Setting the Record Straight on Winter Laminitis

Since I started writing about winter laminitis several years ago the topic has appeared with increasing frequency in other places.  Spreading the word is always good but several things have been transformed in translation.

Cortisol as a cause.  While it’s true cortisol levels may be somewhat higher with cold stress, they are with heat stress too and we don’t recognize a parallel situation of summer induced hoof pain. If cortisol was a key mechanism it would also put all horses at the same risk, not just those with EMS. While cortisol can sensitize vessels to constrictors, it doesn’t cause constriction itself. Endothelin-1 is the most likely culprit here.

Thyroid hormone as a cause.  It’s not true that thyroid hormone reduces blood flow to the hooves.

Arteriovenous shunts function.  Several discussions of the role of arteriovenous shunts got the mechanism backwards. These shunts bypass the local tissues and send blood back to the interior of the body without perfusing the local cells.  They do not close in cold weather; they open.

Endothelin-1 action.  Again, I’ve seen this described as the reverse of its actual role. Endothelin-1 does not dilate vessels, it contracts them.

Hyperlipidemia from running out of hay as a cause.  There is no evidence that going without hay for short periods causes hyperlipidemia and that in turn causes vasoconstriction. After a  single feeding, it takes at least 6 hours for the stomach and small intestine to empty into the cecum and at least 2 days for the cecum and colon to empty. Hay is primarily digested by fermentation in the cecum and colon so that process doesn’t even begin for 6 hours after eating the hay.  In the meantime, the horse is still working on fermenting hay that was eaten long before that.

If the horse does not have enough  calories coming in from the digestive tract and production of glucose in the liver, more triglycerides from fat storage will be released into the blood to make up the deficit. This will not occur after just a short (hours) period without hay. There is also no evidence that these physiological levels of triglycerides cause vasoconstriction.


To review:

  • High levels of insulin are associated with insulin resistance
  • Insulin resistance in blood vessels leads to unopposed action of the very potent vasoconstrictor endothelin-1, known to be elevated in endocrinopathic laminitis
  • Cold-triggered vasoconstriction on top of the endothelin-1 dominated state could lead to painfully impaired circulation to the feet
  • Damage to the vessels from prior laminitis bouts may also increase risk

Much more research into the phenomenon of cold-induced hoof pain is needed but evidence to date and response to treatments is pointing to a problem with excessive vasoconstriction and insufficient blood supply.

Eleanor Kellon, VMD

About Dr. Kellon

Graduate of University of Pennsylvania Veterinary School. Owner of Equine Nutritional Solutions,, industry and private nutritional consultations, online nutritional courses. Staff Veterinary Expert at Uckele Health and Nutrition.
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7 Responses to Setting the Record Straight on Winter Laminitis

  1. Roxanne says:

    Dr. K,

    Can you post the resources to your conclusions above? I’m interested in learning more but am not sure where to start.

  2. Deborah Tompkins says:

    BRAVO for setting that straight. Now add the other culprit, lamina already under stress from long toes and under-slung heels are more susceptible to the added stressors at any time of year.

  3. Susan Normab says:

    Growing up around horses/ponies in England 1950/60’s we were always told not to trot endlessly on tarmac roads but to use the grass verges whenever they were available for “ fear of causing road founder.” Indeed some hunt horses would occasionally come down with this. But perhaps they had a metabolic issue already ongoing that was not recognised back then and just trotting on hard surface brought it to the fore?? I would love to hear your thoughts on this!
    Thank you. I appreciate all your time and effort you put into educating us about laminitis

    • Dr. Kellon says:

      Yes, I think you are probably very right. Horses with high insulin levels have been documented to have pathology in their laminae even if they haven’t shown an acute, obvious episode of laminitis. This tissue weakening would predispose them to mechanical damage.

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