Dr. Brian Eitelman, DVM, CJF, and Aggie Vet and Farrier Services provide veterinarian and farrier services in Parker, CO, Elizabeth, CO, Franktown, CO, Castle Rock, CO, Sedalia, CO and Larkspur, CO. To learn more, please visit us at www.vetandfarrier.com
In this series, Dr. Brian Eitelman, DVM, CJF, discusses the main metabolic diseases in horses.
In part 1, we go over Equine Metabolic Syndrome or EMS and Pituitary Pars Intermedia Dysfunction or PPID, insulin resistance, and most importantly, why horses suffer from these diseases.
As a veterinarian and farrier, I encounter laminitis and founder in horses a lot - metabolic diseases in horses are one of the most common causes of laminitis and founder in a horse, and can make these conditions worse.
Two main diseases I am going to talk about are Equine Metabolic Syndrome or EMS and Pituitary Pars Intermedia Dysfunction or PPID. Let’s just shorten this to EMS and PPID. Later on I will touch briefly on insulin resistance in horses.
Equine Metabolic Syndrome (EMS)
This is sometimes called “peripheral cushings.” We’re not going to do that. It is confusing. Either use the full name “Equine Metabolic Syndrome” or “EMS.” There is not a cut and dry definition for this condition - it is a grouping of symptoms. So, the textbook definition is - you are an EMS horse if you have these traits: abnormal fat deposits, too much insulin production (more on that later), and are pre-disposed to laminitis. In reality, I am worried that your horse has EMS if it is too fat, has weird fat deposits in weird places, can’t lose weight, and especially if it has sore feet.
The classical presentation for EMS is a younger horse up to teens. The breeds that are pre-disposed to this condition are usually breeds selected for efficiency - gaited breeds, arabs, ponies, mustangs. Why do these breeds get picked on? Well, the common thread among these types of horses is they were bred to endure LOTS of exercise and consume very little in the way of nutritious forage. Take ponies for example - pulling mine carts for hours and hours per day down where there is very limited room for hay. What about Arabs, Mustangs? - cover vast distances every day -50-60 miles - with minimal time for quality grazing
But nowadays we’ve switched that - we give our horses LOTS of rich food and very little exercise, instead of what they’re designed for - LOTS of exercise and running and very little nutritious food.
- Abnormal fat deposits on neck, shoulder, top of rump
- “Easy keepers”/Can’t lose weight
- Tend to be obese over entire body BUT being fat doesn’t necessarily mean it is metabolic and metabolic doesn’t necessarily mean it is fat.
Pituitary Pars Intermedia Dysfunction (PPID)
This is usually what people are talking about when they say “Cushings” but again, stick with PPID for clarity. So what is PPID - essentially it is an excess production of steroid in the body - called cortisol. When I use the term steroid, I am specifically referring to CORTISOL. Cortisol steroid regulates a bunch of stuff in your body and in your horse too - it is the main hormone produced when the body undergoes stress!!
The classic presentation for a horse with PPID is an older horse that is abnormally hairy (doesn’t shed in summer, too much hair, or rough weirdly-curly coat), and usually tend to look “skinny.”
Importantly, these guys can actually look more like EMS horse in the early stages with abnormal fat deposits. But later on in the disease, and more commonly, there is actually a loss of muscle mass that makes the horse look skinny. Again this is why testing is important to distinguish between these two conditions because they can look similar initially! The skinny appearance comes from excess cortisol (aka steroid) in the body causing loss of muscle mass.
- Hypothalamus (located in brain) regulates the pituitary gland (right next to it in the brain). The pituitary gland, in turn, regulates the adrenal glands (located in kidneys). The adrenals produce cortisol (steroid). The hypothalamus produces dopamine. When there is MORE dopamine production, there is LESS activity in the pituitary gland, which means LESS activity of the adrenal glands, which means LESS steroid (cortisol) produced. Functionally, dopamine acts like brakes in the car. By default, the brakes are on. When the body needs more cortisol, the foot comes off the brake until cortisol needs have been met and then back on the brakes.
In PPID, dopamine receptors aren’t as responsive as they should be so basically the brakes are out. This causes part of the pituitary gland to enlarge and produce too much ACTH (one of the main things we test for). This, in turn, causes the adrenals to produce too much cortisol (steroid) and this excess steroid is the main cause of our problems.
So the medication we use in PPID increases the sensitivity to dopamine and essentially puts on new brake pads.