October 22, 2026 | John Wise

Evolutionary Ghost Stories: The 98 Percent Zombie

It is high time to let
the evolutionary zombies
rest in their graves

 

The Evolutionary Ghost (98%) vs. the Living Skeleton
How a debunked cliché haunts science,
while data reveals a declining genome

by John D. Wise, PhD

Halloween is the season when the dead walk. In evolutionary biology, however, the truly terrifying apparitions are not ghosts or goblins; they are thoroughly debunked textbook myths that refuse to stay in their graves.

We satirized this intellectual necromancy in our video short, “The Lingering Dead: debunked but still on the syllabus.” In that piece, long-refuted icons, from Ernst Haeckel’s fraudulent embryo drawings to Kettlewell’s dead peppered moths pinned to tree trunks, whisper from the shadows of an institutional hallway: “We live… we live in the curriculum!”

In this second book, Jonathan Wells gives more examples of discredited Darwinian icons that keep rising from the dead.

Just as you turned your back, hoping to get on with life, another undead phantom rises from its grave:

What makes us human? A first atlas of functional DNA Changes offers new clues, (McGill University press release, 15 October 2026). Announcing a new scientific paper by an international research team led by Yizhi Yan and David Gokhman, the university press office wastes no time trotting out the most persistent corpse in the evolutionary gallery:

“Human and chimpanzee genomes are more than 98 per cent identical, but until now we had no way to know which genetic differences had meaningful biological effects,” said first author Yizhi Yan.

To anyone tracking genomics over the last two decades, that statement produces immediate consternation. If you are a genomics researcher publishing in Nature (or for that matter a peer-reviewer or editor at this prestigious scientific journal) shouldn’t you know better?

A Charitable Concession and the T2T Reality

To be charitable, one could forgive earlier researchers for clinging to that soundbite. When the draft chimpanzee genome was announced back in 2005, sequencing technology was primitive by today’s standards. The celebrated 98.8 percent identity figure was obtained through a massive bioinformatic sleight of hand that few who knew acknowledged, and of which almost no one else was aware: researchers compared only single-nucleotide substitutions within short, pre-aligned, highly similar segments of DNA. Everything else was discarded. Insertions and deletions (indels) were ignored, highly repetitive regions, centromeres, copy number variations, and entire swaths of sequence that could not be linearly aligned were tossed out of the calculation.

That excuse, however, vanished with the arrival of Telomere-to-Telomere (T2T) assemblies, first introduced in 2020 and routine by mid-decade. When geneticists sequence complete primate genomes from telomere to telomere, accounting for structural variations, indels, and species-specific duplications, this high-profile illusion dissolved. As independent geneticists like Richard Buggs (and Jeff Tompkins of ICR) pointed out, when you perform a true base-by-base comparison of the actual genomes, the sequence identity drops into the ~85 percent range.

That 15 percent difference represents hundreds of millions of genetic letters, novel genetic architectures, and taxonomically restricted sequences. As we quipped (in Shakespearean English) in our CREV Theater short, “The Tragedy of King Charley”:

“98 percent? Nay, the tale is ancient! Near 15 percent we differ, a genetic chasm! … 400 million base pairs now stand! A canyon wide ‘twixt beast and man!”

To repeat the 98 percent slogan today is not an innocent oversight. It is to deliberately channel an embalmed relic of a bygone era.

Bypassing the PR Gloss: The Paper Behind the Press Release

When you leave the popular press release behind and open the technical paper, titled The gene-regulatory evolution of the human skeleton (Nature, 23 September 2026), the 98 percent slogan disappears. The researchers are not dealing with a tiny handful of minor genetic tweaks. They had to synthesize and screen a massive library of regulatory sequences just to get a handle on what separates human skeletal genomics from that of apes:

“To investigate the regulatory effects of fixed or nearly fixed human-derived substitutions, we designed a library of 732,804 sequences encompassing the human and great ape allele of each cCRE, and assayed their activity using MPRAs… Overall we synthesized 366,402 sequence pairs containing 561,410 single-nucleotide substitutions.”

The authors examined more than half a million human-specific regulatory substitutions fixed across our lineage. Using Massively Parallel Reporter Assays[1] (MPRAs) in fetal cells responsible for building cartilage and scaffolding bones (called chondrocytes) alongside human-ape hybrid allotetraploid cells,[2] the team sought to identify which regulatory switches actually changed gene expression.

What they discovered was not the creative emergence of new evolutionary hardware. Instead, they uncovered a massive, coordinated downregulation of the extracellular matrix (ECM). Specifically, the human lineage displays an extensive, system-wide suppression of glycosaminoglycan (GAG) biosynthesis:

“Integrating the hybrid cells with MPRA measurements produced genome-wide atlases of human-specific changes in cis-regulatory expression, and the sequence variants that drive them. These atlases reveal an extensive rewiring of the extracellular matrix (ECM), including a marked suppression of glycosaminoglycan (GAG) biosynthesis, leading to an approximately three-to-fourfold reduction in joint GAG content in humans compared with non-human apes.”

The Cartilage Shock Absorber

To understand what the researchers found, you need to understand how the skeleton’s high-performance bio-hydraulic shock absorbers work. The extracellular matrix (ECM) is the structural framework of your cartilage, capping the ends of the bones at every moveable joint. Think of it as a dense, three-dimensional mesh of high-tensile steel cables holding the entire pad in shape.

But a structural cage alone can’t absorb repeated impacts; it needs hydraulic resistance and rebound. That is where GAGs come in, acting like microscopic, water-trapping sponges woven directly into the ECM. Because they carry dense negative electrical charges, they drink in water through osmotic pressure and create internal swelling pressure like an over-inflated tire. Every time your foot hits the pavement, you don’t smash bone on bone. The trapped water absorbs the blow, distributes the load, and springs right back.

The 62 Percent Deficit: Engineering or Pathology?

Now, here is the bombshell from the Nature study. When researchers measured the actual cartilage matrix in humans compared to chimpanzees, gorillas, and orangutans, they discovered that across eight different joints – knees, hips, elbows, and fingers – humans have an astonishing 62 percent deficit in their shock-absorbing cushion in comparison to apes.

In clinical medicine, losing just 25 to 38 percent of our cartilaginous matrix means that we suffer from agonizing osteoarthritis, slipped discs, or chronic joint failure. Yet healthy humans walk around with a built-in 62 percent deficit. Our shock absorbers are engineered right at the edge of structural failure.

“The evolutionary change we detected in humans compared with great apes is twice as large (-62%), suggesting that it might have pushed human cartilage towards a threshold of vulnerability – such that all humans carry a baseline GAG deficit that primes the joint for degeneration. Indeed, humans have a substantially higher prevalence of degenerative skeletal diseases than do non-human primates. The most notable difference is observed in osteoarthritis: this highly heritable disease is the most common skeletal disorder in humans… However, in great apes, it is much rarer, even after accounting for age, sex and environment.”

The Adaptationist Trap

How does evolutionary storytelling explain a massive, system-wide drain of our cartilage matrix that leaves our entire species uniquely vulnerable to crippling joint disease? By telling a bedtime story about “evolutionary trade-offs.”

In genetics, when an entire biochemical factory dials down production of necessary equipment across the board, the diagnosis is straightforward: the genetic programming is wearing down. The machinery to build robust shock absorbers is still sitting inside our DNA, but human regulatory switches have dialed down the output. Yet the researchers cannot bring themselves to view this as biological decline:

“Whereas great apes show conservation in the GAG pathway at both the genetic and the phenotypic level, the shift in human GAG biosynthesis shows mixed signatures of selection. On the one hand, some observations are compatible with a relaxation of negative selection, because in the absence of selection, gene expression levels are more likely to decrease than they are to increase… On the other hand, several other observations are more difficult to reconcile with purely relaxed constraint, and instead point to non-neutral, potentially adaptive changes… Regardless of whether these changes reflect adaptation or relaxation of negative selection, they point to a shift in the selective pressures[3] shaping human skeletal biology, with implications for both skeletal morphology and health.” (emphasis added)

Notice the verbal gymnastics. In evolutionary thinking, a loss is never allowed to simply be a loss. If our joint cushioning drops by more than half, it must somehow be an evolutionary upgrade in disguise! We are asked to believe that natural selection deliberately drained our ECM shock absorbers to help sculpt a flatter face, a higher forehead, and an upright posture, accepting chronic, lifelong joint failure as the clever price for walking on two feet.

Does that sound like a good deal to you?

As we saw with the recent collapse of the “obstetrical dilemma” myth, secular anthropology habitually mistakes human vulnerability for evolutionary compromise. When something breaks or wears down, researchers invent an evolutionary just-so story to explain away the physical breakdown. But rather than viewing osteoarthritis as a brilliant evolutionary compromise for walking upright, the actual data points to a familiar reality: an upright, specialized human architecture is operating near its mechanical limits in a world running down under the effects of real-world decay.

The popular press continues to parade the “98 percent” corpse because it protects the comfortable myth of gradual ape-to-human ascent. Meanwhile, the actual laboratory data reveals an unbridgeable architectural gulf, over half a million fixed regulatory changes, and an engineered skeletal framework that defies simplistic Darwinian storytelling.

It is high time to let the evolutionary zombies rest in their graves. And it is high time we stop ignoring that death is the penalty for sin, not the architect of life.

For more examples of dead theories walking, read this book.

Related CEH Reading

Footnotes

[1] Massively Parallel Reporter Assays (MPRAs): Think of non-coding DNA elements as dimmer switches that turn genes up or down. Traditionally, biologists had to test these switches one by one in a slow, laborious process. Pioneered between 2009 and 2012 by marrying high-speed DNA printing with modern sequencing, an MPRA allows researchers to test hundreds of thousands of genetic switches all at once in a single dish. Each test sequence is tagged with a tiny molecular barcode; by simply counting which barcodes get copied into RNA, scientists can instantly measure which switches are active and compare how strongly human switches fire compared to ape versions.

[2] Human–Ape Hybrid Allotetraploid Cells: Before your imagination conjures a creature from a horror movie, rest assured this does not refer to breeding a hybrid animal. It is a strictly microscopic, dish-based laboratory technique. Scientists take a cultured human stem cell and physically fuse its outer membrane to an ape stem cell, combining their chromosomes into a single, shared nucleus. Why do this? To create a perfectly controlled test. Normally, if a human cell and an ape cell behave differently in separate dishes, you cannot easily tell whether the difference is caused by the DNA switches themselves (cis) or by subtle differences in the surrounding cellular bath (trans). By placing the human and ape chromosomes in the exact same cellular room, any difference in output between them must be driven by the hardwired programming of the DNA sequence itself.

[3] I am beginning to grow weary of these evolutionary oxymorons. If “selection pressure” is pressure, then it isn’t selective, and if it is selective, it isn’t pressure. Pressure is a real force, and selection requires a mind. Want a diagnostic tool for spotting Hegelian dialectical thinking? Look for this sort of terminological contradiction.


John Wise received his PhD in philosophy from the University of CA, Irvine in 2004. His dissertation was titled Sartre’s Phenomenological Ontology and the German Idealist Tradition. His area of specialization is 19th to early 20th century continental philosophy.

He tells the story of his 25-year odyssey from atheism to Christianity in the book, Through the Looking Glass: The Imploding of an Atheist Professor’s Worldview (available on Amazon). Since his return to Christ, his research interests include developing a Christian (YEC) philosophy of science and the integration of all human knowledge with God’s word.

He has taught philosophy for the University of CA, Irvine, East Stroudsburg University of PA, Grand Canyon University, American Intercontinental University, and Ashford University. He currently teaches online for the University of Arizona, Global Campus, and is a member of the Heterodox Academy. He and his wife Jenny are known online as The Christian Atheist with a podcast of that name, in addition to a YouTube channel: John and Jenny Wise.

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