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Equine Laminitis or Founder

Laminitis represents a huge source of pain and suffering for our equine companions every year. There are many known causes of laminitis (or founder) in equids, some of which are related to underlying endocrine diseases and some of which are related to illness or environmental factors. While we have figured out what the risk factors are for episodes of laminitis, the exact cellular pathways by which it occurs are a source of ongoing research.

Endocrinopathic (endocrine disease-related) laminitis

While horses may develop a number of endocrine diseases, two of the most common and important are Equine Metabolic Syndrome and Pituitary Pars Intermedia Dysfunction (PPID or Equine Cushing’s).

Equine Metabolic Syndrome (EMS), as defined by the Equine Endocrinology Group, is a collection of risk factors for endocrinopathic laminitis with insulin dysregulation as a central feature. Other components include obesity (specifically a crested neck appearance), resistance to weight loss, known episodes of laminitis, and altered hormone and cell signaling molecules within the horse’s body. EMS is more common in certain breeds, such as mustangs, Peruvian Pasos, Paso Finos, Warmbloods, Andalusians, and Morgans, among others. Researchers hypothesize that members of these breeds were naturally selected for the presence of the “thrifty” gene, which allowed them to thrive on sparse forage in harsh environments. Unfortunately the presence of this gene, which allows many of our horses to be easy keepers, works against them in an environment with such easy access to high quality food, leading to insulin dysregulation and EMS.

Insulin is a hormone that is released within the body in response to increases in glucose (sugar). It acts on cells within the body, allowing them to take in the glucose for energy to maintain normal function. The cells of horses with EMS are not as sensitive to insulin, so they require higher insulin concentrations to be able to take up glucose for energy. This leads to both higher blood glucose and insulin concentrations; measurement of these two values forms the basis of our screening for EMS. There are also dynamic tests such as the Oral Sugar Test and Insulin Tolerance Test that veterinarians may utilize to diagnose the disease. Treatment of EMS, at its core, involves dietary management. Recommendations will often include cutting out grain, reducing/minimizing grazing, and soaking hay prior to feeding. All of these actions reduce the amount of sugar a horse takes in, with the hope of reducing both blood glucose and insulin. Increased exercise levels will help with weight loss and appropriate glucose metabolism, assuming the horse is not currently dealing with laminitis. Additionally, medications such as Thyro-L may help to increase and support your horse’s metabolism. Metformin is a medication used for people with Type 2 diabetes that can be used in the horse to increase insulin sensitivity and decrease blood glucose. 

Pituitary Pars Intermedia Dysfunction (PPID, Equine Cushing’s) results in an abnormal production of the hormone, ACTH, from the horse’s pituitary gland. Excess ACTH causes the release of excess cortisol from the adrenal glands, resulting in the clinical signs associated with PPID. Early signs of PPID may include lethargy, decreased athletic performance, failure to shed the haircoat or a thicker haircoat than normal, loss of topline, and abnormal sweating (among other signs). Horses in the later stages of PPID show these signs as well as increased urination, recurrent infections, recurrent foot abscesses, and laminitis, among others. Your veterinarian may test for PPID with either a baseline ACTH or TRH stimulation test. The TRH stimulation test gives a more comprehensive look at the current function of the horse’s pituitary and adrenal glands. The TRH stimulation test is usually recommended over the baseline ACTH, though the baseline ACTH may be a good starting point in some cases. The TRH stimulation test has only been validated during non-fall months (approximately mid-November to mid-July), as horses experience a natural, seasonal increase in cortisol in the fall that may affect results of the TRH stimulation test. Baseline ACTH levels may be measured year-round. Treatment for PPID involves Prascend or pergolide. This medication inhibits the pituitary gland’s overproduction of ACTH, thereby reducing the horse’s circulating cortisol levels and clinical signs. Treatment with Prascend is generally very effective, though it is recommended to periodically check that the current dosage of Prascend is adequately controlling levels of ACTH.

While the diseases described above are well characterized, the mechanisms by which they cause laminitis are still under study. Both cortisol and insulin are thought to directly affect the health of the laminae. Specifically, high levels of these hormones are deleterious, causing laminitis. One study observed the ability of insulin to bind to specific (IGF-1) receptors in the laminae. When insulin bound to these receptors, it altered the growth of the laminae in a harmful way, weakening the laminar connections. Other studies have proposed altered glucose metabolism in the laminae and altered blood flow within the hoof as potential mechanisms of laminitis secondary to endocrine disease. Additionally, horses with either disease may show increases in regional adiposity (“fat pads”); fat is an inflammatory tissue and increased amounts of it cause the horse to have higher levels of inflammatory molecules circulating in the bloodstream.


Other, non-endocrine mechanisms of laminitis

Unfortunately for us and our horse companions, there are other ways for horses to founder than having endocrine disease. These mechanisms of founder may occur in horses with or without endocrine disease. One of these is Pasture-Associated Laminitis. During the spring, warmer weather and increased periods of sunlight cause grass to grow and produce sugars at a high rate. One specific type of sugar, fructans, passes through the horse’s small intestine after it is consumed without being processed. It is finally processed once it reaches the large intestine (cecum and large colon) by hindgut bacteria, one prominent species being Streptococcus bovis. These bacteria consume the fructans molecules and produce lactic acid. The problem begins when the horse consumes a high level of fructans (seen in lush, green grass), resulting in a high level of lactic acid production by hind gut bacteria. The excessive lactic acid reduces the internal pH of the large intestine, causing the wall of the intestine to become “leaky.” This results in translocation of endotoxin, bacteria, and other potentially harmful microorganisms into the bloodstream. This ultimately may lead to laminitis. Similarly, the presence of bacteria (sepsis) or endotoxin (endotexemia) in the bloodstream and the related systemic inflammatory response can lead to laminitis in horses with systemic infections or certain, severe types of colic.


Take Away

Laminitis is an unfortunately common problem in our equine populations, especially in this area where grass becomes very lush in the spring and summer. The best treatment for laminitis is prevention. Early intervention for both Cushing’s and EMS is critical for preventing laminitis. TRH stimulation and insulin testing should be performed on any horses that are slow to shed in the spring or have fat deposits typical of either disease such as a cresty neck, excess fat around the tail head, or fat pads under the saddle area. Over the past decade testing and treatment for equine endocrine diseases have improved dramatically. Piedmont Equine has seen a significant drop in the incidence of laminitis since we started testing and treatment at the first sign of endocrine disease. Owners of at risk horses should be aware of the hazards of grazing on lush grass and consider options such as muzzling their horses or allowing grazing during times of the day when grass sugars are lower (typically the morning hours). If your horse does develop laminitis, work closely with your veterinarian and farrier team to explore all options available to make your horse more comfortable and get him or her through the episode. We know so much more about laminitis and endocrine disease than we used to, however continued research is still of utmost importance as we strive to create the best lives for our equine companions.



Baskerville, C.L., S. Chockalingham, P.A. Harris, et al. 2018. “The effect of insulin on equine lamellar basal epithelial cells mediated by the insulin-like growth factor-1 receptor.” Peer Journal, 2018, 6:e5945.

Equine Endocrinology Group. “Pituitary Pars Intermedia Dysfunction (PPID).” American Association of Equine Practitioners, 2017.

Equine Endocrinology Group. “Recommendations for the Diagnosis and Treatment of Equine Metabolic Syndrome (EMS). American Association of Equine Practitioners, 2018.

Graves, E.A. “Equine Endocrine Diseases: The Basics.” American Association of Equine Practitioners, 2015,

Harlow, B.E., I.A. Kagan, L.M. Lawrence, et al. “Effects on inulin chain length on fermentation by equine fecal bacteria and Streptococcus bovis.” Journal of Equine Veterinary Science, 2017, 48:113-120.

Morgan R.A., Keen J.A., Walker B.R., Hadoke P.W.F. “Vascular dysfunction in horses with endocrinopathic laminitis.” PLoS ONE, 2016, 11(9): e0163815.