The Role Of The Hind Gut in Laminitis

A lot of attention has been directed to bacterial endotoxins, MMP enzyme activators and fructan or starch fermentation as factors in laminitis but how much are they really involved?

With laminitis, it’s usually hormones, not the hind gut

In the “horse broke into the feed bin” scenario, too much starch reaches the hind gut where it is fermented to lactate. A significant acidosis develops which weakens the lining and allows bacteria, bacterial endoxins and other factors to enter the circulation.

The same lining damage and bacterial invasion happen with experimental fructan overload, colic/colic surgery, intestinal infections like Potomac Horse Fever or Salmonella, colitis and uterine infections from retained placenta. These horses have SIR – systemic inflammatory response. They are obviously very ill with dehydration, fever, elevated white count, usually diarrhea. In fact, most of these horses are in hospitals.

When laminitis occurs without the horse being seriously ill and with no overconsumption of grain, there is at least a 90% chance the cause is high insulin from equine metabolic syndrome or pituitary pars intermedia dysfunction (PPID).

Why is this important? The focus in treating endocrinopathic laminitis should be on lowering insulin, not the hind gut, but many supplement sites to this day talk about hind gut factors – and, of course, sell stuff for that. There is even dangerous advice, like suggestions to feed alfalfa because it does not contain fructan when alfalfa is a laminitis trigger for many horses.

The bottom line here is that unless the horse is obviously also ill, you should be focusing on insulin, not the hind gut. For more in-depth information go to, especially the 2017 NO Laminitis proceedings, and for a list of products safe for metabolic horses, see .

Eleanor Kellon, VMD

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Copper and Zinc

Rich, fade-proof colors require adequate copper and zinc

Copper and zinc are two of the most common trace mineral deficiencies around the world and the symptoms often intertwine and overlap so discussing them together just makes sense.

In addition to the levels of these two minerals often being too low in the diet, factors such as high iron intake and high sulfate in water or forage makes the situation even worse by interfering with absorption.

While other deficiencies may not be easily visible, zinc and copper problems often present in ways that are readily seen.

A dead giveaway of copper and zinc deficiency is bleaching of the coat and red ends on black manes and tails. This is typically blamed on sun exposure, which is true, but horses with adequate levels of melanin will not experience these changes.

Melanin is the pigment that gives skin and hair its color. Melanin also protects against UV radiation and chemical  damage. Copper (all colors) and zinc in combination with copper (darker colors) are essential for the production of generous amounts of melanin.

Hoof quality also suffers with copper and zinc deficiency. Deficiencies of either copper or zinc have been linked to:

  • Soft feet
  • Cracks
  • Sole hemorrhages
  • Abscesses
  • Thrush

Dramatic improvements in hoof quality are often seen following adequate zinc and copper supplementation.

Only dietary analysis can tell you the precise amounts needed but consider a ballpark figure of 250 mg of copper and 850 mg zinc as the starting point for horses showing outward evidence of deficiency.

Eleanor Kellon, VMD

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Don’t Fear Selenium

While it is true that selenium can be toxic, so can many other nutrients.  Focusing on toxicity leads to unjustified fears of supplementing this mineral which can do more harm than good.


Selenium is needed for conversion of thyroid hormone to its active form, for maintenance of key antioxidant enzyme systems and for immune function. Deficiency in pregnant mares leads to foals with the often fatal white muscle disease. It is also implicated in myopathies of adult horses.

In the map of soil selenium levels above, adequate only means that there might be enough selenium in the crops to support the bare minimum requirements for selenium – not necessarily that there will be.  Local soil conditions, especially pH, will also influence levels in the crops.

Poisoning may occur when horses are on range grazing for many months with poor grass availability and easy access to weeds that concentrate selenium (seleniferous plants).  Selenium toxicity from properly formulated and manufactured supplements, grains or from hays is virtually unheard of, even if you use more than one source of selenium.

The recommended minimum daily intake of selenium for an average sized, idle, adult, nonbreeding horse is 1 mg/day, or 0.1 mg/kg (= 0.1 ppm) in the total diet.  The suggested maximum safe intake, above which toxicity many develop over weeks or months, is 20 mg/day or 2 mg/kg (2 ppm).  That’s a big difference.

Let’s take a look at how this might break down for an average horse.  We’ll assume the hay is coming from an adequate selenium area and provides 1 mg/day.  This horse is also getting 5 lbs/day of a supplemented grain which has 0.6 ppm.  That’s 0.6 mg per kg or 0.6 x 5/2.2 (2.2 lbs in one kilogram) = 1.36 mg for a total of 2.36 mg.  Let’s say the owner is also feeding a vitamin and mineral concentrate with 3 mg/dose.  That brings the total to 5.36 mg/day.  Even if you add a vitamin E and selenium supplement with 1 to 2 mg/dose (35 to 70 ppm if you feed 1 ounce/day), you are still way, way below the upper safe limit of 20 mg/day.

An additional factor to consider is that arsenic and sulfate, often present in generous levels in waters and feeds from adequate or high selenium areas, decrease the absorption of selenium.  So does copper which is present in supplemented grains and mineral supplements.

Finally, the minimum requirement of 1 mg/day for inactive adult horses can change significantly with work, allergy, inflammation or infectious disease challenge, as well as high levels of minerals that interfere with absorption.  For example, many endurance riders feed 5 to 7 mg/day routinely.

If you are concerned about the amount of selenium you are feeding, either too much or too little, consider blood testing.  Whole blood selenium levels are a good estimate of total body selenium content.

Eleanor Kellon, VMD

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Emergency Care for Metabolic Laminitis

Research has shown about 90% of laminitis cases are metabolic (endocrinopathic) which means the key to successful treatment is controlling insulin.

High insulin is the cause of most laminitis

Everyone’s first instinct is to reach for phenylbutazone or some other NSAID medication to control pain but these are only minimally effective. The reason is endocrinopathic laminitis is not inflammatory and they do nothing to control insulin. They should not be used for longer than 5 days but horses often get caught in a prolonged course of NSAIDs because the insulin level and trim have not been adequately addressed.

A useful acronym to keep you focused on the comprehensive treatment is DDT:

  • D: Diagnosis
  • D: Diet and Drugs
  • T: Trim

If the horse has not been tested for metabolic syndrome and Cushing’s with insulin and ACTH this can be done after the condition has stabilized. In the meantime, starting metformin at 30 mg/kg twice a day can help control insulin. If the horse also has PPID (Cushing’s disease), pergolide will be necessary to lower insulin.

The emergency diet should be soaked grass hay only, fed at 1.5% of current body weight or 2% of ideal weight, whichever is larger. Plain beet pulp which has been well rinsed then soaked can be used to carry supplements and medications. No pasture, alfalfa or clover. No grains including those that claim to be safe, and no balancers since their base is often not safe. Safe means less than 10% sugar and starch combined.

A general vitamin and mineral supplement can be added but it is far better to have the hay analyzed so that one can be chosen which actually matches what the horse needs. Also analyze for sugar and starch to see if you need to continue soaking. Vitamin E 2000 IU for the average size horse and 4 to 6 oz of ground flax should be added as well as salt.

The feet should be radiographed as soon as possible. Remove shoes and trim the horse to have a short rounded toe and palmar angle no higher than 5 degrees to minimize stress to the laminae. Styrofoam blocks or boots and pads are best for comfort.

If you focus on diagnosis, diet and trim, not just pain control, outcome will be much improved. For more detailed information, visit .

Eleanor Kellon, VMD

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Whole Food For Horses

The “whole food” claim is being used to market some feeds and supplements for horses but what is a whole food and are these products really superior?

Does this look like whole food to you?

The term whole food is not currently regulated so it can mean anything the company using it wants it to mean. “Whole food” was originally coined in the 1940s and referred to produce “without subtraction, addition or alteration”, harvested and eaten fresh, raised without pesticides, herbicides or chemical fertilizers – in other words, both unprocessed and organic.

Whole food in horse products is definitely not the same as organic. If you don’t see the USDA seal of certification, it’s not organic. Non-GMO is not the same thing as organic either and no guarantee the product does not contain chemicals even far more dangerous than glyphosate.

If you don’t see the USDA seal, it’s not organic.

Whole food is supposed to mean not processed in any way – like eating an apple or peach. Reference might be made to minimal necessary processing. This should include things like peeling a banana to eat it, rinsing dirt off a carrot or cracking open a nut. However, in one prominent feed that plays the whole food card the only actual whole food in it is oats. Everything else has been ground, skinned, pelletized, dried, heat dehydrated (and possibly preserved with sulfur dioxide), dehulled, cleaned, exposed to strong magnetic fields, steamed (split peas), polished, or solvent extracted.

The reality is that very few whole foods will escape rotting inside a feed bag without processing or preservatives. Even drying and grinding leads to loss of some vitamins and fragile fatty acids. What starts out as a whole food loses some critical portions of its nutrition by the time it goes into a bag and really isn’t a whole food any longer.

Whole food supplements have another problem. In addition to not really being whole foods after they are processed into a powder or bar, the levels of nutrients they provide falls far, far short of being helpful. For example, one “multi” type whole food supplement made from fruits, vegetables, nuts (and some most definitely not whole foods like oils, bran and processed yeast) provides the following amounts of nutrients per daily serving:

  • Protein: 6.2 grams versus requirement of 630 grams (500 kg horse at maintenance)
  • Calcium: 0.8 grams versus requirement of 20 grams
  • Copper: 0.4 mg versus requirement of 100 mg
  • Zinc: 1.35 mg versus requirement of 450 mg

Those are only the rock bottom bare minimum requirements in health. Actual optimal requirements can be much higher. Are these numbers misleading because nutrients in foods are much more bioavailable?  No. That’s a myth. In fact, research has shown minerals in foods are far less bioavailable than minerals in supplements, including inorganic minerals from rock.

There’s nothing wrong with the ingredients that go into these feeds and supplements but the suggestion they are superior to other products does not stand up to scrutiny. For example, I would much rather feed processed wheat bran with its high protein, minerals and vitamin-packed wheat germ intact than the whole wheat grain which is loaded with high glycemic index starch/flour.  The supplements have nice ingredients and are yummy but they’re treats, not supplements.

As much as I favor whole foods like whole oats, it’s not the answer to optimal nutrition for the management scenario of today’s domesticated horse.

Eleanor Kellon, VMD

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Attention Owners of Cushing’s Horses Diagnosed by TRH Response Test

Some horses with Cushing’s/PPID have normal levels of the hormone ACTH but test positive with a TRH stimulation test. How can you monitor their response to medication when ACTH is normal to start with?

Some horses with PPID can only be diagnosed by a TRH Response Test

Testing ACTH levels is the usual way PPID is diagnosed but it’s not always accurate. Many early cases, and even some advanced cases, do not have abnormal levels of ACTH.

We have learned a lot about early PPID, where signs like fall laminitis later in life and unexplained tendon or ligament disease can be signs long before the classical long curly coat and muscle loss. There are even some cases with those late classical signs that do not have high ACTH.

We can diagnose those horses with a TRH Response Test. TRH (thyrotropin releasing hormone) stimulates the intermediate lobe of the pituitary gland resulting in abnormal levels of ACTH after TRH in positive horses.

Once diagnosed, the horse will be treated with pergolide but how do you make sure the dosage is correct and doing its job? We can’t use ACTH since that was normal before treatment. It makes sense that the TRH response would improve or normalize but that has not been documented and can’t just be assumed.

The nonprofit Equine Cushing’s and Insulin Resistance Group, Inc,, wants to change that. They are offering $300 to offset testing costs to anyone with a PPID horse diagnosed by TRH testing who will repeat the test after the horse has been on pergolide for at least 3 weeks.

If your horse was diagnosed by a positive TRH test and has been on pergolide for at least 3 weeks, contact me at drkellon “at”

Eleanor Kellon, VMD

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The Power of Magnesium

Magnesium often receives little attention in equine nutrition. For example, you will rarely see it listed in the analysis on a feed bag. Despite this, it could easily be argued that no other mineral has as many important functions.

Magnesium is required to both store and release cellular energy in ATP

The biochemistry is complicated but basically the energy locked into your horse’s food is transformed and stored as high energy bonds between phosphate molecules. The highest energy form is ATP, adenosine triphosphate. Magnesium is required to stabilize and store ATP as well as to release the energy in those bonds. Without it, all cells would die.

Magnesium is also required for all genetic  material, DNA and RNA, to function and be transcribed. You can’t get much more basic to survival than that.

Science has so far identified over 300 enzymes that require magnesium to function. Virtually any body function you can think of requires adequate magnesium at some step along the line.

While calcium is a major trigger/facilitator of muscle and nerve reactions, magnesium’s function is more often to moderate and regulate.  This shows up clearly in the signs and symptoms of magnesium deficiency.

Low magnesium is a very common cause of behavioral issues such as hypersensitivity to sound or touch and irritability. Aberrant nerve activity, like thumps, can be seen.

In other species, magnesium deficiency has also been clearly identified as both a cause and effect of insulin resistance.

Muscular irritability manifested as twitching in muscles, increased muscle tone, even elevated blood levels of muscle enzymes and signs of tying up can also be caused by magnesium deficiency.  With extreme deficiency, weakness results because of the key function of magnesium in maintaining ATP stores.

Magnesium is present in all equine feeds but levels vary considerably. Acidic soil conditions often result in much magnesium being washed out of the soil by rain. Whole grains, brans, germs and alfalfa tend to have the highest levels but this can be offset by high calcium levels which may compete for absorption.

The only way to determine how much magnesium supplementation may be needed in your horse’s current diet is by diet analysis, especially hay analysis. In general terms, if you suspect a muscular, insulin resistance or behavioral issue with your horse may have a component of inadequate magnesium intake try supplementing with 5 to 10 grams of elemental magnesium per day.

Eleanor M Kellon, VMD

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These May Not Be True Symptoms

There has been an insidiously growing trend to label certain observations as indicators of a disease/disorder when actually they are really almost universal aspects of normal equine behavior. If you are trying to convince an owner to buy a product or service based on these observations you are set to make a killing.  If you are the owner being targeted, you could be wasting a lot of worrying – and money – for nothing.

Some signs and symptoms are too nonspecific to use for a diagnosis

Girthiness:  Resistance to having the girth tightened, or even reaction to pressure along the midline of the lower abdomen, is typically blamed on gastric ulcers.  This makes no sense anatomically since the stomach sits high in the midline of the abdomen with colon between stomach and lower abdominal wall.  Higher up it is flanked on either side by the spleen and the liver.

Furthermore, you have to search far and wide to find any horse that does not react in some way to having the girth tightened. Some just pin their ears. Some take a deep breath and hold it.  Others actually kick or snap.  In short, horses don’t like having the girth tightened.

Flank sensitivity to touch:  Sensitivity to touch in the flank is similarly blamed on a gut problem, typically hind gut “ulcers” or “leaky gut”, sometimes ovarian issues, but once again this is a very common reaction even in normal horses.  The flanks are a vulnerable area.  They lack the thick skin and dense fat layer that protects the hind quarters and without the ribs are a direct portal to internal organs for a predator.  All  horses are protective of their flanks and reactive to touch here, especially if they do not know it is coming.

Weak going to the right:  Weakness traveling to the right or trouble holding the right canter lead, falling to the inside on the right lead have been blamed on a problem with the cecum (usually acidity) or even neurological disorder.  Horses, like people, have a strong and a weak side.  The vast majority of horses are stronger going to the left and similarly most riders are better going to the left – at least in the Northern Hemisphere.

Kidney pain:  Sensitivity to pressure along the topline of the back is sometimes said to indicate kidney disease.  However, the kidneys are well protected underneath the ribs/spine and with a layer of encompassing fat.  Kidney disease is extremely rare in horses.  When it does occur, pain on pressure in this area is not a part of the picture.  With back pain look for bone or muscle disorders as the cause.

What if these findings appear suddenly; are a change from the horse’s normal behavior?  Those are valid observations, and important ones, but it’s also important to remember that increased sensitivity to touch/not wanting to be touched is a common and very nonspecific indicator that the horse is in pain or does not feel well.  It doesn’t necessarily tell you anything about why.  Poor concentration and resistance to cues under saddle are also common nonspecific changes.

With any question about how the horse is moving you should start with a good old-fashioned thorough lameness and neurological examination. Always rule out a training or musculoskeletal issue before buying into more esoteric explanations.

Eleanor Kellon, VMD

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Why “Bute” Doesn’t Work with Endocrine-Related Laminitis

Both you and your veterinarian are anxious to relieve your horse’s pain when there is laminitis. The first thing reached for is usually phenylbutazone or another NSAID drug like Banamine or Equioxx. Unfortunately, they often have little effect.

Laminitis caused by high insulin is different from other types of laminitis

There are many different types of lamintis, including:

  • Mechanical: A horse is overloading one leg because another is injured, stretched laminae and dropped coffin bone from a long toe and/or shoes
  • Inflammatory: Grain overload, experimental fructan overload, retained placenta, Strangles, colic, Salmonella, Lyme, Potomac Horse Fever.
  • Endocrinopathic – EMS or PPID.

Antiinflammatory drugs like the NSAIDs (nonsteroidal antiinflammatory drugs) are most effective with the inflammatory types of laminitis which involve destruction of the basement membrane of the laminae, which does not occur in endocrinopathic laminitis.

The FDA approved instructions on the product inserts for these drugs clearly limits their use to 5 to 14 days only (depending on the drug). This is because of the significant risk of damage to the stomach, colon or kidneys with long term use. Despite these mandated precautions, many horses end up in a cycle of long term pain and NSAID use because the real cause of their pain is not being addressed.

Research has clearly shown that approximately 90% of laminitis cases are endocrinopathic.

Endocrinopathic refers to a problem with the endocrine system, the hormones. In this case it is insulin in horses with Equine Metabolic Syndrome – EMS or PPID – Pituitary Pars Intermedia Dysfunction. High insulin levels cause the laminitis.

NSAIDs do nothing to lower insulin. The white blood cell invasion and basement membrane destruction does not happen with this type of laminitis. The NSAIDs are reasonable for a few days because any damaged or destroyed tissue will trigger an inflammatory reaction but the real focus needs to be on insulin and the effects of insulin.

Insulin is lowered by a low sugar and starch diet. Feed only grass hay soaked for 30 minutes until a hay analysis can be done. No grain including those called “safe” and soaked beet pulp only as a carrier for supplements. For more details see the files at . Those that fail to respond can be started on metformin. It’s also important to do a physiologically correct realigning trim as soon as possible.

Finally, the only clearly documented effect of high insulin is to increase levels of endothelin-1, which causes blood vessels to spasm. The Chinese herb Jiaogulan can counteract this by increasing activity of the eNOS, endothelial nitric oxide synthase, enzyme which produces nitric oxide inside blood vessels to dilate them. Arginine supports this production.

Endocrinopathic laminitis is different but if you approach it with the goal of controlling the cause – insulin – results are good.

Eleanor Kellon, VMD

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Open Letter to the AAEP Regarding Pasture Laminitis

April 7, 2022

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. .

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

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)

In addition to the post on the AAEP Facebook page, multiple materials on the site have similar inaccurate information, e.g.,
Geor 2013 refers to restricting pasture access because of fructan. Parks 2016 No mention of testing and treatment for endocrinopathic
laminitis despite the fact this explains the vast majority of cases. Frank 2018
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.


Eleanor M. Kellon, VMD
Owner, Equine Cushing’s and Insulin Resistance on
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 85282 ! of !2 3

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