10/16/2026
➡️ From Almost Certain Euthanasia to Hope: How Our Understanding of Equine Laminitis Has Transformed
[🚨There is a super juicy part marked in the text‼️be sure to read that bit 😉]
Twenty-five years ago, laminitis was commonly understood to be associated with grain overload, retained placenta, severe gastrointestinal disease, systemic inflammatory disorders (including sepsis), and limb injury resulting in supporting-limb laminitis. Obesity was also recognised as a significant risk factor, however the mechanistic relationship between obesity, insulin dysregulation and laminitis had not yet been established.
A major shift in understanding occurred in 2002 when Dr Philip Johnson proposed a link between obesity, hyperinsulinaemia and laminitis, laying the foundations for what is now recognised as Equine Metabolic Syndrome (EMS).
This marked the beginning of a new concept in which endocrine dysfunction, rather than inflammation alone, was recognised as a major cause of laminitis.
Experimental evidence soon followed with Asplin et al. (2007) demonstrating that it is possible to experimentally induce laminitis in normal ponies by infusing insulin until hyperinsulinaemia (abnormally high levels of blood insulin) occurred. All ponies infused with insulin developed laminitis within 72 hours in all four feet. This was followed by Carter et al. (2009), who showed that hyperinsulineamia preceded the development of naturally occurring pasture associated laminitis in Welsh and Dartmoor ponies. Their work also contributed to establishing the diagnostic thresholds used even today to identify horses at increased risk of EMS-associated laminitis.
In 2010 the American College of Veterinary Internal Medicine (ACVIM) released a consensus statement on EMS as the foundational reference for veterinarians. This established EMS as a legitimate veterinary diagnosis, standardised terminology and diagnostic approaches.
Further support for a causal role of hyperinsulinaemia came from de Laat et al. (2010), who induced hyperinsulinaemia in Standardbred horses and produced laminitis in all treated animals within 48 hours. Importantly, this study incorporated radiographic assessment before and after laminitis induction, confirming that all horses entered the study with radiographically normal feet. Despite the development of clinically and histologically confirmed laminitis, conventional radiographs remained normal throughout the 48-hour experimental period and showed no evidence of distal phalanx rotation or distal displacement.
This finding was significant because it highlights an important limitation of radiography in acute laminitis. Laminitis begins with microscopic injury to the lamellae, the tissues responsible for suspending the distal phalanx (P3) within the hoof capsule.
During the developmental and early acute stages, substantial lamellar injury and pain are present before sufficient structural failure occurs to produce radiographically detectable displacement of P3. In many cases, the distal phalanx remains correctly positioned for up to 72 hours after the onset of clinical signs.
Subsequent studies have reinforced these observations. Arble et al. (2009) demonstrated that advanced imaging modalities, such as MRI are needed to detect lamellar pathology before conventional radiographic changes become apparent, while Skelton et al. (2024) confirmed that traditional radiographic measurements have limited sensitivity for the diagnosis of acute laminitis. Consequently, radiographs should only be used as a tool for assessing disease progression post 72 hours of laminitis onset rather than as a definitive means of excluding early laminitis.
For this reason, clinical assessment remains central to diagnosis. Horses in the acute phase frequently exhibit significant pain and lameness despite minimal or absent radiographic abnormalities (Herthel & Hood, 1999). As Sherlock and Parks (2013) demonstrated, radiographic findings should always be interpreted alongside the clinical picture, as they may substantially underestimate disease severity during the early stages.
The understanding of EMS associated laminitis has now evolved considerably. For many years, metformin was the principal pharmacological option available. Its use was largely based on the assumption that EMS was similar to type 2 diabetes in humans, where improving insulin sensitivity can reduce hyperinsulinaemia. However, it is now recognised that EMS is not simply an equine equivalent of diabetes and therefore metformin was never likely to be the wonder drug it was hoped to be. While insulin resistance may contribute to disease pathophysiology, the strongest evidence links laminitis risk directly to hyperinsulinaemia. This is clearly demonstrated by all the experimental induction studies, in which sustained hyperinsulinaemia alone was sufficient to induce laminitis in otherwise healthy horses and ponies.
More recently, sodium-glucose co-transporter-2 (SGLT2) inhibitors such as velagliflozin, ertugliflozin and canagliflozin have emerged as promising therapeutic options. These drugs reduce renal glucose reabsorption, resulting in increased urinary glucose excretion, lower blood glucose concentrations and, importantly, reduced insulin in the blood.
The first major equine study investigating this class of medication was published by Meier et al. (2018). Ponies treated with velagliflozin for 21 days before exposure to a high (12g/Kg BW/day) non-structural carbohydrate (NSC) diet for up to 18 days remained protected from laminitis, whereas 38.5% of untreated control animals developed clinical disease.
🚨Furthermore, only ponies that developed laminitis showed measurable radiographic evidence of distal phalanx rotation following the dietary challenge. This is a very important study since radiographs were taken before the start of the study and then post NSC diet challenge period (up to 18 days in length).
🚨These findings demonstrate that the 14 ponies which subsequently developed laminitis following the high non-structural carbohydrate (NSC) dietary challenge had radiographically normal feet prior to the onset of disease, with a median distal phalanx rotation of 2.9°. Following the development of clinical laminitis, distal phalanx rotation increased to a median of 5.7°, indicating that structural displacement occurred after the onset of the disease process rather than before it.
‼️This is clear peer reviewed evidence of a direct link between diet, development of laminitis and rotation of the distal phalanx.‼️
Since then, growing clinical evidence has supported the use of SGLT2 inhibitors. Sundra et al. (2023) reported a marked reduction in insulin concentrations following treatment with ertugliflozin in horses with severe hyperinsulinaemia. Subsequently, the same first author, found that more than 85% of owners reported improvements in their horses' quality of life following treatment, with most also reporting substantial reductions in pain (Sundra et al. 2025). It has also been shown that ertugliflozin attenuated the hyperinsulinaemic response associated with intra-articular corticosteroid administration (Page et al. 2026).
Taken together, these studies indicate that the veterinary profession's understanding of laminitis causes and in particular EMS-associated laminitis have advanced rapidly over the past two decades. Hyperinsulinaemia is now recognised as a primary driver of many cases of laminitis, and targeted therapies capable of reducing insulin concentrations are becoming increasingly available. As experience with SGLT2 inhibitors continues to grow and their efficacy and safety become more widely established, there is reason to be optimistic that the number of horses lost to EMS-associated laminitis will decline in the coming years.
For horses experiencing recurrent laminitis despite appropriate dietary and management interventions, assessment for insulin dysregulation should be strongly considered. Identifying and addressing underlying EMS remains one of the most important steps in reducing the risk of future episodes and improving long-term outcomes.
References
Herthel, D.J. and Hood, D.M. (1999) Clinical presentation, diagnosis, and prognosis of chronic laminitis. Veterinary Clinics of North America: Equine Practice, 15(2), pp. 375–394. Available at: https://pubmed.ncbi.nlm.nih.gov/20381743/
Asplin, K.E., Sillence, M.N., Pollitt, C.C. and McGowan, C.M. (2007) Induction of laminitis by prolonged hyperinsulinaemia in clinically normal ponies. Veterinary Journal, 174(3), pp. 530–535. https://doi.org/10.1016/j.tvjl.2007.07.003
Arble, J.B., Mattoon, J.S., Drost, W.T., Weisbrode, S.E., Wassenaar, P.A., Pan, X., Hunt, R.J. and Belknap, J.K. (2009) Magnetic resonance imaging of the initial active stage of equine laminitis at 4.7 T. Veterinary Radiology & Ultrasound, 50(1), pp. 3–12. Available at: https://journals.sujps.com/index.php/sj/article/view/291
Carter, R.A., Treiber, K.H., Geor, R.J., Douglass, L. and Harris, P.A. (2009) Prediction of incipient pasture-associated laminitis from hyperinsulinaemia, hyperleptinaemia and generalised and localised obesity in a cohort of ponies. Equine Veterinary Journal, 41(2), pp. 171–178. https://doi.org/10.2746/042516408X342975
de Laat, M.A., McGowan, C.M., Sillence, M.N. and Pollitt, C.C. (2010) Equine laminitis: Induced by 48 h hyperinsulinaemia in Standardbred horses. Equine Veterinary Journal, 42, pp. 129–135. https://doi.org/10.2746/042516409X475779
Sherlock, C. and Parks, A. (2013) Radiographic and radiological assessment of laminitis. Equine Veterinary Education, 25(10), pp. 524–535. Available at: https://beva.onlinelibrary.wiley.com/doi/10.1111/eve.12065
Meier, A., Reiche, D., de Laat, M., Pollitt, C., Walsh, D., et al. (2018) The sodium-glucose co-transporter 2 inhibitor velagliflozin reduces hyperinsulinemia and prevents laminitis in insulin-dysregulated ponies. PLOS ONE, 13(9), e0203655. https://doi.org/10.1371/journal.pone.0203655
Campolo, A., Frantz, M.W., de Laat, M.A., Hartson, S.D., Furr, M.O. and Lacombe, V.A. (2020) Differential proteomic expression of equine cardiac and lamellar tissue during insulin-induced laminitis. Frontiers in Veterinary Science, 7, 308. https://doi.org/10.3389/fvets.2020.00308
Stokes, S.M., Stefanovski, D., Bertin, F.R., Medina-Torres, C.E., Belknap, J.K. and van Eps, A.W. (2021) Plasma amino acid concentrations during experimental hyperinsulinemia in 2 laminitis models. Journal of Veterinary Internal Medicine, 35(3), pp. 1589–1596. https://doi.org/10.1111/jvim.16095
Sundra, T., Kelty, E. and Rendle, D. (2023) Preliminary observations on the use of ertugliflozin in the management of hyperinsulinaemia and laminitis in 51 horses: A case series. Equine Veterinary Education, 35, pp. 311–320. https://doi.org/10.1111/eve.13738
Skelton, G., Acutt, E., Stefanovski, D. and van Eps, A. (2024) Evaluation of digital radiographic measurements for the diagnosis of acute laminitis. Equine Veterinary Journal. https://doi.org/10.1111/evj.14436
Sundra, T., Kelty, E., Rossi, G., Lester, G. and Rendle, D. (2025) Horse owner experiences and observations with the use of SGLT2i for the management of equine metabolic syndrome and hyperinsulinaemia-associated laminitis. Equine Veterinary Education, 37, pp. 202–209. https://doi.org/10.1111/eve.13975
Thane, K., Voth, R., Klee, R., Warnken, T., Chukwu, V. and Frank, N. (2025) Effects of the sodium-glucose cotransporter-2 inhibitor velagliflozin on insulin concentrations in horses with insulin dysregulation. Journal of Veterinary Internal Medicine, 39(6), November–December 2025, jvim70256. https://doi.org/10.1111/jvim.70256
Page, A.E., McPeek, J.L., McGreevy, E., Carattini, S. and Adam, E.N. (2026) Treatment with ertugliflozin mitigates the hyperinsulinemic response to intra-articular triamcinolone acetonide. Equine Veterinary Journal. https://doi.org/10.1002/evj.70150
Bröjer, J., Hanche-Olsen, S., Fintl, C., Svonni, E., Hellings, I.R., Müller, C. and Lindåse, S. (2026) Efficacy and safety of canagliflozin in insulin dysregulated horses: a 4-week multi-arm, double-blind, randomized, clinical trial. Journal of Veterinary Internal Medicine, 40(3), May–June 2026, aalag107. https://doi.org/10.1093
