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.
- 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