Laminitis in horses is caused by the breakdown of the tissue that connects the hoof wall to the bone inside the foot. The triggers fall into three main categories: hormonal and metabolic disorders, systemic inflammation from illness, and mechanical overload from bearing too much weight on one leg. Of these, hormonal causes are the most common by far. About 2% of all horses experience laminitis in any given year, but on operations that see cases, the impact can be devastating.
How the Hoof Fails From the Inside
To understand the causes, it helps to know what’s actually breaking down. Inside the hoof, interlocking layers of tissue called lamellae suspend the coffin bone (the main bone of the foot) from the hoof wall. These lamellae are anchored by a thin membrane and tiny protein structures that act like rivets, holding the living tissue to the structural hoof.
When laminitis develops, that anchoring system disintegrates. Research using electron microscopy has shown that in affected horses, the anchoring membrane swells to roughly twice its normal thickness, and the number of those protein rivets drops by half. With fewer attachment points and a weakened membrane, the connection between bone and hoof wall begins to fail. If the damage is severe enough, the coffin bone can rotate or sink within the hoof capsule, a condition called “founder.” The specific trigger determines how and why that membrane breaks down, but the end result is the same: structural failure inside the foot.
Metabolic and Hormonal Causes
The most frequent path to laminitis runs through the horse’s endocrine system. Two conditions dominate: equine metabolic syndrome (EMS) and pituitary pars intermedia dysfunction (PPID), commonly called Cushing’s disease. Together, these are referred to as endocrinopathic laminitis.
EMS is characterized by insulin dysregulation, meaning the horse’s body produces abnormally high levels of insulin or responds poorly to it. High insulin levels directly damage the lamellae. Research has shown that excessive insulin drives rapid, disorganized cell growth in the lamellar tissue, which appears to strip away the anchoring structures that hold the hoof together. Horses with EMS are often easy keepers: overweight, with fat deposits along the crest of the neck, behind the shoulder, or above the tail.
PPID occurs as horses age and involves progressive degeneration of neurons in the brain that regulate the pituitary gland. The result is overproduction of hormones including cortisol and ACTH. Classic signs include a long, curly coat that doesn’t shed properly and muscle wasting. About 30% of horses with PPID also have insulin dysregulation, which is the link to laminitis. Knowing whether a PPID horse also has abnormal insulin levels is critical for assessing laminitis risk and adjusting diet accordingly.
Pasture and Diet
Dietary triggers are closely tied to the metabolic causes above. A horse with normal insulin regulation can generally tolerate sugar-rich pasture without issue. But for horses with EMS, PPID, or a history of laminitis, the sugar and starch content in their feed becomes a serious concern.
Grasses store energy as sugars and fructans, and levels fluctuate throughout the day and across seasons. Cool, sunny days with cold nights tend to produce the highest concentrations because the grass produces sugar through photosynthesis but can’t use it for growth in the cold. Spring and fall are typically the highest-risk periods. For sensitive horses, the University of Tennessee recommends keeping total nonstructural carbohydrate (sugar plus starch) intake at 10% or less across all feed sources.
Grain overload is another well-known trigger. When a horse accidentally gets into a feed bin and eats a large quantity of grain, the starch overwhelms the small intestine’s ability to digest it. The excess reaches the hindgut, where it ferments rapidly, disrupts the microbial population, and can release toxins into the bloodstream. This sets off an inflammatory cascade that damages the lamellae.
Infection and Systemic Inflammation
Severe illness can trigger laminitis even in horses with no metabolic problems. This is called sepsis-related laminitis, and it occurs when a widespread inflammatory response sends damaging signals to the blood vessels and tissues of the foot.
Common scenarios include a mare that retains her placenta after foaling, severe colic (especially involving the large intestine), and serious bacterial infections. In these cases, the body’s immune response floods the bloodstream with inflammatory molecules that compromise blood flow to the lamellae and damage the tissue directly. Laminitis in these situations is essentially collateral damage from the body fighting a life-threatening problem elsewhere.
Exposure to certain toxins works through a similar inflammatory pathway. Black walnut shavings used as bedding are a well-documented cause. Even a small percentage of black walnut mixed into normal shavings can trigger a laminitic episode within hours.
Mechanical Overload
When a horse has a severe injury in one leg, the opposite leg bears a disproportionate amount of weight. This is called supporting-limb laminitis, or contralateral limb laminitis, and it’s one of the most feared complications in equine orthopedic cases. It’s the condition that killed the racehorse Barbaro.
The problem starts almost immediately. Blood flow to the lamellae in the supporting foot is compromised as soon as the horse stops loading the injured leg normally. Healthy horses standing at rest shift their weight between their front feet roughly one to five times per minute. This constant, subtle movement maintains blood circulation inside the hoof. When a horse can’t shift weight because the opposite leg is too painful, that cycling stops, and the tissue inside the supporting hoof begins to starve.
Reduced frequency of weight shifting appears to be the primary driver, rather than the extra load itself. Preventing supporting-limb laminitis depends on managing the original injury well enough that the horse can use both legs. Specialized shoeing that positions the foot at a roughly 20-degree angle has been shown to help preserve blood flow to the lamellae during full weight bearing.
Steroid Medications
Steroid injections used to treat joint inflammation or allergic conditions have long been considered a potential laminitis trigger. The reality is more nuanced than the reputation suggests. In healthy horses with no underlying metabolic issues, short-term treatment with steroids carries a very small risk of causing laminitis.
The danger is primarily in horses that already have subclinical lamellar damage, meaning the process has begun but no visible lameness has appeared yet. In these horses, steroids can push the situation over the edge, making it look like the medication caused the problem when it actually accelerated a process already underway. Higher-potency steroids like dexamethasone and triamcinolone carry more risk than lower-potency options like prednisolone. Horses with a history of laminitis should be monitored closely if steroids are necessary for another condition.
Concussion and Hard Work
Excessive work on hard surfaces, sometimes called “road founder,” can damage the lamellae through repeated mechanical trauma. This is most common in horses worked barefoot or with inadequate hoof protection on pavement or packed ground. The constant concussion inflames the lamellar tissue and, if the work continues, can progress to full laminitis. This cause is relatively straightforward to prevent with appropriate footing, hoof care, and conditioning.
Why Some Horses Are More Vulnerable
Laminitis frequency estimates range widely, from about 1.5% to 34% depending on the population studied, which reflects how dramatically risk varies between groups. USDA data found that 13% of U.S. horse operations reported at least one laminitis case in a given year. No specific breed appears to be predisposed after accounting for how common that breed is in the general population. Quarter Horses show up most often in laminitis statistics, but they’re also the most common breed in the country.
The factors that truly increase individual risk are metabolic: obesity, insulin dysregulation, uncontrolled PPID, and a previous episode of laminitis. A horse that has foundered once has already sustained structural damage to the lamellar attachment, making it easier for a second episode to take hold. Managing weight, monitoring insulin levels, and controlling pasture access are the most effective ways to reduce risk in susceptible horses.