10/12/2026
UNDER SCRUTINY
THE DISEASE THAT DOESN'T EXIST
There is a difference between challenging how a disease is managed and claiming that the disease itself is a misunderstanding.
And apparently, laminitis has been misunderstood all along.
According to a rather confident explanation circulating in hoof-care circles, shortening toes and leaving heels elevated creates hoof-capsule distortion, makes P3 appear to rotate and ultimately damages the lamellae.
What veterinary medicine recognises as laminitis is, we're told, fundamentally a mechanical imbalance.
Correct the balance and the problem disappears.
Or, as the claim rather memorably puts it:
"When balance is correct, the so-called disease disappears."
That's quite a proposition.
Particularly when there are controlled experiments in which researchers induced laminitis without first creating the proposed trimming imbalance.
And then examined the resulting pathology under a microscope.
THE EXPERIMENTS
In 2007, Asplin and colleagues published a controlled experiment involving nine clinically healthy ponies.
Five received prolonged insulin infusions while their blood glucose was maintained within the normal range. Four received saline as controls.
The insulin-treated ponies experienced extremely high circulating insulin concentrations, averaging approximately 1,036 µIU/mL.
All five developed clinical and histological laminitis within 72 hours, reaching Obel grade 2 at an average of approximately 55 hours.
None of the controls developed laminitis.
No experimental toe-shortening or heel-elevation protocol was used to induce the condition.
The researchers sustained markedly elevated insulin concentrations. The treated ponies developed laminitis; the controls did not.
In 2010, de Laat and colleagues investigated whether the findings could be reproduced in horses.
Eight clinically normal Standardbreds were studied.
Four underwent a euglycaemic hyperinsulinaemic clamp: insulin was continuously infused, while glucose administration maintained normal blood glucose concentrations.
Four received control infusions.
All four insulin-treated horses developed clinical laminitis within 48 hours.
None of the controls did.
Microscopic examination revealed significant lamellar abnormalities in the treated horses, including elongation and attenuation of secondary epidermal lamellae, changes in basal cell morphology and localised basement-membrane separation.
The severity and distribution of the lesions varied between hooves.
Again, the disease was induced by a controlled metabolic intervention, not an experimental trimming procedure.
These were small studies, and the insulin concentrations were markedly elevated. They demonstrate causation under the conditions studied, not that every naturally occurring case follows precisely the same pathway.
But their central finding is clear.
Prolonged experimental hyperinsulinaemia can cause laminitis.
AND HERE IS WHERE IT GETS PARTICULARLY INTERESTING
The researchers in the 2010 Standardbred study also took radiographs.
Despite the horses developing clinical laminitis and significant microscopic lamellar pathology, the radiographs showed no evidence of pedal bone rotation or sinking during the experiment.
The horses had laminitis.
Their lamellar tissues were abnormal.
Yet the radiographs did not demonstrate rotation or sinking.
The disease was present without radiographically detectable displacement.
That is an important distinction for any explanation that treats laminitis as merely an appearance created by hoof-capsule distortion.
Laminitis and pedal bone displacement are not interchangeable diagnoses.
Displacement can occur when lamellar support is compromised, but it is not a prerequisite for the disease to exist.
A radiograph can provide important information about hoof architecture.
It cannot, by itself, establish that the lamellar tissues are healthy.
And the absence of displacement does not mean that mechanical loading is irrelevant to the disease process.
THE PATHOLOGY IS NOT IMAGINARY
A separate histopathological investigation published by Asplin and colleagues in 2010 examined lamellar tissues from the earlier insulin-induced laminitis experiment in ponies.
The findings included swollen and disorganised epidermal cells, abnormal keratinisation, increased mitotic activity, apoptosis and significant elongation of secondary epidermal lamellae.
Widespread basement-membrane separation was absent. Only minimal separation was identified.
That matters because laminitis is often described in simplified terms as the lamellae physically tearing apart.
The actual pathology can be considerably more complex.
Different forms and stages of laminitis do not necessarily produce identical microscopic lesions.
But the abnormalities were real, measurable and demonstrably different from those in the controls.
They were not a trick of radiographic positioning.
They were not an illusion caused by the external shape of the hoof.
They were changes in living tissue.
And changing the trimming interpretation cannot make those findings disappear.
ONE NAME. MORE THAN ONE PATHWAY.
There is another difficulty with attributing laminitis to one particular trimming configuration.
The condition occurs in several recognised clinical contexts.
Endocrinopathic laminitis is strongly associated with insulin dysregulation.
Sepsis-associated laminitis develops in connection with serious systemic inflammatory disease.
Supporting-limb laminitis can develop when a horse must bear disproportionate weight on one limb for a prolonged period.
These forms do not necessarily share identical initiating mechanisms.
A comprehensive review by Elliott and Bailey in 2023 examined the cellular and molecular evidence across all three and explored possible common pathways involving stress within lamellar epithelial cells.
The precise mechanisms, and how they interact, remain subjects of investigation.
But an incomplete understanding of every cellular step is not evidence that the disease itself is a misunderstanding.
And a theory intended to replace the established understanding of laminitis must account for these different clinical and experimental circumstances.
Not just the appearance of a selected hoof before and after trimming.
MECHANICS ARE PART OF THE STORY. NOT THE WHOLE STORY.
Mechanical forces can play different roles in different forms of laminitis.
In supporting-limb laminitis, prolonged abnormal loading and reduced opportunities for unloading are implicated in altered lamellar perfusion and the development of injury.
The evidence supports an important relationship between loading, perfusion and lamellar health, although the complete causal sequence from altered perfusion to lamellar failure remains unresolved.
In endocrinopathic and sepsis-associated laminitis, mechanical forces can contribute to deformation and displacement as lamellar function becomes compromised.
These are not interchangeable mechanisms.
And acknowledging one does not invalidate the others.
Hoof-capsule distortion is real. Appropriate mechanical management can be an essential part of rehabilitation. Inappropriate trimming can create additional mechanical problems.
But none of that establishes routine trimming imbalance as an initiating cause of endocrinopathic, sepsis-associated or supporting-limb laminitis.
Nor does improvement following corrective trimming establish that trimming caused the original disease.
An intervention can improve the consequences of a condition without having addressed every factor that caused it.
That distinction is fundamental.
THE PROBLEM WITH THE CLAIM
For the proposed explanation to account for laminitis as a whole, it would need to explain why experimentally sustained hyperinsulinaemia produces clinical and histological laminitis in treated animals but not controls.
It would need to account for the cellular abnormalities documented under microscopy.
It would need to explain why those abnormalities can occur without radiographic evidence of pedal bone rotation or sinking.
And it would need to account for lamellar disease arising in substantially different clinical circumstances.
Simply asserting that the hoof capsule is out of balance does not answer those questions.
Nor does demonstrating improved hoof alignment after months of rehabilitation.
Such improvement may be clinically valuable. It may demonstrate successful management of mechanical problems.
But it does not invalidate the experimental findings.
A change in hoof shape cannot retrospectively establish what initiated the original pathology.
WHY THIS MATTERS
The consequences of presenting laminitis as nothing more than an incorrectly balanced hoof extend beyond an argument about terminology.
If the underlying disease process is dismissed, owners may concentrate exclusively on hoof mechanics while overlooking insulin dysregulation, systemic illness or other clinically important factors.
A horse can have a mechanically improved hoof and still have an unresolved metabolic problem.
A horse can have laminitis without radiographically detectable displacement.
And a horse can have hoof-capsule distortion without that distortion establishing the original cause of its pathology.
There is plenty of room to debate trimming methods, mechanical rehabilitation and the interpretation of radiographs.
There is also plenty we still need to learn about the cellular mechanisms of laminitis.
But uncertainty about every detail does not mean nothing has been established.
We have controlled experimental evidence that sustained hyperinsulinaemia can induce laminitis.
We have histopathological evidence of cellular and structural changes within the lamellae.
We have evidence that lamellar disease can exist without radiographically detectable displacement.
And we have different clinical forms of laminitis in which metabolic, inflammatory and mechanical factors contribute in different ways.
None of that is adequately explained by a single proposed trimming error.
The question was never whether hoof mechanics matter.
The question is whether they explain everything.
They don't.
And the lamellar tissues have been telling us that for years.
REFERENCES
Asplin KE, Sillence MN, Pollitt CC, McGowan CM (2007). Induction of laminitis by prolonged hyperinsulinaemia in clinically normal ponies. The Veterinary Journal, 174(3), 530–535. https://doi.org/10.1016/j.tvjl.2007.07.003
de Laat MA, McGowan CM, Sillence MN, Pollitt CC (2010). Equine laminitis: induced by 48 h hyperinsulinaemia in Standardbred horses. Equine Veterinary Journal, 42(2), 129–135. https://doi.org/10.2746/042516409X475779
Asplin KE, Patterson-Kane JC, Sillence MN, Pollitt CC, McGowan CM (2010). Histopathology of insulin-induced laminitis in ponies. Equine Veterinary Journal, 42(8), 700–706. https://doi.org/10.1111/j.2042-3306.2010.00111
Elliott J, Bailey SR (2023). A review of cellular and molecular mechanisms in endocrinopathic, sepsis-related and supporting limb equine laminitis. Equine Veterinary Journal, 55(3), 350–375. https://doi.org/10.1111/evj.13933
