Thursday, 18 June 2026

Malevolent Design - We Have The Ability To Regenerate An Amputated Limb - But It's Turned Off And Hidden

A conceptual graphic shows how growth factors BMP2 and FGF2 are applied to the injury site to stimulate tissue regeneration, highlighting new research into restoring damaged digits.
Credit: Melissa Bristow/Texas A&M University College of Veterinary Medicine and Biomedical Sciences

A–C Representative longitudinal sections and μCT images (insets) of control and FGF2 treated digits 21 days post treatment (DPT). A Control BSA treated digits do not display a regenerative response and are truncated. B The majority of FGF2 treated digits are truncated without displaying a regenerative response. C A minority of FGF2 treated digits produce an ectopic skeletal element distal to the amputation that articulates with the stump bone.

What if humans could regrow tissue? Texas A&M study moves science closer – Texas A&M Stories.

Although the Discovery Institute and its Fellows who advocate for Intelligent Design are usually careful not to identify their putative “intelligent designer” explicitly with the God of the Christian Bible, the dog-whistle signals they use leave their target audience in little doubt. The designer is understood to be the Christian god, merely relabelled for legal and tactical convenience. That being so, and if that god were actively interfering in the design and evolution of living systems — with humans as the supposed pinnacle of creation and occupying a special place in it — we might reasonably expect humans to have been given the best design available.

Instead, nature looks exactly as an unplanned evolutionary process would lead us to expect: a patchwork of compromises, contingencies and inherited limitations. As I describe in my book, The Malevolent Designer: Why Nature's God is not Good, humans are remarkable in some respects, particularly in our relatively large brains and consequent cognitive abilities, but in most other respects we are not especially impressive. We are not the strongest animals, nor the fastest. Birds of prey have far better eyesight; barn owls and dogs have far better hearing in relevant ranges; dogs have a vastly superior sense of smell; elephants and some other long-lived animals have evolved impressive cancer-resistance mechanisms; and the immune systems of many bats are tuned in ways that make our own look distinctly ordinary.

But perhaps the most striking contrast is in the ability of some animals to regenerate lost or damaged body parts. Several species can regenerate structures that humans simply cannot replace. Salamanders can regrow limbs; fish can replace fins and repair tissues that would leave mammals permanently damaged; and some invertebrates can regenerate astonishing portions of the body. Yet, noticeably, all the prayers, incantations and appeals to divine mercy have never once been shown to regrow an amputated human limb, replace a lost eye, repair a severed spinal cord, or restore dead heart muscle after an infarction. Nor do we see cancerous sections of colon removed by surgery obligingly regrowing as healthy tissue in answer to prayer. These are not impossible biological feats in principle; they are just things our lineage cannot normally do.

Now researchers from Texas A&M College of Veterinary Medicine and Biomedical Sciences (VMBS) have found something that should be even more disturbing for Intelligent Design creationists. In a paper recently published in Nature Communications, they report that non-regenerating mouse digit wounds can be induced to move part-way towards regeneration. In other words, the relevant mammalian cells may not be entirely incapable of regeneration; their capacity appears to be suppressed or obscured by the normal wound-healing response. Creationists who reject the evolutionary explanation now need to explain why an intelligent, omnibenevolent designer would leave mammals, including humans, with a latent capacity for regeneration, while allowing that capacity to be overridden by scarring.

The researchers’ explanation makes perfect sense as the outcome of a utilitarian, unplanned evolutionary process. In mammals, rapid wound closure by scar-forming fibroblasts can be life-saving. A quick patch reduces blood loss, closes a route for infection and gives the injured animal a better chance of surviving long enough to reproduce. Regeneration, by contrast, is slower and more complex. Evolution has no foresight and no obligation to produce perfection; it merely preserves what works well enough under the circumstances. The injury is patched up with a near-enough-is-good-enough solution, and the animal lives to pass on its genes.

That, of course, should not have been beyond the wit of an intelligent designer to improve upon. A competent designer could have given us both abilities: rapid wound closure to prevent fatal bleeding and infection, followed by orderly regeneration of the missing structures. Instead, we have the familiar evolutionary compromise: survival first, elegance later — and often not at all.

The problem centres on fibroblast cells, which can follow different developmental routes. In ordinary mammalian wound-healing, they rapidly close the wound and form scar tissue. In strongly regenerative animals, similar cells can organise into a blastema — a temporary structure that seals the wound while also providing the cellular basis for rebuilding missing tissues. The Texas A&M team showed that, after the wound had first closed, applying fibroblast growth factor 2 (FGF2), followed later by bone morphogenetic protein 2 (BMP2), could redirect the response. The result was imperfect regeneration, but it included bone, tendon, ligament and joint-like structures.

The conclusion is not that humans are about to start regrowing limbs, nor that a mouse digit is the same as a human arm or leg. It is more interesting than that. The potential for regeneration in mammals may not have vanished completely. It may still be there, hidden beneath the faster, rougher, scar-forming response that natural selection has favoured. For creationists, that raises the awkward question of why their supposed designer would equip other animals with regenerative abilities, leave traces of the same capacity in mammals, and then arrange matters so that, when humans most need it, the system normally fails.

Background^ Animals With Remarkable Powers of Regeneration. Regeneration is the ability to replace lost or damaged cells, tissues, organs or even whole body parts. Humans can regenerate some tissues, such as skin and parts of the liver, but our ability to replace complex structures such as limbs, eyes, spinal cord tissue or heart muscle is very limited. Other animals show what biology can do when evolution has taken a different route.
  • Axolotls and other salamanders – Among the champions of vertebrate regeneration. Axolotls can regenerate limbs, tail, spinal cord, parts of the heart and other complex tissues, usually without the heavy scarring seen in mammals.
  • Zebrafish – These small freshwater fish can regenerate fins and can also repair damage to the heart, retina, optic nerve, spinal cord and other tissues. This makes them important laboratory models for regenerative medicine.
  • Planarian flatworms – Famous for their almost absurd powers of regeneration. A small fragment of a planarian can regenerate into a complete animal, because these worms contain abundant adult stem cells called neoblasts.
  • Hydra – These tiny freshwater relatives of jellyfish can regenerate whole bodies from pieces of tissue. Their simple body plan and continuously active stem cells make them useful for studying how animals organise and rebuild themselves.
  • Sea stars – Commonly called starfish, many sea stars can regrow lost arms. In some species, a detached arm can even regenerate into a new individual, although most require at least part of the central disc to be present.
  • Sea cucumbers – Some sea cucumbers can expel parts of their internal organs as a defensive response and then regenerate them. The digestive tract, in particular, can be rebuilt after evisceration.
  • Lizards – Many lizards can shed their tails to escape predators and later grow a replacement. The new tail is not usually a perfect copy of the original, but it is functional enough for survival.
  • Crabs and other crustaceans – Many crustaceans can regenerate lost legs, claws or antennae over successive moults. A missing claw may return small at first and then increase in size after further moulting.
  • African spiny mice – Unlike most mammals, these mice can heal large skin wounds with little scarring and can regenerate structures in damaged ears, including skin, hair follicles and cartilage.
  • Deer – Male deer shed and regrow antlers annually. Antlers are among the fastest-growing organs in mammals and show that even mammals retain some impressive, though highly specialised, regenerative abilities.

These examples do not suggest that regeneration is magic, nor that every animal should be expected to regenerate every structure. They show instead that regenerative capacity varies widely across the animal kingdom. Evolution has produced many different compromises between rapid wound closure, scar formation, infection control, energy cost and the slower, more complex process of rebuilding lost tissue. Humans sit on the poor-regeneration side of that trade-off.
The paper in Nature Communications was accompanied by a press release from Texas A&M by Camryn Haines:
What if humans could regrow tissue? Texas A&M study moves science closer
Researchers have successfully regenerated skeletal and connective tissue — even if not perfectly formed — demonstrating the next, critical step in limb regeneration.
For centuries, the inability to regrow lost body parts has been considered a defining limitation of humans and other mammals. While animals like salamanders can regenerate entire limbs, humans are left with scar tissue.

But new research from the Texas A&M College of Veterinary Medicine and Biomedical Sciences (VMBS) suggests that this limitation may not be permanent. Instead, the capacity for regeneration may still exist — hidden within the body’s normal healing process.

Why some animals can regenerate and others, particularly humans, can’t is a big question that has been asked since Aristotle. I’ve spent my career trying to understand that.

Professor Dr. Ken Muneoka, senior author
Department of Veterinary Physiology and Pharmacology
College of Veterinary Medicine and Biomedical Sciences
Texas A&M University, TX, USA.

In their study, published in Nature Communications, Muneoka and his colleagues detail a newly developed two-step treatment that led to the regeneration of bone, joint structures and ligaments. While the results were imperfect, the team believes this approach could be used more immediately to reduce scarring and improve tissues repair after amputations.

Redirecting the body’s natural response

In mammals, injuries typically trigger fibrosis, a process in which fibroblast cells rapidly close the wound and form scar tissue. This response prioritizes survival by sealing the injury quickly, but also limits the body’s ability to rebuild missing structures.

In regenerative species, like salamanders that can regrow lost limbs, those same types of cells organize into a blastema, a temporary structure that enables tissue regrowth.

It’s as if these cells can move in two different directions. They could either make a scar or make a blastema. Our research focused on redirecting the behavior of fibroblasts already present at the injury site.

Professor Dr. Ken Muneoka.

To test whether mammalian healing could be shifted toward regeneration, researchers developed a sequential treatment using two well-studied growth factors.

The first step involved applying fibroblast growth factor 2 (FGF2) after a wound had already closed. This timing allowed the body to complete its typical healing response, and then the team “changed what happens next,” Muneoka said.

FGF2 stimulated the formation of a blastema-like structure — something that does not normally occur in mammals following this type of injury; several days later, a second treatment — using bone morphogenetic protein 2 (BMP2) — was applied, triggering those cells to begin forming new structures.

This is really a two-step process. You first shift the cells away from scarring, and then you provide the signals that tell them what to build.

Professor Dr. Ken Muneoka.

Challenging assumptions about regeneration

A key implication of the study is that regeneration does not depend on adding external stem cells, as many current approaches in regenerative medicine attempt to do.

This is really a two-step process. You first shift the cells away from scarring, and then you provide the signals that tell them what to build. You don’t have to actually get stem cells and put them back in. They’re already there — you just need to learn how to get them to behave the way you want.

Professor Dr. Ken Muneoka.

Dr. Larry Suva, a VTPP professor who worked on the study, said the findings shift how researchers think about the limits of mammalian healing.

The cells that we thought to be unprogrammable, in fact are. The capacity is not absent — it’s just obscured.

Professor Dr. Larry J. Suva, co-author
Department of Veterinary Physiology and Pharmacology
College of Veterinary Medicine and Biomedical Sciences
Texas A&M University, TX, USA.

The study also showed that cells can be redirected to form structures beyond their original location — a concept known as positional re-specification, which plays a critical role in development.

This means cells that would normally contribute to one part of the body can be instructed to rebuild a different structure after injury.

Imperfect but complete regrowth

Although the regenerated structures were not exact replicas of the original anatomy, researchers were able to restore all the expected components removed during amputation, such as the bone, tendon, ligament and joint.

The results included both skeletal elements and connective tissues, organized in a way that reflects the natural structure.

We regenerated what you would expect to see at that level of injury. The structures are there — just not in a perfect form.

Professor Dr. Ken Muneoka.

The findings also revealed that regeneration occurs through multiple biological pathways, indicating that rebuilding tissue is more complex than relying on a single mechanism.

Potential applications in human healing

While the research is still in early stages, it may have more immediate applications in improving how wounds heal.

Rather than focusing solely on regrowing entire structures, researchers believe the approach could first be used to reduce scarring and improve tissue repair.

People should start thinking about using these signals during the healing process. Even shifting the response slightly away from scarring could have real benefits.

Professor Dr. Ken Muneoka.

Because BMP2 is already FDA approved for certain medical uses and FGF2 is in multiple clinical trials, the pathway to clinical exploration may be more accessible for entirely new therapies.

A new direction for regenerative medicine

The study represents a shift in how scientists understand regeneration in mammals — not as a lost ability, but as one that remains present but inactive.

This changes the way we think about what’s possible. Once you show that regeneration can be activated, it opens the door to asking entirely new questions.

Professor Dr. Larry J. Suva.

For Muneoka, those questions have guided decades of research — and now, finally, have a new foundation.

Regenerative failure in mammals can be rescued. Now we have a model to begin figuring out how.

Professor Dr. Ken Muneoka.

Publication:


Abstract
Epimorphic regeneration in mice is stimulated at a non-regenerative digit amputation by sequential treatment with FGF2 and BMP2 (FGF2→BMP2). FGF2 stimulates digit amputation wound cells to form a blastema and BMP2 induces blastema differentiation to regenerate the amputated distal phalangeal element, albeit imperfectly. The formation of a phalangeal growth plate suggests that the induced regenerate recapitulates embryonic development and cell lineage studies show that wound cells that enter the blastema cells are positionally re-specified during regeneration. FGF2→BMP2 treatment also stimulates a blastema-independent response that regenerates a synovial joint complex containing stump-derived tendon, ligament and a sesamoid-like bone. Together the blastema-dependent and blastema-independent responses can result in the regeneration of all skeletal structures removed by amputation. The induced regeneration response demonstrates the availability of regeneration competent cells at a non-regenerating wound, and that FGF and BMP signaling is sufficient to trigger a regenerative outcome at wounds that heal by fibrosis.


So once again, we find that the real world looks nothing like the work of a perfect designer producing optimal solutions for its favoured species. It looks like evolution: an accumulation of workable compromises, shaped by selection, constrained by ancestry, and indifferent to suffering. In mammals, the immediate priority after injury is rapid wound closure. That may well have been good enough to keep an injured animal alive long enough to reproduce, but it comes at the cost of scarring and the loss of the more elegant regenerative abilities seen in other branches of the animal kingdom.

That is precisely the kind of trade-off an evolutionary process would produce. Natural selection does not plan for the future, nor does it aim at perfection. It simply preserves traits that improve reproductive success in the environments in which organisms live. A crude repair that prevents infection and bleeding today may be favoured over a more sophisticated repair that takes longer and carries greater immediate risk. Evolution has no reason to care whether the result leaves a person paralysed, disfigured, disabled or missing a limb.

For Intelligent Design creationists, however, the problem is harder to evade. If their designer is the omniscient, omnipotent and benevolent god they imply but dare not name in court, then this arrangement is difficult to excuse. Why give salamanders, fish, flatworms and hydra such remarkable regenerative powers, leave mammals with what may be traces of the same latent ability, then arrange human wound-healing so that scarring normally blocks regeneration? Why produce a system that is good enough for survival in the wild, but not good enough to restore function, relieve suffering or repair catastrophic injury?

The usual creationist answer, when one is offered at all, is to retreat into mystery: we cannot know the designer’s reasons; perhaps there is some hidden purpose; perhaps suffering is part of a greater plan. But that is not science. It is merely a way of protecting a belief from evidence. The scientific explanation, by contrast, requires no special pleading. Regeneration, scarring, wound closure and tissue repair are the products of inherited developmental systems modified by evolution. Different lineages have taken different routes, and mammals have inherited one that favours rapid patching over elegant rebuilding.

The Texas A&M study does not mean human limb regeneration is just around the corner, and it would be misleading to pretend that a treated mouse digit is equivalent to a human arm or leg. What it does show is more subtle and, in some ways, more revealing: the biology of regeneration may not be wholly absent in mammals. It may be masked by the very wound-healing programme that keeps us alive after injury. That is a fascinating finding for regenerative medicine, but an awkward one for anyone who insists that humans were specially designed as the pinnacle of creation.

As so often, the evidence points not to a perfect designer, but to an imperfect history. We are not the product of foresight, benevolence or engineering excellence. We are the descendants of survivors, carrying the compromises that helped our ancestors live long enough to reproduce. That explains why nature is full of animals that can do what no prayer has ever achieved: regenerate what was lost.




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