Understanding insulin resistance in horses: The silent threat behind most laminitis cases

Insulin resistance represents the most significant—and preventable—metabolic threat facing horses today, directly responsible for approximately 90% of laminitis cases. Yet many owners remain unaware their horse is affected until painful hoof damage has already occurred. The good news: with proper identification and management, horses with insulin dysregulation can live long, comfortable lives and maintain successful careers.

This metabolic disorder disrupts how the body processes glucose, triggering a cascade of hormonal imbalances that ultimately weaken the delicate laminar structures inside the hoof. Understanding the condition empowers owners to recognize warning signs early and implement evidence-based strategies that can prevent devastating outcomes. Recent advances, including promising new medications and refined diagnostic protocols, have transformed our ability to manage even the most challenging cases.

How insulin resistance develops and damages the body

In a healthy horse, the pancreas releases insulin after a meal, signaling cells throughout the body to absorb glucose from the bloodstream for energy. Insulin binds to specialized receptors on muscle, liver, and fat cells, triggering a cascade that moves glucose transporters to the cell surface. The system operates with elegant efficiency.

In insulin-resistant horses, this signaling pathway breaks down. Tissues respond sluggishly to insulin’s message, absorbing glucose at dramatically reduced rates despite adequate—or even elevated—insulin concentrations. The pancreas compensates by producing ever-higher levels of insulin, creating a state called hyperinsulinemia. Blood glucose typically remains normal or only slightly elevated because the body keeps increasing insulin output to maintain balance. This compensatory mechanism masks the underlying problem until significant metabolic dysfunction has developed.

The condition rarely appears in isolation. Obesity accelerates insulin resistance through multiple pathways: enlarged fat cells become metabolically dysfunctional, producing inflammatory compounds and hormones called adipokines that further impair insulin signaling. Adipose tissue deposits, particularly in the neck region, actively worsen the metabolic picture. However, obesity isn’t required—some horses develop insulin dysregulation while maintaining lean body condition, a phenomenon researchers have termed the “non-obese EMS phenotype.”

The devastating connection to laminitis

The most consequential aspect of hyperinsulinemia is its direct effect on hoof structures. Research has definitively established that sustained high insulin concentrations cause laminitis independently of other factors. In experimental studies, maintaining insulin levels at concentrations commonly seen in metabolically affected horses induced clinical laminitis within 48 to 72 hours.

The mechanism involves a case of mistaken molecular identity. Lamellar cells in the hoof contain few insulin receptors but abundant receptors for a related hormone called insulin-like growth factor-1 (IGF-1). At high concentrations, insulin binds to these IGF-1 receptors, triggering uncontrolled cell proliferation in the laminar tissue. This causes the delicate secondary epidermal lamellae to stretch and elongate, compromising their structural integrity and ultimately their ability to suspend the coffin bone within the hoof capsule.

Unlike sepsis-related laminitis, hyperinsulinemia-associated laminitis shows minimal inflammation in early stages—it’s primarily a proliferative lesion rather than an inflammatory one. This distinction has important implications: by the time obvious lameness appears, significant structural damage has often already occurred. Many horses show evidence of chronic lamellar changes, including divergent hoof rings and stretched white lines, before their metabolic condition is ever diagnosed.

Equine Metabolic Syndrome: More than just obesity

Equine Metabolic Syndrome (EMS) describes a collection of metabolic abnormalities centered on insulin dysregulation—the defining feature that creates laminitis risk. The condition typically manifests in horses between 5 and 15 years of age, though it can appear earlier in predisposed individuals.

While obesity frequently accompanies EMS, it’s neither required for diagnosis nor sufficient to establish it. The critical diagnostic criterion is demonstrating insulin dysregulation through appropriate testing. Horses can be overweight without insulin problems, and lean horses can harbor dangerous hyperinsulinemia. This distinction matters enormously for identifying at-risk animals.

Regional fat deposits provide more reliable indicators than overall body condition. A cresty neck score of 3 or higher (on a 0-5 scale) indicates five times greater odds of insulin dysregulation compared to horses with lower scores. Other concerning fat accumulations include deposits behind the shoulder, above the eyes (supraorbital fat pads), around the tailhead, and in the sheath region of males.

Affected horses often display additional metabolic abnormalities including elevated triglycerides, high leptin levels, and reduced adiponectin—a hormone that normally enhances insulin sensitivity. Cardiovascular changes such as increased blood pressure may also develop.

When PPID complicates the picture

Pituitary Pars Intermedia Dysfunction (PPID), commonly called Cushing’s disease, presents a related but distinct condition affecting primarily horses over 15 years old. This disorder originates from dysfunction in the pituitary gland, causing excessive hormone production that can exacerbate or trigger insulin resistance.

Approximately 30% of horses with PPID demonstrate concurrent insulin dysregulation, and this combination significantly elevates laminitis risk. Importantly, horses with PPID alone—without accompanying insulin problems—rarely develop laminitis. When a PPID horse experiences laminitis, insulin dysregulation should be strongly suspected.

The two conditions can be distinguished by their characteristic features. PPID produces hirsutism (a long, curly coat that fails to shed normally), muscle wasting particularly along the topline, and often increased thirst and urination. EMS horses typically maintain normal coats and muscle mass but show regional adiposity. However, because horses can have both conditions simultaneously—especially middle-aged and older animals—comprehensive testing for both is recommended in any horse over 10 years old presenting with metabolic concerns or laminitis.

Recognizing the warning signs

The clinical presentation of insulin resistance often proves frustratingly subtle until laminitis develops. Owners may notice their horse is an “easy keeper” who maintains weight on minimal feed, or one who seems perpetually hungry yet gains weight readily. Some horses show decreased performance, lethargy, or difficulty losing weight despite appropriate diet and exercise.

Physical examination reveals characteristic patterns. Body condition scoring using the Henneke 1-9 scale often shows values of 7 or higher in affected horses. More specifically, evaluating regional fat deposition provides crucial diagnostic information. The cresty neck score deserves particular attention: a crest that has begun forming an arch, shows palpable fat deposits, or has become so enlarged it falls to one side indicates significant concern.

Hoof changes may appear before obvious lameness develops. Divergent growth rings—wider at the heel than the toe—suggest episodes of lamellar stress. A widened white line, flat or convex soles, and recurring foot abscesses can all indicate subclinical laminitis damage accumulating over time. Veterinarians often recommend radiographs even in horses without apparent lameness to detect subtle coffin bone changes that would confirm previous lamellar injury.

When laminitis does manifest, it typically affects both front feet and may recur seasonally, with peak incidence during spring and early summer when pasture carbohydrate content surges. Recurring mild lameness episodes, reluctance to walk on hard surfaces, and increased digital pulses warrant immediate investigation.

Diagnostic approaches that reveal hidden risk

Identifying insulin dysregulation before laminitis occurs offers the greatest opportunity to prevent harm. Testing protocols have evolved considerably, with current recommendations emphasizing dynamic challenges that reveal how the body actually handles carbohydrates rather than relying solely on single-point measurements.

Baseline testing provides a starting point

Resting insulin and glucose measurements offer an accessible screening option. Horses should not receive grain or rapidly absorbed carbohydrates within four hours of blood collection, though hay or pasture access beforehand is acceptable. Morning sampling between 8 and 10 AM in a low-stress environment yields the most reliable results.

A resting insulin concentration exceeding 20 μIU/mL suggests insulin dysregulation, while values above 50 μIU/mL are definitively diagnostic. However, baseline testing has significant limitations: approximately 44% of horses with insulin resistance test normal on resting insulin alone. Equivocal results or strong clinical suspicion despite normal baseline values warrant dynamic testing.

Dynamic testing unmasks hidden problems

The Oral Sugar Test (OST) has emerged as the preferred dynamic assessment for most situations. After overnight fasting with only one flake of hay permitted before midnight, horses receive corn syrup orally—either a low dose (0.15 mL/kg) or high dose (0.45 mL/kg). Blood sampling at 60 or 90 minutes measures the insulin response to this carbohydrate challenge.

For the low-dose protocol, insulin exceeding 45-60 μIU/mL indicates dysregulation. The high-dose version uses a cutoff of 110 μIU/mL at 60 minutes. Importantly, the Equine Endocrinology Group confirms these tests do not trigger laminitis when performed as directed.

Alternative protocols include the Oral Glucose Test, which uses dextrose powder mixed into feed, and the Combined Glucose-Insulin Test, an intravenous procedure offering excellent sensitivity and specificity for research settings or complex cases. The insulin tolerance test directly assesses tissue responsiveness by measuring glucose decline after insulin administration.

Testing considerations that affect accuracy

Several factors can falsely elevate insulin results, potentially leading to misdiagnosis. Stress, excitement, pain, recent exercise, and systemic illness all increase circulating insulin. Alpha-2 agonist sedatives like xylazine and detomidine also affect results. Testing during acute laminitis episodes proves unreliable due to pain-induced hormonal changes.

Seasonal variation adds another layer of complexity. Insulin responses to oral carbohydrate challenges tend to be higher in summer months, while glucose tolerance shows different patterns across seasons. This variation doesn’t invalidate testing but should inform interpretation, particularly for borderline results.

Sample handling significantly impacts accuracy. Blood should remain chilled from collection, with serum or plasma separated within four hours. For ACTH testing (used to diagnose PPID), heat and time on red cells cause degradation that produces falsely low results—a critical consideration when shipping samples.

Which horses face greatest risk

Certain breeds demonstrate dramatically higher susceptibility to insulin dysregulation, reflecting genetic adaptations that proved advantageous during evolutionary history but create metabolic vulnerability in modern management conditions.

Ponies lead the risk hierarchy, particularly British native breeds including Welsh, Shetland, and other hardy types that evolved to thrive on sparse forage. Their exceptional metabolic efficiency—sometimes called the “thrifty gene” phenotype—becomes pathological when combined with abundant feed and limited exercise. Morgan horses, Arabians, Paso Finos, and Spanish Mustangs share similar predisposition. Norwegian Fjords, American Saddlebreds, Warmbloods, donkeys, and miniature horses also face elevated risk.

Quarter Horses, Tennessee Walking Horses, and Rocky Mountain Horses occupy a moderate-risk category. Thoroughbreds and Standardbreds, bred for athletic performance rather than metabolic efficiency, show comparatively lower susceptibility.

Genetic research has begun identifying specific markers associated with EMS. Studies in Welsh ponies and Morgan horses confirmed moderate to high heritability for key metabolic traits including insulin levels, triglycerides, and adipokine concentrations. Genome-wide association studies have pinpointed candidate genes near FAM174A in Arabian horses and variants on chromosomes 15 and 17 in other breeds. This genetic contribution likely involves multiple alleles with breed-specific distributions.

Beyond genetics, management factors powerfully influence risk. Physical inactivity impairs insulin sensitivity. Diets high in non-structural carbohydrates—including grain, sweet feeds, and lush pasture—challenge metabolic capacity. The combination of genetic predisposition, overfeeding, and limited exercise creates a perfect storm for metabolic dysfunction.

Evidence-based management transforms outcomes

Successful management of insulin-resistant horses requires a comprehensive approach addressing diet, exercise, weight, and sometimes medication. The ECEIM Consensus Statement emphasizes this represents “a long-term strategy requiring diligence and discipline.” With commitment, most horses achieve excellent outcomes.

Dietary intervention forms the foundation

Diet modification alone successfully manages most EMS cases. The fundamental principle involves restricting non-structural carbohydrates (NSC) to less than 10% of hay dry matter—combining water-soluble carbohydrates and starch into this calculation. For the most severely affected horses, targeting less than 10% ethanol-soluble carbohydrates plus starch provides an extra margin of safety.

Hay testing is essential because NSC content varies dramatically between batches, ranging from 5% to over 25% in cool-season grasses. Late-maturity grass hay typically contains lower energy and carbohydrate levels than early-cut material. Timothy, orchardgrass, and bromegrass cut at mature stages often meet requirements. Alfalfa sometimes surprises owners by testing lower in sugar and starch than grass hay, though its higher calorie density requires portion control.

When hay testing reveals excessive NSC, soaking reduces water-soluble carbohydrate content by 24-43% depending on conditions. Warm water requires 30 minutes; cold water needs 60 minutes. Maximum soak time should not exceed two hours to prevent bacterial growth. The resulting hay should be fed immediately, and the water discarded away from areas where horses might access it. Soaking leaches minerals, making supplementation necessary.

All grains, sweet feeds, and molasses-containing products must be eliminated entirely. Low-calorie ration balancers provide essential vitamins and minerals without problematic carbohydrates—typically one to two pounds daily for an average-sized horse. Unmolassed beet pulp serves as an acceptable carrier for supplements due to its low glycemic index.

Feeding management also matters. Multiple small meals distributed throughout the day—four to six feedings ideally—produce smaller insulin responses than large meals. Slow feeders and small-hole hay nets extend eating time, reducing consumption speed and mimicking natural grazing patterns. One study found these devices extended eating time from 120 to 193 minutes for restricted hay rations.

Exercise enhances insulin sensitivity

Physical activity improves metabolic function through multiple mechanisms. Exercise increases muscle mass while reducing fat deposits, enhances insulin receptor sensitivity, produces anti-inflammatory effects, and burns calories. Both acute exercise sessions and consistent conditioning programs benefit insulin regulation.

For non-laminitic horses, current recommendations specify low-to-moderate intensity exercise exceeding 30 minutes, performed more than five times weekly. Target heart rates of 130-170 beats per minute—corresponding to fast trot through canter work—produce the most consistent metabolic benefits. Lower-intensity programs show disappointingly inconsistent results.

A practical protocol involves 5 minutes of walking to warm up, 15-20 minutes of brisk trotting, and 5 minutes of walking to cool down. Consistent application of this simple routine improves insulin regulation within weeks.

Horses recovering from laminitis require special consideration. Exercise should not begin until clinical lameness has fully resolved, baseline insulin has normalized, any coffin bone rotation has been corrected, and veterinary clearance obtained. Initial work should involve low-intensity movement on soft surfaces, gradually increasing based on individual response while monitoring carefully for recurrent lameness.

Weight loss requires patience and precision

Overweight horses should target body condition scores of 5 on the Henneke scale, with 6 representing the maximum acceptable. The cresty neck score should be tracked alongside overall condition, as neck fat correlates most strongly with metabolic dysfunction.

Safe weight loss proceeds at 0.5-1% of body weight weekly—approximately 2.5-5 kg (5.5-11 lbs) for a 500 kg horse. Faster losses increase circulating triglycerides and free fatty acids, potentially triggering hyperlipemia, a dangerous condition particularly in ponies, miniatures, and donkeys.

Initial forage allocation typically starts at 1.4-1.7% of actual body weight as fed. If weight loss stalls after 30 days, this can be reduced to 1.25% of ideal body weight. The absolute minimum—1.0% of body weight as dry matter intake—should only be implemented with close veterinary monitoring. Adding straw (up to 30% of total forage) can increase intake volume while limiting calories, though gradual introduction prevents impaction risk.

Monthly weighing with a consistent method tracks progress accurately. Photographs from multiple angles, neck circumference measurements, and periodic body condition assessments document changes that scales alone might miss. Notably, body condition scores may not change immediately despite weight loss, as visceral fat loss occurs first.

Pharmaceutical support when management falls short

Medications serve as adjuncts to—never replacements for—dietary and lifestyle management. Several options exist for horses requiring additional intervention.

Metformin (15-30 mg/kg orally every 8-12 hours) works primarily in the intestinal tract, reducing glucose absorption rather than improving systemic insulin sensitivity as once believed. Administration 30-60 minutes before feeding blunts postprandial glucose and insulin spikes. It’s useful during initial management implementation or for horses with persistent postprandial hyperinsulinemia despite optimal diet.

Levothyroxine sodium (48 mg daily for an average horse) increases metabolic rate to accelerate weight loss in resistant cases. Horses with EMS are not truly hypothyroid—this represents a pharmacological rather than physiological intervention. Treatment continues for 3-6 months maximum, with gradual weaning. Because it stimulates appetite, strict dietary control must continue throughout treatment.

SGLT2 inhibitors represent the most promising recent pharmacological advance. These medications (canagliflozin, ertugliflozin, velagliflozin) block renal glucose reabsorption, causing glucose loss through urine and subsequently reducing blood insulin concentrations. Case series have reported dramatic improvements in horses with refractory hyperinsulinemia, including resolution of laminitis pain and normalization of abnormal fat deposits. Current recommendations reserve these drugs for cases failing dietary management, exercise, metformin, and levothyroxine. Monitoring serum triglycerides during initiation is advised.

For horses with concurrent PPID, pergolide addresses the pituitary dysfunction and often improves insulin regulation secondarily.

Pasture poses the greatest challenge

Grass presents a constant temptation and a genuine danger for insulin-resistant horses. Cool-season pastures can contain NSC levels of 10-20%, with dramatic variation based on weather, time of day, and growth conditions.

High-risk periods include spring flush, autumn regrowth, days following cold nights (below 40°F/5°C) with subsequent sunshine, drought-stressed grass, and afternoon hours when photosynthesis has maximized sugar accumulation. Overgrazed short grass concentrates sugars and poses particular danger.

The safest grazing windows occur from late night through early morning—ideally before sunrise—and during or after prolonged cloudy periods when plants have utilized stored sugars through respiration. Second consecutive overcast days offer the lowest-risk grazing opportunity.

Grazing muzzles reduce dry matter intake to approximately 77-83% of unmuzzled consumption and preferentially allow access to leaf tips, which contain somewhat less sugar than stem bases. However, muzzles create stress for some horses and may cause abnormal tooth wear with prolonged use. They work best combined with limited turnout time rather than as all-day solutions.

Many affected horses require complete pasture restriction, at least during initial management or high-risk seasons. Dry lot confinement with hay provided in slow feeders offers safe turnout while eliminating grazing risk. Multiple feeding stations distributed throughout the area encourage movement. Pea gravel sections around water and high-traffic zones improve footing and provide additional hoof stimulation.

Track systems (Paddock Paradise) create narrow pathways around pasture perimeters, encouraging movement while grass quickly becomes depleted on the narrow strips. These systems offer mental stimulation and exercise opportunity superior to small dry lots, though research suggests movement increases may be modest compared to traditional turnouts—the primary benefit lies in grass restriction rather than dramatically increased activity.

Living well with insulin resistance

With appropriate management, horses with insulin dysregulation can maintain excellent quality of life and continue successful careers. The condition cannot be cured—the underlying genetic and metabolic predisposition persists—but it can be effectively controlled indefinitely.

Owners should expect to maintain dietary vigilance permanently, with seasonal adjustments as pasture conditions change. Regular retesting at 3-12 month intervals once stable confirms ongoing metabolic control. Horses may gradually resume restricted pasture access as their condition improves, though this requires careful monitoring.

Success should be measured by insulin normalization, not just weight loss. Some horses achieve excellent metabolic control while remaining slightly heavier than ideal body condition suggests, while others reach target weight without fully correcting their hyperinsulinemia. Dynamic testing provides the definitive assessment.

Horses over 10 years old require ongoing monitoring for PPID development, which affects approximately 30% of horses with pre-existing insulin dysregulation. Annual ACTH testing or TRH stimulation testing catches early disease when treatment is most effective.

Prevention protects at-risk horses

For breeds with known susceptibility, proactive management offers the best protection against metabolic disease. Maintaining body condition at 5-6 on the Henneke scale throughout life prevents the adipose dysfunction that accelerates insulin resistance. Owners should resist the temptation to let “easy keepers” carry extra condition simply because they maintain it effortlessly.

Regular exercise beginning early in life and continuing throughout maintains insulin sensitivity and prevents inappropriate weight gain. Dietary NSC restriction—avoiding grain and sweet feeds, limiting pasture access, testing hay—should be standard practice for predisposed breeds regardless of current metabolic status.

Annual screening with dynamic insulin testing starting at age 5-7 identifies developing problems before damage occurs. The cost of testing is trivial compared to laminitis treatment and the potential loss of an otherwise healthy horse.

The evolving science of equine metabolism

Research continues advancing our understanding of insulin dysregulation. Genetic studies have confirmed significant heritability of key metabolic traits, with ongoing work seeking to identify specific markers that could enable breeding decisions or targeted early intervention. The enteroinsular axis—the communication between gut hormones and insulin secretion—has emerged as an important factor in postprandial hyperinsulinemia, potentially explaining why some horses respond better to metformin than others.

Microbiome research shows preliminary evidence that horses with EMS harbor less diverse gut bacterial populations, with specific changes resembling patterns seen in humans with glucose intolerance. This opens possibilities for microbiome-targeted therapies, though practical applications remain investigational.

The 2024 Equine Endocrinology Group recommendations reflect accumulated evidence favoring dynamic testing, earlier PPID screening, and stepwise medication protocols culminating in SGLT2 inhibitors for refractory cases. Terminology has evolved from “insulin resistance” toward “insulin dysregulation” to capture the full spectrum of abnormalities—though some experts continue debating whether even this terminology adequately describes the condition.

Practical commitments for long-term success

Managing an insulin-resistant horse requires consistent effort but rewards that commitment with a healthy, comfortable animal. Testing hay for NSC content, eliminating grain and sugary treats, using slow feeders, restricting or eliminating pasture access during high-risk periods, implementing regular exercise, and monitoring body condition and insulin status form the core of successful management.

Working closely with a veterinarian who understands equine metabolic disorders ensures appropriate testing, medication when needed, and guidance through challenging periods. Owner compliance remains the single greatest predictor of outcomes—understanding why these measures matter helps maintain the discipline required for success.

The horses themselves seem to adapt readily to their new routines. Slow feeders satisfy the drive to forage. Track systems and dry lots with enrichment provide mental stimulation. Regular exercise, even in older horses, becomes an enjoyable part of daily management. What initially feels restrictive eventually becomes simply how one cares for a particular horse.

Conclusion

Insulin resistance represents a manageable condition rather than a death sentence, but it demands respect and attention. The metabolic dysfunction that allows a horse to thrive on sparse forage becomes dangerous liability when combined with modern management practices and abundant feed. Understanding this fundamental mismatch—and bridging it through thoughtful diet, exercise, and monitoring—transforms outcomes.

The connection between hyperinsulinemia and laminitis places metabolic management at the center of hoof health for susceptible horses. Testing identifies problems before hooves suffer damage. Dietary intervention corrects most cases. Exercise and weight management address underlying contributors. Medications provide options when other approaches prove insufficient. Prevention remains far preferable to treatment, and early intervention dramatically outperforms delayed response.

For owners of at-risk breeds, metabolic awareness should inform every management decision from the beginning. For those whose horses have already developed insulin dysregulation, the path forward is clear: commit to the necessary changes, work with knowledgeable veterinary partners, monitor progress through appropriate testing, and expect a horse who can live comfortably and well for years to come.