Monday, March 9, 2026

PET 2 LEVIN

 

Planaria Memory & Xenobots: Detailed Breakdown


PART 1: PLANARIA AND MORPHOLOGICAL MEMORY

Background: Why Planaria?

Planaria (Dugesia japonica and related species) are freshwater flatworms with an almost absurd capacity for regeneration. Cut one into 200 pieces, and you get 200 new worms. Every fragment — even a tiny tail segment with no brain tissue whatsoever — will regenerate a complete, properly oriented animal.

This alone is remarkable. But Levin's lab discovered something far stranger.


The Classic Setup: Polarity and Bioelectrics

Every planarian has a defined anterior-posterior axis — a head end and a tail end. This polarity is maintained by a gradient of bioelectric signals across the body, particularly involving:

  • Gap junctions — protein channels that directly connect neighboring cells, allowing ions and small molecules to flow between them
  • Ion pumps (especially V-ATPase, an H⁺ pump) that create voltage differentials across tissues
  • Neurotransmitters like serotonin that act as patterning signals even outside the nervous system

The key insight: this bioelectric pattern is not just a readout of genetic instructions. It is itself instructive — it tells cells where they are and what they should become. It functions like a map or a blueprint held in electrical form across the tissue.


The Experiment: Erasing and Overwriting the Memory

Here is what Levin's lab did, step by step:

Step 1 — Cut the worm A planarian is cut transversely, producing a head fragment and a tail fragment. Normally:

  • The head fragment regenerates a new tail at the wound site
  • The tail fragment regenerates a new head at the wound site

This is normal polarity — the body "knows" which end is which.

Step 2 — Pharmacological intervention during regeneration While the tail fragment is regenerating (the critical window is the first ~24 hours after cutting), researchers bathe it in octanol — a drug that blocks gap junctions, severing the bioelectric communication between cells.

What happens? The tail fragment, unable to read its normal bioelectric positional information, sometimes regenerates a head at both ends — a two-headed worm. The chemical disruption confused the tissue's sense of axis.

Step 3 — The crucial discovery: the memory persists Here is where it gets extraordinary. After the two-headed worm is fully regenerated, researchers:

  • Remove the drug (restore normal chemical environment)
  • Allow the worm to live normally for weeks
  • Then cut it again — no drugs, no intervention

A normal worm, cut in this state, would regenerate with correct polarity. But these worms regenerated two-headed worms again — even though no drug was present during the second regeneration.

The altered bioelectric state had become self-sustaining. The tissue had "learned" a new body plan and perpetuated it across generations of regeneration without any genetic change and without ongoing chemical intervention.


What Is Actually Being "Remembered"?

This is not memory in the neural sense — there are no neurons storing an engram. What's happening is:

Bioelectric state as memory: The pattern of ion flows, membrane voltages, and gap junction connectivity across the tissue constitutes a stable attractor state — a self-reinforcing electrical pattern that cells maintain and propagate when they divide and communicate.

Think of it like a standing wave in a medium. The wave pattern persists not because any single molecule holds it, but because the dynamics of the system continuously recreate it. When you cut the worm, the new cells inherit the electrical environment of their neighbors and reproduce the same pattern.

The "Body Plan Morphogenetic Field": Levin frames this in terms of a morphogenetic field — a distributed representation of target anatomy encoded not in DNA sequence but in the bioelectric state of the tissue. DNA provides the parts list (what proteins are available); the bioelectric field provides the blueprint (how those parts should be assembled).

The planaria experiments show this blueprint can be:

  • Altered (by disrupting gap junctions)
  • Stabilized in its new form (self-reinforcing dynamics)
  • Transmitted across regenerative events (new cells adopt the electrical state of existing cells)
  • Maintained without ongoing external signals

The Deeper Implication

This means the worm's body plan is not simply computed fresh from the genome each time. There is a second layer of information — above the genome, encoded in bioelectric dynamics — that stores and propagates the target morphology.

Levin uses the analogy of computer hardware vs. software: the genome is the hardware (fixed, inherited), but the bioelectric pattern is the software running on top — and that software can be edited, corrupted, and rewritten independently of the hardware.

This is teleological in a deep sense: the tissue is not just following chemical gradients passively. It is actively comparing its current state to a stored target state and making corrections. When that target state is altered, the corrections drive toward the new target.



PART 2: XENOBOTS — LIVING MACHINES AND KINEMATIC SELF-REPLICATION

What Are Xenobots?

Xenobots were first reported in 2020, created collaboratively by Levin's lab at Tufts and Josh Bongard's computational lab at the University of Vermont.

They are made from Xenopus laevis — the African clawed frog — specifically from ectodermal cells (cells that would normally become skin) harvested from early embryos.

Crucially: these cells are removed from their normal developmental context. They are no longer receiving the chemical signals that would tell them "you are part of a frog embryo, become skin." Freed from that context, they exhibit novel, emergent behaviors that no frog has ever exhibited — and that were never programmed.


Stage 1: Self-Assembly and Spontaneous Organization

When ectodermal cells are harvested and placed in a dish as a loose aggregate, something remarkable happens over ~24 hours:

  • The cells do not die (as isolated cells typically would)
  • They reorganize — moving, adhering, and arranging themselves into a compact, roughly spherical or ovoid body
  • Cells with cilia (hair-like projections, normally used to move mucus across skin) reorient those cilia outward, creating a coordinated propulsion system
  • The resulting structure, roughly 500–700 micrometers across, moves through fluid in a directed way

No blueprint was given. No morphogen gradient was applied. The cells used their existing genetic toolkit — developed for one purpose (being frog skin) — to build a novel functional organism suited to their new context.

This is a profound demonstration of context-dependent agency: the cells are not executing a fixed program, they are solving the problem of "what should I be?" given their current situation.


Stage 2: The AI-Designed Body Plans

In the 2020 paper, Bongard's team used an evolutionary algorithm running on a supercomputer to design optimal xenobot body shapes for specific tasks (like moving in a particular direction or pushing objects).

The process:

  1. Simulate thousands of random arrangements of frog cells in silico
  2. Evaluate which arrangements best accomplish a target behavior
  3. Select the best performers, mutate them, repeat
  4. Take the winning design and build it in real life using microsurgery on real frog cells

Strikingly, the real xenobots closely matched the behavior of their simulated counterparts — confirming that the cells were indeed executing coherent, predictable behaviors, not random activity.

But the spontaneously self-assembled xenobots (without AI design) were arguably more interesting, because they required no external design at all.


Stage 3: Kinematic Self-Replication (2021)

The 2021 PNAS paper reported something that genuinely shocked the scientific community.

The setup: Researchers placed xenobots in a dish containing a large supply of loose, dissociated frog cells — essentially raw cellular material.

What happened: The xenobots spontaneously began to gather the loose cells, sweeping them together into piles using their ciliary motion.

Those piles of gathered cells then self-assembled into new xenobots.

Those new xenobots could, in turn, gather more loose cells and produce another generation.

This is kinematic self-replication — replication through motion and behavior rather than through chemical template copying (like DNA replication). It is an entirely different category of reproduction from anything previously documented.


Why "Kinematic" Is the Key Word

In biology, replication almost always means template-directed chemical copying: DNA unzips, complementary bases are added, you get two copies. The information is in the molecule.

Kinematic self-replication is different: the information is in the behavior and shape of the organism. The xenobot "replicates" not by copying its molecules but by doing things in the world — moving, gathering, organizing — that result in a new entity similar to itself.

This is closer to how a whirlpool "reproduces" (by creating conditions for new whirlpools) than how a bacterium reproduces. But xenobots are vastly more complex and directed.

Von Neumann had theorized kinematic self-replicators in the 1940s as a thought experiment. Xenobots are the first biological instantiation.


The Shape Discovery: C-Shape Matters

A critical finding from the 2021 work: the default spherical xenobots replicate poorly — they gather some cells but the process is inefficient and quickly dies out after 1–2 generations.

When the AI evolutionary algorithm was again applied — this time to optimize for replication efficiency — it discovered that a C-shaped or pac-man-shaped xenobot was dramatically more effective at gathering and corralling loose cells into the interior of the C, where they could aggregate and self-organize.

This C-shape does not exist in frog biology. It was discovered by an algorithm, then built, then confirmed to work. The frog cells — never having "intended" to replicate this way — executed the replication faithfully when given the right body shape.


The Philosophical Payload

The xenobot work raises several deeply unsettling and important questions:

1. What is an organism? Xenobots are made of frog cells, carry frog DNA, but are not frogs. They have never existed in nature. They exhibit goal-directed behavior (moving, replicating) that no frog exhibits. Are they a new species? A new category of being?

2. What is reproduction? Xenobots don't pass on genetic information to their "offspring" — the daughter xenobots have the same genome as the parent, inherited from the original frog embryo. What's being transmitted is form and behavior, not genetic novelty. This blurs the line between reproduction and construction.

3. Where does the "goal" come from? The xenobots were not programmed to gather cells and replicate. This behavior emerged from the interaction of cell-level properties (cilia, adhesion, motility) with the physical environment. The goal-directedness is real — measurable, reproducible — but it wasn't designed in. It emerged.

Levin argues this shows that agency and teleology can be genuine properties of matter — not imposed from outside by a designer or genome, but arising from the dynamics of sufficiently complex, self-organizing systems.


Connecting Planaria and Xenobots: The Unified Theme

Both experiments point to the same conclusion:

PlanariaXenobots
SubstrateAdult flatworm tissueEmbryonic frog cells
Context changeChemical disruption of polarity signalsRemoval from embryonic context
ResponseAdopt and maintain new body planSelf-assemble novel body plan
Memory/GoalBioelectric target stateEmergent morphogenetic goal
Key findingMorphological memory above genomeGoal-directed behavior without programming

In both cases, cells are doing something more than executing a genetic program. They are reading their environment, computing a response, and pursuing a target state — even when that target state has been altered or is entirely novel.

This is Levin's core claim made flesh: biology is cognitive all the way down, and the gap between "mere matter" and "minded agent" is not a gap at all, but a continuum we are only beginning to measure.

Michael Levin - teleology in biology

 Michael Levin is a developmental biologist at Tufts University whose work is reshaping how we think about intelligence, agency, and goal-directedness in living systems. Here's an overview of his revolution:

The Core Idea: Intelligence Is Not Brain-Specific

Levin argues that cognition and agency are substrate-independent — they don't require neurons or brains. Instead, any system capable of pursuing goals, remembering states, and problem-solving in a flexible way deserves to be called "intelligent" in some meaningful sense.

Teleology Rehabilitated

Classical science largely banished teleology (goal-directedness) from biology after Descartes and the mechanistic revolution. Levin is helping bring it back — not as mysticism, but as a legitimate, measurable property of biological systems.

His key insight: organisms at every scale — from single cells to tissues to whole animals — exhibit goal-directed behavior toward specific target states (like a body plan or organ shape). This isn't metaphor; it's observable, manipulable, and quantifiable.

The Planaria & Xenobot Experiments

Levin's lab produced some of the most striking evidence:

  • Planaria (flatworms) remember their head-tail polarity even when cut and regrown in reversed chemical environments — their tissues "remember" a target morphology.
  • Xenobots — living robots made from frog stem cells — spontaneously self-assembled, moved, and even exhibited a crude form of kinematic self-replication, a behavior no one programmed.
  • Anthrobots (2023) — made from human lung cells — self-assembled and promoted neural repair in lab dishes, again without explicit programming.

These organisms pursue goals that weren't hardcoded — they compute solutions to problems using biological hardware.

The Cognitive Light Cone

One of Levin's most important theoretical contributions is the "cognitive light cone" — the idea that different agents have different scales over which they integrate information and pursue goals:

  • A bacterium has a tiny cognitive light cone (milliseconds, micrometers)
  • A brain has a larger one (years, the whole body)
  • A society or ecosystem might have an even larger one

This gives a continuous, non-binary framework for intelligence — dissolving the sharp line between "dumb matter" and "minded beings."

Bioelectricity as the Medium

Levin's lab focuses heavily on bioelectric signaling — electrical patterns across cell membranes (not just in neurons) that encode positional and morphogenetic information. These signals function like a body-wide "blueprint memory":

  • Disrupting bioelectric patterns causes radical morphological changes (e.g., making flatworms grow two heads)
  • Restoring correct bioelectric patterns can cure cancer in tadpoles or induce limb regeneration

Bioelectricity appears to be a proto-cognitive medium — a way that non-neural tissue computes and communicates goal-states.

Implications Across Fields

Philosophy of mind: Mind and agency exist on a continuum; we need new frameworks beyond neurocentric consciousness theories.

AI & robotics: True intelligence may require goal-directedness and embodiment, not just computation. Levin collaborates with Daniel Dennett and others on these questions.

Medicine: Cancer may be a failure of cellular agency — cells "forgetting" their role in the larger collective and reverting to unicellular selfishness. Treating it bioelectrically rather than just chemically is an active research direction.

Ethics: If intelligence is a spectrum, where does moral consideration begin? Levin takes this seriously — his lab has published on the ethics of creating novel cognitive entities (like xenobots).

The Deeper Philosophical Bet

Levin is essentially arguing that teleology is real, physical, and measurable — that "what is this system trying to do?" is a legitimate scientific question at every scale of biology. This cuts against both naive mechanism and mystical vitalism, carving out a rigorous third path: computational teleology, where goal-states are physically encoded and causally efficacious.

It's one of the most ambitious research programs in contemporary science — simultaneously experimental, theoretical, and deeply philosophical.

OW LITTLE WE UNDERSTAND. READ THE NEXT TWO POSTS TO ENTER A NEW WORLD OF BIOLOGY

Tuesday, February 3, 2026

Worth investigation

 Terminal lucidity

From Justapedia, where neutrality meets objective truth

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Terminal lucidity, also known as paradoxical lucidity, rallying or the rally, is an unexpected return of mental clarity and memory, or suddenly regained consciousness that occurs in the time shortly before death in patients with severe psychiatric or neurological disorders.[1][2][3] This condition has been reported by physicians since the 19th century.

History

Several case reports in the 19th century described the unusual condition of an improvement and recovery of the mental state in patients days or weeks before death. William Munk, for instance, in 1887 called the phenomenon "lucidity before death".[4] According to historical reviews headed by the biologist Michael Nahm, who also has an interest in mediumship and near-death experiences,[5] the phenomena have been noted in patients with diseases which cause progressive cognitive impairment, such as Alzheimer's disease, but also schizophreniatumorsstrokesmeningitis, and Parkinson's disease.[6][7][8] However, terminal lucidity is not currently listed as a medical term.[9]

According to Nahm, it may be present even in cases of patients with previous mental disability.[10] Nahm defines two subtypes: one that comes gradually (a week before death), and another that comes rapidly (hours before death), with the former occurring more often than the latter. There may be plenty of cases reported in literature, although the phrase terminal lucidity was coined in 2009.[11] Interest in this condition, which dwindled during the 20th century, has been reignited by further studies.[4] A 2020 research screened for what the authors preferred to call "paradoxical lucidity", a general term for unexpected remissions in dementias, independent of whether it followed a terminality process or not; it found strong association of the condition as a near-death phenomenon and stated that it can overlap the concept of "terminal lucidity" in some cases.[6] Such a paradoxical condition is considered a challenge to the irreversibility paradigm of chronic degenerative dementias such as Alzheimer's.[12]

Causes

The earliest attempt at explanation was issued by Benjamin Rush in 1812, which proposed the hypothesis that a reawakening could be due to a nervous excitation caused by pain or fever, or else because of dead blood vessels, released by a leakage of water in the brain chambers. Johannes Friedreich, in 1839, proposed that the factors causing impairments may be reversed shortly before death, analogous to the reabsorption in terminal patients with hydrocephalus, and that high fever may be a cause of it. According to Macleod (2009)[13] in his observations, explanative causes could not be found for the variety of cases, but it was suggested that due to the modern pharmacology in terminal cases, the condition may be less common today.[4] A recent proposed mechanism includes a non-tested hypothesis of neuromodulation, according to which near-death discharges of neurotransmitters and corticotropin-releasing peptides act upon preserved circuits of the medial prefrontal cortex and hippocampus, promoting memory retrieval and mental clarity.[14]

References

1.   Koczanowicz, Leszek (2020). "Chapter 12 - The Anxiety of Clairvoyance: Terminal Lucidity and the End of Culture". Anxiety and Lucidity: Reflections on Culture in Times of Unrest. Routledge. pp. 162–198. ISBN 978-0367218232.

2.   Mendoza, Marilyn A. "Why Some People Rally for One Last Goodbye Before Death". Psychology Today (blog). Retrieved 26 August 2019.

3.   Bursack, Carol Bradley. "When Loved Ones Rally Before Death". AgingCare. Retrieved 26 August 2019.

4.   Chiriboga-Oleszczak, Boris Alejandro (2017-03-28). "Terminal lucidity". Current Problems of Psychiatry. 18 (1): 34–46. doi:10.1515/cpp-2017-0003ISSN 2353-8627.

5.   Michael Nahm

6.   Batthyány, Alexander; Greyson, Bruce (2020-08-27). "Spontaneous remission of dementia before death: Results from a study on paradoxical lucidity". Psychology of Consciousness: Theory, Research, and Practice. 8: 1–8. doi:10.1037/cns0000259ISSN 2326-5531S2CID 225192667.

7.   Nahm, Michael; Greyson, Bruce (December 2009). "Terminal lucidity in patients with chronic schizophrenia and dementia: a survey of the literature". Journal of Nervous and Mental Disease. 197 (12): 942–944. doi:10.1097/NMD.0b013e3181c22583ISSN 1539-736XPMID 20010032.

8.   Nahm, Michael; Greyson, Bruce; Kelly, Emily Williams; Haraldsson, Erlendur (July–August 2012). "Terminal lucidity: a review and a case collection". Archives of Gerontology and Geriatrics. 55 (1): 138–142. doi:10.1016/j.archger.2011.06.031ISSN 1872-6976PMID 21764150.

9.   Webster Medical Dictionary

10.                     Nahm, M.; Greyson, B. (2014). "The Death of Anna Katharina Ehmer: A Case Study in Terminal Lucidity". OMEGA. 68 (1): 77–87. doi:10.2190/OM.68.1.ePMID 24547666S2CID 1265185.

11.                     Bering, Jesse (2017). "One Last Goodbye: The Strange Case of Terminal Lucidity". Scientific American Blog Network.

12.                     Mashour, George A.; Frank, Lori; Batthyany, Alexander; Kolanowski, Ann Marie; Nahm, Michael; Schulman-Green, Dena; Greyson, Bruce; Pakhomov, Serguei; Karlawish, Jason; Shah, Raj C. (2019-06-19). "Paradoxical lucidity: A potential paradigm shift for the neurobiology and treatment of severe dementias". Alzheimer's & Dementia. 15 (8): 1107–1114. doi:10.1016/j.jalz.2019.04.002ISSN 1552-5260PMID 31229433.

13.                     Macleod, AD (December 2009). "Lightening up before death". Palliative & Supportive Care. 7 (4): 513-516. doi:10.1017/S1478951509990526PMID 19939314.

14.                     BostanciklioÄŸlu, Mehmet (January 2021). "Unexpected awakenings in severe dementia from case reports to laboratory". Alzheimer's & Dementia. 17 (1): 125–136. doi:10.1002/alz.12162ISSN 1552-5279PMID 33064369S2CID 222840626.

 

Saturday, November 22, 2025

Important update on the Human-chimpanzee DNA fiasco

 Are human populations 99.9% identical?

How a correct finding has been incorrectly interpreted.

Nov 21

https://www.aporiamagazine.com/p/are-human-populations-999-identical

 

Written by Peter Frost.

You’ve probably heard that humans and chimpanzees are genetically 98 to 99% the same. 

You’ve probably also heard that human populations are 99.9% the same. The second finding

 has often been cited, for example by Hillary Clinton. In a speech to high school graduates,

 the former First Lady mentioned “genetic research that shows humans are 99.9 percent the same”.

The differences in how we look — in our skin color, our eye color, our height — stem from 

just one-tenth of 1 percent of our genes. And the differences among us — our cultures, our 

religious beliefs, the music we like — it is all so small a distinction in our sea of common humanity.

Of course, one tenth of one percent is still a lot. In a post criticizing Clinton’s speech, anthropologist 

John Hawks observed that “one-tenth of 1 percent of 3 billion is a heck of a large number —

 3 million nucleotide differences between two random genomes” (Hawks, 2007). He added, 

“We differ by one-tenth of 1 percent of nucleotides, this is enough to make coding differences 

 in a large fraction of our genes.”

In other words, the 0.1% figure is not the percentage of genes that are different. It’s the percentage 

of individual nucleotides that are different. A single gene is a long chain of nucleotides, often

 a very long one, and a single nucleotide mutation can significantly alter how the entire gene works. 

In theory, then, each and every human gene could work differently from one population to another.

Moreover, as Hawks himself showed in a study published the same year, at least 7% of the human 

genome has changed over the last 40,000 years — mostly the last 10,000 (Hawks et al., 2007). 

This was when our ancestors were spreading over the globe and differentiating into today’s geographic

 populations. Those populations cannot all share the 

same 7% change.

Clearly, 0.1% isn’t the fraction of genes that differ among human populations. The true figure is certainly

 larger. Again, each and every gene could differ among human populations by 0.1%, and such a 

 difference could affect how each and every one functions. Also, genes do not differ solely in 

nucleotide sequences. They also differ in the way those sequences are arranged on the chromosomes. 

The same sequence may be repeated consecutively or it may be copied and inserted somewhere else.

 Such rearrangements can likewise affect how a gene functions. “Structural variations, such as 

copy-number variation and deletions, inversions, insertions and duplications, account for much more human genetic variation than single nucleotide diversity” (Wikipedia, 2025).

This structural variation became apparent during the first complete sequencing of a human genome:

Of the 4.1 million variations between chromosome sets, 3.2 million were SNPs, while nearly 

one million were other kinds of variants, such as insertion/deletions (“indels”), copy number variants, 

block substitutions, and segmental duplications. While the SNPs outnumbered the non-SNP types of 

variants, the non-SNP variants involved a larger portion of the genome. This suggests that human-to-human variation is much greater than previously thought. (Phys.org, 2007; see also Levy et al., 2007)

If we return to comparing humans and chimpanzees, we can measure the total genetic difference

 between them by looking at what the genes make, i.e., proteins. The two species differ in about 80% 

of their proteins — a figure far higher than the 1 to 2% difference in their nucleotide sequences

 (Glazko et al., 2005).

Even this 80% figure is not the whole story. Some genes regulate how other genes are expressed, 

often thousands of others, and thus play a key role in growth and development. These “regulator” 

genes are much fewer in number than other genes but far greater in their effects. Plus, they differ 

much more between humans and chimpanzees than other genes do. Whereas the two species are 

almost identical in the nucleotide sequences of their genes and the amino acid sequences of their 

proteins, and relatively similar in the proteins that make up their tissues, they differ radically 

in the way their tissues grow and develop, notably the neural tissues of the brain.

This was already clear to two researchers, Mary-Claire King and A.C. Wilson, when, half a century ago,

 they discovered the startling similarity of nucleotide sequences and amino acid sequences between 

humans and chimpanzees:

The molecular similarity between chimpanzees and humans is extraordinary because they differ far 

more than sibling species in anatomy and way of life. Although humans and chimpanzees are rather 

similar in the structure of the thorax and arms, they differ substantially not only in brain size but also

 in the anatomy of the pelvis, foot, and jaws, as well as in relative lengths of limbs and digits. Humans

 and chimpanzees also differ significantly in many other anatomical respects, to the extent that nearly 

 every bone in the body of a chimpanzee is readily distinguishable in shape or size from its human 

counterpart. Associated with these anatomical differences there are, of course, major differences in 

posture, mode of locomotion, methods of procuring food, and means of communication. Because of 

these major differences in anatomy and way of life, biologists place the two species not just in separate

 genera but in separate families …

The contrasts between organismal and molecular evolution indicate that the two processes are to a large

 extent independent of one another. Is it possible, therefore, that species diversity results from molecular 

changes other than sequence differences in proteins? … According to this hypothesis, small differences 

in the time of activation or in the level of activity of a single gene could in principle influence 

considerably the systems controlling embryonic development. The organismal differences between 

 chimpanzees and humans would then result chiefly from genetic changes in a few regulatory systems, 

while amino acid substitutions in general would rarely be a key factor in major adaptive shifts. (King & Wilson, 1975, pp. 113–114)

Genetic distance between humans and chimpanzees, compared to genetic distances in other taxa.

 (King & Wilson, 1975, p. 113)

In this context, the two researchers were thinking not only about the human-chimpanzee difference 

but also about the differences within our species:

[The human-chimpanzee] distance is 25 to 60 times greater than the genetic distance between human 

races. In fact, the genetic distance between Caucasian, Black African, and Japanese populations is less 

than or equal to that between morphologically and behaviorally identical populations of other species. (King & Wilson, 1975, p. 113)

The above paragraph appears in the middle of a discussion about the human-chimpanzee genetic d

istance, and its paradoxical smallness. In fact, the two researchers highlight this paradox right after:

However, with respect to genetic distances between species, the human-chimpanzee D value is e

xtraordinarily small, corresponding to the genetic distance between sibling species of Drosophila or 

 mammals. Nonsibling species within a genus … generally differ more from each other, by e

lectrophoretic criteria, than humans and chimpanzees. The genetic distances among species from 

different genera are considerably larger than the human-chimpanzee genetic distance. 

(King & Wilson, 1975, p. 113)

How should we measure the genetic distance between two human populations? There is no easy answer

 because few species resemble our own. Our species is unusual in that it evolved rapidly at the very 

time it was splitting up into populations across different environments — not only natural environments 

from the equator to the arctic but also an ever-wider range of cultural environments. In fact, this entry 

into so many environments largely explains the concurrent rapidity of human genetic evolution. 

Natural selection has thus shaped human populations in highly divergent ways (Akbari et al., 2024

Cochran & Harpending, 2009Frost, 2023aHawks et al., 2007Kuijpers, et al., 2022

Libedinsky et al., 2025Piffer & Kirkegaard, 2024Rinaldi, 2017).

In such a situation, differences in selection contribute much more to genetic diversity between 

populations than to genetic diversity within populations. Keep in mind that natural selection causes 

a population to diversify only in certain limited cases (e.g., frequency-dependent selection). In most 

cases, a population is diversified by stochastic processes of little adaptive consequence, since everybody

 is adapting to the same environment and the same selection pressures.

We thus return to the same paradox: Fst is relatively low in our species even though human populations 

differ much more anatomically than do most sibling species in the animal kingdom. As Charles Darwin 

noted, a naturalist would consider some human groups to be “as good species as many to which he had 

been in the habit of affixing specific names.” The paradox exists because humans split rapidly to 

colonize highly divergent environments, with the result that genetic diversity between populations is 

 much more consequential than genetic diversity within populations. We are therefore comparing apples

 to oranges when we calculate human Fst (Darwin, 1936 [1888], pp. 530-531; King & Wilson, 1975;

 Frost, 2023b).

What’s more, relatively little of our evolution has been at the level of nucleotide sequences or amino 

acid sequences. It has been largely at a higher level — the duplication, rearrangement and regulation of 

 existing DNA in new ways (Yoo et al., 2025). This point came up in a recent discussion on X:

The widely cited Chimpanzee-Human 98-99% DNA similarity figures refer exclusively to nucleotide s

equence similarity within alignable genomic regions, which become misleading when portrayed as the t

otal amount of DNA shared. While this metric is important, as it highlights the strength of the 

evolutionary constraints within the protein-coding and non-coding sequences found in alignable r

egions, it ignores the structural and regulatory differences that are key for shaping the phenotypic 

differences between Chimpanzees and Humans. When combining these metrics, total 

 Chimpanzee-Human DNA similarity figures drop to ~84.7% (Origins Unveiled, 2025)

Admittedly, I have no idea how the author combined these metrics.

I don’t blame Hillary Clinton for drawing the wrong conclusion from the 99.9% estimate, but I’m less 

forgiving toward those who have silently gone along with this fallacy while knowing better. Two 

decades ago, John Hawks pointed out its flaws in a post criticizing Hillary’s speech. The post remained 

on his website until he deleted it in 2021 — when many American academics got the memo that Hillary 

had been right all along… on this issue and on any other.

“Nice research lab you have there. Pity if anything happened to it.”

When academics choose the path of silence, and withhold their objections, they help create a fake 

consensus that ultimately brings academia into disrepute.

Peter Frost has a PhD in anthropology from Université Laval. His main research interest is the

role of sexual selection in shaping highly visible human traits. Find his newsletter here.


References

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