The Barefoot Bloke

05/09/2026

05/09/2026

With the warmer weather, a few points to consider:
Adipose tissue (fat) functions as an endocrine organ in horses, just as it does in humans.
In both species, white adipose tissue is far more than an energy-storage depot. It actively secretes bioactive molecules called adipokines (and adipocytokines) that act locally or systemically to influence energy balance, appetite, insulin sensitivity, inflammation, and other processes. 
Key similarities
• Leptin: Secreted in proportion to fat mass. Higher body fat → higher circulating leptin. It signals satiety to the brain and is elevated in obese horses.
• Adiponectin: Produced almost exclusively by adipocytes. It improves insulin sensitivity and has anti-inflammatory effects. Levels generally fall as fat mass rises; low adiponectin is linked to insulin dysregulation and higher laminitis risk in horses.
• Other factors: Inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6, CCL2) and other adipokines are produced, especially when adipose tissue becomes dysfunctional in obesity.
• Steroid hormone metabolism: Adipose tissue contains enzymes (such as 11β-HSD1) that locally activate glucocorticoids, influencing metabolism and adipocyte differentiation.
These functions are well-documented in equine research, particularly in the context of obesity and equine metabolic syndrome (EMS). EMS shares parallels with human metabolic syndrome: excess adiposity, insulin dysregulation, chronic low-grade inflammation, and increased risk of related problems (laminitis in horses versus type 2 diabetes/cardiovascular disease in people). 
Notes on differences in knowledge depth
Scientific understanding of the equine adipocyte “secretome” is less complete than in humans or rodents, but the core endocrine role is clearly established. Regional fat depots (e.g., nuchal/cresty neck fat, visceral/peri-renal, retroperitoneal) can differ in activity and inflammatory profile, which is clinically relevant for EMS risk assessment.
In short, the recognition of fat as an endocrine organ applies to horses in the same fundamental way it does to humans, with important implications for managing equine obesity and metabolic health.

Equine metabolic syndrome (EMS) is a common endocrine disorder in horses, ponies, and donkeys. It is defined as a collection of risk factors centered on insulin dysregulation (ID) that greatly increases the risk of hyperinsulinemia-associated laminitis (HAL), the most common form of laminitis in the general equine population (accounting for >90% of cases in many studies). 
EMS is not a single disease but a syndrome arising from the interaction of genetic predisposition and environmental factors (especially diet and management). It is analogous in some ways to human metabolic syndrome, though the primary clinical concern in horses is laminitis rather than cardiovascular disease or type 2 diabetes.
Core Features
• Insulin dysregulation (ID) — the consistent, defining component. This includes any combination of:
• Resting (basal) hyperinsulinemia
• Exaggerated or prolonged insulin response after eating or carbohydrate challenge (postprandial hyperinsulinemia)
• Tissue insulin resistance (peripheral or hepatic)
• Increased adiposity — generalized obesity (body condition score typically ≥7/9) and/or regional adiposity (cresty neck, fat pads over the tailhead/rump, behind the shoulder, prepuce, or mammary gland). Note: Lean phenotypes with regional fat deposits also exist (“lean EMS”).
• Predisposition to laminitis (acute episodes or chronic/subclinical with divergent hoof rings).
• Variable additional findings: altered lipid metabolism (e.g., hypertriglyceridemia), abnormal adipokine levels (high leptin, low adiponectin), and sometimes mild hypertension or reproductive changes in mares.
Obesity is common and exacerbates the problem but is not required for diagnosis—ID is the essential feature. 
Pathophysiology
ID develops through a combination of excessive pancreatic insulin secretion in response to nonstructural carbohydrates (NSCs — sugars and starches), reduced hepatic insulin clearance, and tissue insulin resistance. High circulating insulin is toxic to the digital laminae of the hoof, leading to HAL.
Adipose tissue plays a key role as an endocrine organ (as discussed previously). Dysfunctional fat secretes elevated leptin and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, CCL2) while producing less adiponectin (an insulin-sensitizing and anti-inflammatory adipokine). This contributes to systemic inflammation, further impairs insulin signaling, and promotes a vicious cycle of worsening ID and adiposity. 
Genetic factors (a “thrifty” or easy-keeper genotype) interact with modern management: high-NSC diets (lush pasture, grain, treats), overfeeding, and insufficient exercise.
Predisposed Groups
Higher risk in ponies, donkeys, miniature horses, and certain horse breeds including Morgans, Arabians, Andalusians/Iberian breeds, Paso Finos, Saddlebreds, and some Warmbloods. Thoroughbreds and Standardbreds are less commonly affected. It typically appears in young-to-middle-aged animals (often 5–15 years), though it can occur at any age and may coexist with pituitary pars intermedia dysfunction (PPID/Cushing’s) in older horses.
Diagnosis
Diagnosis relies on history, physical examination (body condition scoring, cresty neck score, evidence of current or past laminitis), and laboratory confirmation of ID. Visual assessment of obesity alone is insufficient.
Recommended tests (per Equine Endocrinology Group / EEG guidelines):
• Oral sugar test (OST) — preferred dynamic test: measure insulin (and sometimes glucose) after administering corn syrup. Detects exaggerated postprandial insulin responses and is useful for assessing laminitis risk.
• Insulin tolerance test (ITT) — evaluates tissue insulin resistance.
• Resting (basal) insulin and glucose — useful for screening moderate-to-severe cases but less sensitive for mild ID.
• Additional tests may include adiponectin measurement or ruling out concurrent PPID (e.g., ACTH testing) in older animals.
Testing is recommended for at-risk horses, those with unexplained laminitis, before corticosteroid use, or as part of wellness/pre-purchase exams. 
Management and Treatment
The foundation is management, not just medication:
1. Dietary control (most important):
• Strict restriction of NSCs (ideally forage NSC

31/08/2026

Beautifully worded.
The question this raises is the same, if one correctly understands how the hoof functions is a steel rim shoe the appropriate course of action??? I would argue that it is not.

So what is the journey of a TED clinic actually supposed to achieve?

There is a deliberate order to the way I teach my clinics..

We don’t begin with shoes. We don’t even begin by asking what the “ideal hoof” should look like.

We begin much further back than that.

First, we have to understand what the hoof actually is.

The hoof capsule is not a rigid box surrounding the foot. It is a living, growing, highly deformable biological structure with anisotropic, elastic, plastic and viscoelastic material properties.

It is continually growing while simultaneously being subjected to hundreds of thousands of loading cycles.

So before we can intelligently discuss changing hoof shape, we first have to understand why hoof shape changes at all.

That takes us into material science, functional anatomy and physics.

We explore how forces enter the hoof, how those forces are transmitted through its internal structures, how the capsule deforms under load, and how repeated loading interacts with growth to progressively influence morphology.

Suddenly, flare, crushed heels, migration, asymmetry and distortion stop simply being things that we need to “trim away.”

They become evidence of the mechanical environment in which that hoof has been living.

And that creates the next question.

If forces can progressively change hoof morphology, what mechanical environment should we actually be trying to create?

That takes us into biomechanics.

We look at ground reaction force, centres of rotation, centres of pressure, moments, lever arms, tissue strain, phalangeal alignment and the interaction between internal and external forces.

And eventually we arrive at one of the central questions of the clinic.

What do we actually mean by hoof balance?

For generations we have described hoof balance qualitatively.

We want the hoof to be “balanced.”

We want good proportions.

We want appropriate load distribution.

We want to minimise tissue strain and improve biomechanical efficiency.

All perfectly reasonable aspirations.

But they describe what balance should achieve. They don’t actually define the mechanical condition that constitutes balance.

So we move from qualitative descriptions towards a quantitative mechanical definition.

Rather than asking where the hoof should look balanced, we ask where the forces acting on the digit must resolve.

At midstance, the problem becomes one of equilibrium.

The external moment created by ground reaction force must be resolved against the internal moments of the distal limb. The spatial relationships between the centre of rotation, Point of Balance, pressure-bearing solar surface and actual centre of pressure determine whether the system is operating close to equilibrium or whether additional rotational demands are being imposed upon it.

And this is where hoof balance stops being a two-dimensional exercise.

It becomes a four-dimensional problem. Three-dimensional spatial balance expressed through time.

The hoof is growing. The surface underneath it changes. The direction and magnitude of force change through stance. The horse moves. The centre of pressure migrates. The tissues deform. So balance cannot simply be a measurement frozen in a photograph.

We are trying to create the spatial conditions that allow the system to organise towards mechanical equilibrium with the lowest unnecessary internal energetic and tissue cost.

This is also why there cannot simply be one prescribed shoe, trim or external geometry for every horse.

Equilibrium is the objective. The intervention is merely how we attempt to create the conditions for it.

When constraints are removed, we can actually observe the limb self-organising towards a mechanically efficient solution. That is an important distinction. We are not trying to force the horse into an arbitrary geometry. We are trying to create the conditions in which the system can find equilibrium with minimal internal cost.

But then the clinic deliberately gets bigger.

Because the hoof isn’t attached to a table. It is attached to a horse. And the horse is not simply standing above the hoof passively.

Changing distal mechanics can change proprioceptive input, limb orientation, stabilisation requirements, muscular tone and ultimately posture.

But equally, changing posture alters limb orientation and the direction and timing with which forces return to the hoof.

So the relationship is not

Hoof → Horse.

It is

Hoof ⇄ Horse.

A continuous, bi-directional feedback loop.

Alter the hoof and the horse reorganises around the new boundary condition. Alter the horse and you change the mechanical environment experienced by the hoof. Alter that environment repeatedly enough and the hoof itself adapts and changes morphology.

And then we expand the lens again.

Because posture itself doesn’t exist in isolation.

The horse has a whole world acting upon it.

Movement.

Training.

Rider.

Tack.

Confinement.

Feeding position.

Surfaces.

Pain.

Stress.

Handling.

Social environment.

Autonomic state.

Every one of these can influence muscle tone, movement strategy, posture and limb orientation. And every change in limb orientation has the potential to change how force ultimately arrives back at the ground.

The clinic describes posture as the negotiated outcome between these different boundary constraints. The hoof is an enormously important one, but it isn’t the only one.

So by the end of the journey, we have travelled from the microscopic architecture and material behaviour of hoof horn…

to the physics governing its deformation…

to how repeated loading creates morphology…

to a quantitative definition of hoof balance…

to equilibrium of the distal limb…

to proprioception and posture…

to whole-body force transmission…

and eventually to the horse’s environment, management and lived experience.

And then, only then, do we come back to practical farriery.

What should we trim?

Where should we put the shoe?

What material should we use?

What should we support?

What should we unload?

Because once we understand the system, those decisions stop being recipes.

They become applications of first principles to the individual horse standing in front of us.

That is really what I want these clinics to be.

Not two days of me telling people how I shoe horses.

Two days of developing a framework that allows practitioners to understand why they are doing what they are doing, what mechanical outcome they are trying to achieve, and how to reason their way towards it regardless of which tools happen to be in their toolbox.

Understand the system first.
Define the desired mechanical outcome second.
Choose the intervention last.

That is the journey. So if you haven’t already booked on, is this something you want to miss?

26/08/2026