The Most Common Deficiency Impacting Equine Performance

Diet is critical to performance so it only makes sense that people look to diet and supplements to enhance it. What is the most common deficiency limiting performance? Is it E and selenium, carbohydrate type, hay type, some critical amino acid or metabolite? None of the above.

The most common deficiency impacting performance is salt.

All of those things are important but the most common deficiency is plain salt. Most horses have some sort of salt block available, even boxed loose salt, but do you pay attention to how much they are ingesting? In cool weather, a horse should go through a standard stall size block in about a month. In hot weather, in two weeks. If working, even less time.

Even a lightly sweating horse will double his sodium requirement with one hour of work. When sweating heavily for an hour, the sodium requirement goes up 500%. Rock bottom requirement to match losses, cool weather, no work, average size horse, is about 1 oz/day.

Every cell in the horse’s body works like a mini battery. It performs its functions by maintaining a gradient between the concentration of sodium outside versus inside the cell. Electrolyte fluxes are involved with everything from absorption of nutrients in the gut to brain, nerve, heart and muscle function. Sodium and chloride are also the major electrolytes in blood and the fluid around cells. Without sufficient sodium, the body tissues cannot hold normal levels of water and the kidney is unable to conserve water. Dehydration rapidly ensues.

The consequences of salt and water depletion begin before you can even tell that the horse is dehydrated by common tests like the skin pinch. Reduced performance is the first sign. Muscle cramping is common. Humans report experiencing nausea (? colic or gut motility changes in a horse). This is followed by more obvious exercise intolerance and “hitting the wall”.

The horse has a sensitive hormonal system that “reads” osmolality/sodium concentration in the blood and tells the horse to eat salt and drink water when needed. Before that even happens, urine production slows down.

This works well to preserve blood volume but it is at the expense of fluid and sodium surrounding the cells if the horse does not have access to, and consume, enough salt. Because blood volume and sodium is normal, the drives for salt and water are not triggered so the tissues stay dehydrated.

There is a fairly large amount of sodium in equine bone but we don’t know how available that is to the rest of the body. You should do your best to replace salt losses as they occur and never, ever restrict access to water after exercise.

Figure one ounce of salt for each hour of light sweating, up to 5 ounces for an hour of drenching sweat. These must be replaced during or after exercise. Anything give farther out than 30 minutes before exercise will end up in the urine.

Salt can be divided between meals, post exercise water (always with plain water available as well) and sprinkled onto moistened hay. The other major electrolyte in sweat is potassium but this is present at the lowest concentration and pasture or hay typically contains anywhere from 2 to 4 times the potassium the horse needs.

There are many possible explanations for poor performance and your nutritionist can help you with a check list but remember the first thing on that list should be salt.

Eleanor Kellon, VMD

Equine Science Update

This will be a short one.

Lay magazines, and sometimes even scientific ones, have a penchant for going for the headlines when reporting on a scientific study. They can leave out important details, blow up the significance of findings, etc.. It’s a real disservice to the reader without a scientific background.

If you don’t already subscribe to this report, I highly recommend it https://equinescienceupdate.blogspot.com/ . It will be the best thing you read all month. The research is reported exactly as it was; no embellishment or sensationalizing. You can read past entries also.

Eleanor Kellon, VMD

MIM is Not a New Muscle Disease

I have been receiving an increasing number of questions regarding how to treat a horse with MIM. What is MIM?

MIM is being proposed as a new term for horses with PSSM2

MIM stands for muscle integrity myopathy. It’s unclear where it originated but apparently it was in Europe, possibly with the German genetics lab Generatio.

PSSM2 is currently the moniker for any biopsy showing accumulation of glycogen in abnormal locations that is not positive for the genetic test for PSSM1 – the GYS-1 mutation.

While the name polysaccharide storage myopathy does not tell you anything about the disease process, it is descriptive of the pathological changes. Muscle integrity myopathy isn’t an improvement. In fact, it is described as a group of exertional myopathies, which means exercise brings it on, but they go on to describe some with weakness and muscle atrophy, with no mention of exercise as a trigger.

The main problem though is this entire collection of myopathies is based entirely on the test results from the EquiSeq screen, which has never been validated as actually detecting any genetic myopathy, even after being in business for 8 years and promising to publish.

EquiSeq even has the nerve to state on their web site that the University of Minnesota is collaborating with them, when scrutinizing would be more accurate.

Reaction among the veterinary community in Europe has not been positive either, from the premier equine community at Utrecht University https://www.uu.nl/en/news/pssm-in-horses-a-summary-of-the-scientific-facts to the British Equine Veterinary Association https://www.veterinary-practice.com/2023/beva-warns-against-the-use-of-unvalidated-genetic-tests-for-pssm2-mfm-and-mim .

Pay particular attention to the two articles linked in the BEVA statement which specifically refute the validity of several of EquiSeq’s tests. The American College of Genetics and Genomics in conjunction with the Association for Molecular Pathology has published guidelines for describing genetic variants as pathogenic, likely pathogenic, uncertain, likely benign or benign and what needs to be done to ascertain the significance of any given variant https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4544753/ . There is no evidence that EquiSeq or it’s cohort Generatio are doing that.

There seems to be no shortage of unproven approaches to diagnosis and treatment of horses. That will probably continue as long as people like the founder of EquiSeq describe horse owners as “a niche market with money to burn” https://www.krqe.com/news/albuquerque-entrepreneurs-pitch-for-shark-tank-like-contest/

Don’t get taken in.

Eleanor Kellon, VMD

Inflammation is Essential

Inflammation is always talked about as something you need to avoid or control.  There is a staggering number of medications, supplements and therapy devices that target inflammation. However, inflammation is an essential part of how your horse’s body function

Thermography detects inflammation by surface temperature

Most people define inflammation as pain, swelling and heat but these are the outwardly detectable consequences of inflammation, not inflammation itself. Inflammation is the immune system’s response to infection, injury, foreign/irritating substances and abnormal or dead cells. Even cellular stress that does not cause serious damage will trigger an inflammatory response.

Inflammation can be localized, as in an injury or abscess, or systemic like a viral infection. Inflammation itself triggers release of anti-inflammatory countermeasures and as the cause of the inflammation comes under control, e.g. organisms neutralized or dead tissue cleaned up by scavenger white cells, these anti-inflammatory forces become dominant and the inflammation resolves. Inflammation is also necessary for the release of various growth factors which take over the job of repairing tissues. Without inflammation, these healing messengers would not be released.

Inflammation has a role to play in responses to things other than trauma or infection. When the horse is in training there is ongoing stress to the muscles and joints which results in microscopic damage that is so slight you can’t tell anything is going on. These stressors  trigger the release of inflammatory chemicals and in turn growth factors. The ultimate result is bigger and/or stronger muscles and bones.

An important thing to remember about inflammation is that it has to be turned on by some need. There is always a trigger. On a day to day basis inflammation is involved in normal cellular housekeeping like removing cells as they die, repairing minor damage to the intestinal lining or neutralizing irritants in inhaled air. When the job is accomplished, inflammation is turned off again.

What about inflammation causing disease? We hear a lot about that these days in reference to human health conditions. However, even when increased inflammatory activity is clearly associated with something it is never the cause. The real cause is whatever is turning on the inflammatory response.

There is also a lot of talk about diet causing – or curing – inflammation. Despite a lot of theory and hype there is no evidence that things like high omega-6 fatty acid intake can actually cause inflammation. In fact, there is mounting recent evidence that it doesn’t.  On the flip side, antiiinflammatory dietary elements like omega-3 fatty acids, vitamin E and trace minerals don’t cure inflammation either but they will provide the body with the raw materials it needs to mount its own normal antiinflammatory activity if any of these nutrients are deficient.

In summary, while inflammation can cause your horse pain and certainly signals there is an issue, it is not the cause of the problem.  Once the trigger of the inflammation is removed the inflammation will resolve itself within 72 hours if your horse has a sound diet. The horse then enters a stage of healing that wouldn’t be possible without the inflammatory response.

Eleanor Kellon, VMD

Open Letter to the AAEP Regarding Pasture Laminitis

This is a repost from 2022 because this information is important.

Emma Read, DVM, MVSc, DACVS, President
David L. Foley, CAE, Executive Director
Sally Baker, Director of Marketing & Public Relations
American Association of Equine Practitioners
4033 Iron Works Parkway
Lexington, KY 40511

Dear President Dr. Read, Mr. Foley, and Ms. Baker,

We are writing to you in reference to a post put up on the AAEP Facebook page April 5, 2022 regarding pasture-associated laminitis. The post was subsequently taken down, presumably due to the large volume of negative feedback on the content. We were disappointed in that action. It would have been more fruitful to have a dialog.

Please allow me to elaborate on why fructan is not the issue in pasture laminitis.

In 2006, van Eps and Pollitt reported the induction of laminitis by administering a bolus of pure chicory root oligofructose (a fructan) by stomach tube. The amount required was 7.5 g/kg to induce laminitis in one foot; 10 to 12.5 g/kg for systemic reaction and multifoot laminitis. For a horse to take in that much over a 24 hour period of grazing would require a pasture with 37.5% fructan on a dry matter basis. Perennial ryegrass
improved varieties growing under extreme conditions in areas of the world that are cool and rainy might have the potential to reach that level, at least transiently, but no grass in North America comes even close. The average difference between WSC (sugars + fructans) and ESC (sugars) is only 2% in the Dairy One database.
https://dairyone.com/services/forage-laboratory-services/feed-composition-library/ .

Crawford et al., 2007 fed 3 g/kg chickory fructan to ponies with and without a history of pasture laminitis. Despite a moderate drop in fecal pH from 6.89 to 6.18, there was no evidence of illness or laminitis, no increase in blood levels of fecal amines, or D-lactate (bacterial) which would indicate a compromised colonic barrier. They concluded there is a threshold for fructan to have negative effects.

In 2006, Trieber et al., reported following a herd of 160 ponies on pasture and found a prelaminitic metabolic profile was defined on the basis of body condition, plasma triglyceride concentration, RISQI, and MIRG. (RISQI and MIRG are proxies for insulin sensitivity.) Meeting > or = 3 of these criteria differentiated prelaminitic from never-laminitic group ponies with a total predictive power of 78%. Onset of spring laminitis
in the ponies at risk coincided with a flush of clover and increased pasture starch, not fructan.

Coleman et al., 2018 did a large epidemiological study of horses in North America and identified obesity and regional adiposity, and pre-existing endocrinopathy as risk factors.

Menzies-Gow et al., 2017 followed 446 animals for a period of 3 years and monitored multiple factors to identify those which would be predictive of laminitis developing at pasture. They concluded: “Risk factors for future laminitis prior to disease occurrence include low plasma adiponectin and high serum basal insulin or insulin post-dexamethasone concentrations. “

Fructan-induced laminitis is a carbohydrate overload model with SIRS, endotoxemia, fever and diarrhea – none of which are seen with pasture laminitis. There is no question endocrinopathic laminitis is behind spring
pasture laminitis. Borer et al., 2016 demonstrated chicory fructan produces minimal changes in glucose or insulin which is not surprising considering fructan is not a sugar, and not absorbed. It is a storage form of carbohydrate composed of fructose chains but is no more a sugar than cellulose, which is a chain of glucose
molecules.

The AAEP post further went on to suggest legumes would be safe. This is not correct. In addition to Trieber’s 2006 study documenting the starch in clover pasture as a trigger, Kagan et al., 2020 compared red and white clover samples collected in the morning and afternoon and found significant diurnal variation in starch content
from morning to afternoon; red clover 13-51 g/kg; white clover 24-52 g/kg freeze-dried weight. At 10 kg/day dry matter intake, this represents a range of 130 to 520 grams of starch intake alone. This, combined with the WSC fraction which, given the lack of fructan, would be comprised of simple sugars, led the authors to conclude that grazing clover is not recommended for horses at risk of endocrinopathic (insulin-induced)
laminitis.

In addition to the post on the AAEP Facebook page, multiple materials on the AAEP.org site have similar inaccurate information, e.g.,
Geor 2013 https://aaep.org/sites/default/files/issues/GeriatricGeor2.pdf refers to restricting pasture access because of fructan. Parks 2016 https://aaep.org/issue/laminitis-0 No mention of testing and treatment for endocrinopathic
laminitis despite the fact this explains the vast majority of cases. Frank 2018 https://aaep.org/sites/default/files/issues/proceedings-08proceedings-z9100108000341.PDF
does discuss endocrinopathic issues, but also alludes to gastrointestinal overload as a cause of pasture laminitis.

We urge you to take the above into consideration and update your information on pasture laminitis. Correct treatment and future management of these animals depends on it.

Sincerely,

Eleanor M. Kellon, VMD
Owner, Equine Cushing’s and Insulin Resistance on groups.io
Veterinary Consultant, Equine Cushing’s and Insulin Resistance Group Inc.

Kathleen M. Gustafson, PhD
Research Director, Equine Cushing’s and Insulin Resistance Group Inc.

Nancy C. Collins
President, ECIR Group Inc.
The ECIR Group Inc., 2307 S. Rural Road, Tempe, AZ

Chicken or Egg: Obesity and Insulin

Obesity is widely believed to cause insulin resistance in people but that’s not necessarily the case in horses.

In people, it is generally accepted that weight gain can lead to the development of insulin resistance and type II diabetes but that’s where parallels with the equine situation end. As obesity develops in people, so does a clear picture of higher inflammatory cytokines circulating in their blood and increasing insulin levels reflecting insulin resistance. This does not hold true for horses.

Banse et al [2016] found that markers of inflammation in skeletal muscle were actually lower in horses that were obese, and lowest of all in obese horses with elevated insulin – the exact opposite of what would be expected in a human.

What about obesity causing high insulin and equine metabolic syndrome? Nope. Lindase et al [2016] induced obesity in horses that already had moderately elevated insulin by feeding additional fat but the resultant 10% weight gain did not worsen insulin resistance.  Similarly, Bamford et al [2016] studied normal horses and induced obesity by feeding excess fat with or without a once daily high simple carbohydrate meal. Again, the weight gain did not result in insulin resistance in either group. Contrary to expectations, the horses receiving the high carb meals actually had better insulin sensitivity. [This has also been reported in earlier studies and represents an adaptation to the higher carbohydrate feeding in normal horses.]

If obesity doesn’t cause EMS, where did that idea come from? As above, there is a connection in people but it’s also true that you will find a higher percentage of obese horses with abnormally high insulin than in horses of normal weight.  However, the reason for this is probably that horses with insulin resistance gain weight more easily, not because the weight gain causes EMS – a good reminder that association is not causation https://wp.me/p2WBdh-Ex .

This doesn’t mean you can just ignore it if you horse is overweight. Excess weight puts a lot of unnecessary strain on the heart and skeletal system, reduces exercise tolerance, makes it more difficult to breathe and interferes with temperature regulation in the heat or when exercised.  These all improve with weight loss. To achieve weight loss, change the diet to 2% of ideal weight or 1.5% of current weight (whichever is larger) in grass hay, no pasture, no grain and meet mineral and vitamin needs with a supplement rather than a “balancer” which adds calories.

Obesity per se does not cause laminitis either – high insulin does. Being normal weight won’t protect from laminitis or guarantee normal insulin, but a normal weight in conjunction with a physiologically sound trim will certainly help to mechanically reduce the damage it causes.

In the chicken or egg world of obesity and EMS, it’s the EMS that comes first.

Eleanor Kellon, VMD

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Sulfate and Your Horse

Sulfur in the form of sulfate is essential for life in organisms from bacteria to plants to horses.  Sulfate is an ion with a negative charge, SO₄^-2

Copper sulfate – preserving animal health since the 18th century

Bacteria in the soil form sulfate from sulfur and oxygen. Soil sulfate may complex with other minerals or be absorbed by plants in its free form.  Most of the sulfate in plants is used to manufacture the sulfur containing amino acids. Plants also need sulfate to make chlorophyll and chemicals that protect them from insects.

Sulfate  forms of trace minerals like zinc and copper are highly bioavailable. The intestinal tract can also absorb the sulfate and has a special receptor for it called NaS1 – the sodium sulfate cotransporter. The same receptor is found in the kidney and reabsorbs sulfate from filtered blood to retain what the body needs. Sulfate absorption decreases when supply is abundant and vice versa.

While the body can, and does, absorb sulfate ions, sulfate can be generated from sulfur amino acids and this is the major source.  Sulfate is formed in the terminal breakdown of those amino acids.  Studies have shown that a completely sulfur/sulfate free diet will still support life if it supplies the required amounts of sulfur containing amino acids.

Free sulfate ions combine with ATP to form a compound called PAPS which supplies the sulfate for all body functions which require it – and there are a lot of them:

• sulfation – adding a sulfur group – is one of the main pathways for detoxifying and then excreting things like heavy metals and toxins of many different kinds including xenobiotics
• production of bile salts
• glycosaminoglycan synthesis (sulfates of chondroitin, heparin, dermatan)
• elimination of steroid and thyroid hormones
• building muscle
• activation of some hormones and cellular receptors
• mucus production, including the mucus which protects the stomach from ulceration
• essential for the formation of myelin sheaths which protect the nerves

The level of sulfur amino acids and sulfate in the diet is decreasing in many areas.  Air pollution control legislation has dramatically reduced the amount of sulfur dioxide in the air.  This used to be a rich source of sulfur for the soil, where bacteria converted it to sulfate.  Since sulfur is a key nutrient for plant growth, fertilizer mixtures increasingly need to contain sulfur.

You can check for the adequacy of sulfur amino acids in your horse’s hay by making sure the analysis includes the percentage of sulfur then check the N:S – nitrogen sulfur ratio. To determine nitrogen, divide the percentage of crude protein by 6.25. The N:S should be between 10:1 and 15:1. Also, to support normal amino acid production in the hay the sulfur should be at least 0.2%. These recommendations are from research on cattle but since most sulfur in the diet is in the form of sulfur amino acids it should work as a minimum guideline for the horse as well.

In summary, sulfate is an important nutrient for the horse.  Some comes directly from sulfate in the diet but most is derived from the metabolism of sulfur amino acids. Levels in the diet are dropping as sulfate in soil becomes less plentiful. Guard against this by supplementing 2.5 to 5 grams of methionine/day for the average size horse – more if you know your hay is low in sulfur.

Eleanor Kellon, VMD

You Can’t Just Follow Your Gut with an EMS Horse

Following your gut instinct is good advice in some situations but gut, and even good old common sense, can also be wrong.  This is where fact and science come in.

Correctly caring for a horse with insulin resistance takes some major lifestyle changes. It is up to the caretaker to implement those changes. This can be a major advantage for the horse, who doesn’t have to rely on his own will power, or it can throw any number of obstacles in his path.

We hear things like ‘The horse can’t possibly be happy without pasture’, despite the fact that millions of horses around the world are; many of which do not even have pasture as an option. Another is that they can’t possibly be healthy on a diet restricted in amounts or types of food, when in truth it is the human imposing their own emotional reaction to that possibility on the horse.

Most dangerous are objections that sound like they are based in science when they are not. One is that not permitting an IR horse 24/7 access to food will cause stress and a cortisol increase that will actually make him worse.  This has a ring of truth to it, but it’s wrong.

Sticker et al 1995 fed mares either 100% of requirements or restricted calories by 50%.  The restricted mares had a drop in cortisol levels.

DePew et al 1994 fasted mares and stallions for 19 hours then fed a pellet and hay meal. Cortisol rose after feeding and did not change in response to fasting for 19 hours.

Glunk et al 2015 fed adult Quarter horses a restricted hay diet of 1% of their body weight either as loose hay or from slow feeder nets, divided into two feedings with 15 hours between the afternoon and morning  meals.   The floor fed horses finished their meals much quicker.  There was no difference in cortisol levels between the two types of feeding. Cortisol dropped in both groups over the 28 day trial despite the markedly restricted feeding and weight loss. [Horses were sampled every 30 minutes after meals and hourly between feedings.]

Storer et al fed both normal and hyperleptinemic (IR) mares either constant pasture, free choice hay or hay and pellets only once daily.  The mares fed only once daily had an expected exaggerated insulin and glucose peak after feeding but their cortisol levels were lower than the mares with constant access to hay or pasture at all testing times.

Freestone et al 1991 did find small (but not statistically significant) rises in cortisol in ponies fasted 24 to 72 hours, consistent with the tendency of ponies, but not horses, to develop exaggerated release of fat into the bloodstream with fasting. The metabolism of ponies (and minis, donkeys) is distinctly different from horses.

What about the fact that feral horses spend 18 to 20 hours a day eating? This observation does not automatically mean horses have to spend this much time eating to be metabolically healthy.  You have to remember that grass is over 70% water while hay is typically around 10% and a much more concentrated calorie source than pasture.  They have to spend that much time eating native pasture to get enough calories.

By all means feed your insulin resistant horse with a slow feeding set up to avoid long gaps with no food that might lead to insulin peaks and also just to keep her busy but don’t worry that going without food for even short periods will increase cortisol and make IR worse. Research has proven that’s simply not the case. In fact, in study after study a drop in cortisol has been found with fasting or restricted feeding of horses.

Eleanor Kellon, VMD

Fiber is Food for Horses

Horses can derive significant calories from things that are indigestible for us.

You’ve heard your horse’s intestinal tract referred to as a furnace.  Obviously that’s not literally what happens.  It is where bacterial fermentation takes place.  Fermentation reactions produce cheese and your favorite adult beverage but that’s not what is going on either.

One of the attention grabbing factoids they threw at us early in veterinary school was that cows could survive by fermenting nothing but newspaper. They won’t be healthy for very long doing this but the point was that newspaper can be converted to calories to sustain life.  This hasn’t been tried with horses but all would agree that we couldn’t survive on hay the way horses do.

Fermentation is the enzymatic breakdown of a substance with the enzymes in this case coming from bacteria, yeast and protozoa.  Cellulose, hemicellulose, complex plant carbohydrates, fructans and soluble fibers like pectin and betaglucans are all indigestible by the horse’s digestive enzymes but can be fermented in the large intestine.  The organisms use some of the energy contained in these food fractions for themselves and what is left over, the products of fermentation, are readily absorbed into the blood stream and are what the horse uses as energy sources.

The products of fiber fermentation are primarily acetate, butyrate and propionate.  Simple sugars, starch and fructans also produce lactate.  These fermentation products can account for 60% or more of the calories absorbed by the horse.

Most people have a misguided poor opinion of lactate.  It is an important fuel that can be converted to pyruvate and burned for energy, or converted into glucose or glycogen.  Acetate is a very efficient energy source, ready as-is to enter the mitochondria to be burned.  Acetate also spares glucose which can then be used for other things like replacing glycogen stores.  Acetate is the major fermentation product of hay with even larger yields from beet pulp or soybean hulls.

If butyrate reaches the liver it can be converted to fat but most of it is used by the intestinal lining cells.  Propionate, also produced in smaller amounts than acetate, can be converted to glucose.

Now if someone asks you why horses don’t get drunk from fermenting their  food (don’t laugh, I’ve seen a claim that they can!), you’ll know why.

Eleanor Kellon, VMD

Silver Bullets are for Werewolves

I have been a strong proponent of the role of nutrition in health and optimal function for four decades but with the understanding that while it is pivotal it’s not the sole answer to everything.  Scientifically unrealistic claims for the benefits of supplements mislead owners/caretakers and end up eroding confidence in the power of nutrition.

No silver bullet supplements can guarantee safe grazing for all horses.

Some things are straightforward. Pregnant mares with severe selenium deficiency can give birth to foals with white muscle disease. Supplement those mares with adequate selenium when pregnant and this doesn’t happen. It’s rarely that simple.

For example, there’s been a mini proliferation of “topline”/muscle supplements lately. They typically are 30 to 60% protein and deliver essential amino acids (the building blocks of protein) in dosages ranging from miniscule to sufficient to correct a deficiency state in some circumstances.

The problem is you cannot build muscle just by feeding protein unless there is a dietary deficiency, and there certainly is no supplement that can specifically target the topline. There are several potential causes of topline wasting that cannot be fixed with protein. These include aging, Cushing’s Disease, chronic lung disease, poor saddle fit, Equine Motor Neuron  Disease, EPM and Equine Polysaccharide Storage Myopathy.

The back and croup are also normally covered by a thick layer of fat. Weight/fat loss alone will cause lack of definition along the topline.  The other key “ingredient” to building muscle bulk in any location is exercise.

Then there is the persistent myth that there is a widespread issue with hindgut acidity and hind gut ulcers, with a corresponding assortment of supplements that claim to address it.  The pH of the hindgut normally varies with diet – highest with hays, lower with pasture and hay/grain diets.

There is not one shred of credible evidence showing these normal  variations cause ulcers, pain or behavioral and gait issues. The most recent study that set out to investigate colonic ulcers and causes found ulceration in 12 of 56 (21%), 9 of which were clearly caused by parasites. Only 3 horses (5%) had colonic ulcerations with no clear cause visible but the health and drug (phenylbutazone) history of those horses was not known. http://onlinelibrary.wiley.com/doi/10.1111/evj.24_12732/full

Worse yet are claims for supplements that will let you put any horse out on spring pastures without having to worry about laminitis. Pasture-associated laminitis is caused by higher starch and simple sugar levels in the new growths of grass. Supplement ingredients that address hindgut fermentation (e.g. hops) are irrelevant. Ingredients supporting blood sugar control in humans are also useless since insulin is the problem, not high blood sugar.

It’s true that mineral nutrition is important to the health of hyperinsulinemic horses, but there is no evidence that mineral deficiencies  can actually cause hyperinsulinemia or that correcting those deficiencies or megadosing minerals alone can protect from high insulin levels and laminitis. Please don’t be fooled.  The only way to protect horses prone to hyperinsulinemia from pasture associated laminitis in the spring is to keep them off the pasture.

It’s human nature to want a quick fix, a simple solution to make everything normal. Unfortunately, that’s rarely possible. Nutrition and appropriate supplementation is just one piece of the puzzle. Silver bullets are for werewolves.

Eleanor Kellon, VMD