Vitamin C – Friend or Foe

Vitamin C [ascorbate/ascorbic acid] is a water soluble vitamin which functions as an important antioxidant and is needed for the synthesis of L-carnitine, catecholamines like epinephrine and dopamine, as well as collagen, the major protein in all connective tissues, including tendons and ligaments, even blood vessels.  Deficiency causes a disease called scurvy, beginning as weakness and muscle pain, progressing to bleeding gums, loose teeth, poor healing and eventually mental changes and death.

Fresh, live grass in an excellent source of Vitamin C.

Unlike humans, the horse can synthesize enough vitamin C in its body to prevent the development of a full blown deficiency state (scurvy). However, the ability of this synthesis
to maintain normal vitamin C levels and the role of dietary C is poorly understood. We do know that heavy exercise and chronic disease, especially lung disease, lead to decreased vitamin C blood levels in unsupplemented horses, as does stabling versus pasture access. Low blood levels have also been linked to poor wound healing in horses.

Although information is limited, a “conditionally essential” status may best describe the need for additional vitamin C in the diet of horses that are recovering from illness or surgery, or exercising heavily, when requirements may exceed the body’s ability to make it. The NRC states that information about vitamin C levels in common feedstuffs is lacking but a study from 1938 measured ascorbic acid in many common feeds, hays and references levels in grasses.

The figures are presumably on a dry matter basis and they report 20 to 136 mg/100 gram in fresh pasture; 1.3 mg/100 g in 50:50 alfalfa/grass hay; 0.9 mg/100 g in grass hay; 1.3 to 1.8 mg/100 g in alfalfa; 0.7 mg/100 g in beet pulp; about 0.6 mg/100 g in grains (this would only apply to whole grains). A stabled horse on a grass hay based diet would be taking in less than 1 gram of C from its diet daily while an average horse on pasture is getting a minimum of 20 grams/day (quite possibly part of the value of “Dr. Green”!).

In the early 1970s, Dr. Linus Pauling was recommending megadoses of vitamin C for maximum health and disease prevention. As usually happens, many of these claims were debunked and the pendulum actually swung so far to the other side that megadosing was proposed to be toxic.  Once again, the truth is somewhere in between.

With specific reference to the horse, toxicity in the form of diarrhea usually begins with dosages of 20 grams/day and above. This may be more of a local irritation than a toxicity.  There are two other properties of vitamin C that would dictate caution in horses known or suspected to be iron overloaded. One is that vitamin C increases iron absorption in the intestine. It also can act as a pro-oxidant rather than anti-oxidant in the presence of excess iron in the circulation or tissues.

A reasonable level of supplementation is 3 to 10 grams/day for an average size adult horse, keeping to the lower levels with iron overload.  For additional antioxidant support vitamin C can be combined with other antioxidants such as resveratrol from grapeseed, citrus bioflavonoids, MSM, herbals with good antioxidant activity such as Jiaogulan or Spirulina and vitamin E for fat soluble coverage.

Eleanor Kellon, VMD





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Neurological Herpes Infections

Neurological Herpes, aka EHM – equine herpesvirus myeloencephalitis – is usually caused by a specific strain of the EHV-1 virus which is equine herpesvirus 1. EHV-1 typically causes mild respiratory tract disease or “colds” in young horses. Most adults develop immunity but at least 75% continue to carry the virus which may be shed in nasal secretions during times of stress.

The EHV-1 virus can also cause abortions and illness of infected foals that survive. The neurological form is caused by a specific mutation of the EHV-1 virus which causes damage to the blood vessels of the spinal cord and/or brain. The horse may be infected with that strain or it may mutate from a more common respiratory strain after infection. It has a strong tendency to attack areas of the spinal cord which control the hind legs and ability to urinate.

Country fairs, rodeos, shows, racetracks and other places where horses congregate are ideal for spreading viral infections

EHM outbreaks occur after large numbers of horses have congregated, such as at shows or racetracks, but the virus can also be carried back to infect home barns. There have always been scattered cases of EHM seen during outbreaks of respiratory EHV-1 disease but in the last decade or so it has become clear that outbreaks of EHM, often without respiratory disease, are becoming more common. Anywhere from approximately 29% to 71% of EHM cases are euthanized due to the severity of their disease.

Despite the fact that EHV-1 vaccinations are often required by barns, shows or racetracks, there are no vaccines that can prevent EHM although preliminary research has suggested the modified live vaccine, Rhinomune, may be somewhat better than inactivated vaccines. The good news is that state officials do a spectacular job of controlling spread of the virus when a case has been reported.

Your best protection is strong biosecurity measures such as:

  • Isolate new horses on the premises for at least 2 weeks
  • Pick boarding facilities with little to no horse movement if your horse rarely travels off the farm
  • Always thoroughly strip and disinfect stalls before using them the first time, at home and when away
  • Disinfect trailers between trips
  • Bring your own buckets, bedding, pitchforks, etc when you travel
  • Use a small mesh wire muzzle or completely sealed muzzle when using turnout facilities or temporary holding stalls away from home to prevent contact of the muzzle or tongue with surfaces
  • Do not allow direct muzzle contact with other horses away from home

The individual’s best defense is a strong immune system and antioxidant defenses. This must start with a quality, well balanced diet with adequate protein. Pay attention to the antioxidant and homeostatic nutrients often low in unsupplemented diets such as selenium, zinc and copper as well as vitamin E and omega-3 fatty acids if not on fresh pasture. Avoid added iron, and minimal to no manganese is needed in most areas. Lysine is also very important for immune function in general and because a low lysine level facilitates growth of EHV-1. Supplement 10 grams/day routinely, with a second or third dose daily if the horse has been exposed.

Exposed or symptomatic horses may also benefit from higher than normal doses of vitamin E to help them maintain normal levels of this key antioxidant in the nervous system. Plant based antioxidants, particularly resveratrol from grapes and citrus bioflavonoids, support antioxidant activity and structural integrity in blood vessels.

EHM is not preventable by vaccination but you can limit exposure by good biosecurity measures. As with any infection, a robust immune system will limit the activity of the organism in the horse’s body. If your horse does get infected, good antioxidant levels will help control damage and sound nutrition contributes greatly to recovery.

Eleanor Kellon, VMD

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Nutrition for the Lactating Mare

There is a reason the horse evolved to foal in the Spring. The rich, tender, high moisture young vegetation provides the energy and protein dense nutrition the mare needs to make sufficient milk.

In peak lactation the mare needs 1.8X more calories than when she is not milking. That’s the easy part. She also needs 2.5X more protein and 3X more lysine, calcium and phosphorus.  If her diet was only providing enough protein, lysine and minerals to support adult, nonpregnant body condition, simply feeding enough to meet calorie needs is going to leave sizeable deficits in protein/lysine, calcium and phosphorus. Even diets adjusted for late pregnancy will not have a sufficient concentration of protein, lysine and minerals.

Nature gives precedence to providing for the foal. If the mare’s diet is deficient in protein she will begin to break down her own muscle tissue to obtain amino acids for the milk. This leads to both loss of muscle mass and weight loss in general.  Milk production also suffers with insufficient protein. To get the minerals she needs she will leach calcium and phosphorus from her bones, trace minerals as needed from any stores she has in the liver and kidneys. This is not a sustainable situation for her future health and fertility.

What she needs will, as always, depend on what is in the base diet. If the mare is turned out on sufficient high quality young pasture, calories, protein, lysine, vitamin and essential fatty acid requirements will be met.  The only hole will be minerals. Working with a professional will help you be more precise but generally these mares do very well with a carrier feeding of 1 lb each alfalfa pellets and plain oats with 1.5 to 2 times the regular dose of a  vitamin/mineral supplement with a calcium:phosphorus ratio of 1.2:1.

If the mare is on hay with a protein level of at least 11%, her crude protein needs will be met but she will need mineral supplementation as above plus key amino acids of lysine, methionine and threonine, double the usual dose of 10-5-2 grams per day.  Mares not on fresh pasture also need vitamin E and essential fatty acids from flax or chia.

If the hay is below 11% protein, substitute up to 2 pounds of a 25% protein vitamin and mineral supplement for the plain minerals above. If this isn’t enough to make up the protein deficit, add a 40% protein supplement to avoid excess minerals or too much bulk.  Decrease the triple essential amino acid supplement to one dose and finish off with the vitamin E and flax.

One more thing extremely important for lactating mares is salt. Add 2 oz directly to food or sprayed on hay and keep loose salt available in a small feeder.

As the foal grows and eats more solid food, milk production will drop and you will see the mare start to gain weight. When this happens, begin decreasing how much she is fed and cut back on all supplements by the same percentage – e.g. 25% drop in food and 25% drop in supplements.

You can get away with a lot when feeding lactating mares but the rewards of doing it correctly are immediately obvious in the condition and health of both the mare and her foal.

Eleanor Kellon, VMD

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Diet or Trim – What’s More Important for Hoof Health?

If you ask me which is more difficult for an owner to get right, I’d say the trim. If you ask a talented hoof professional, they would usually say diet. It’s actually a trick question.  Both are critical and one can’t produce a healthy hoof without the other.


There is an acronym I use for reminding owners what needs to be done to effectively treat a laminitic horse – DDT.

  • D – Diagnosis, to identify and remove the cause
  • D – Diet, correct calories, protein, essential fatty acids, vitamins and mineral balance
  • T – Trim, to make the “shoe” (hoof capsule and solar structures) fit the “foot” (bones)

Cut corners on any of these and you won’t get good results. With hoof issues other than laminitis which do not have a systemic disorder cause, it is still equally important to address both the diet and the trim.

Trim is critical whether the horse is shod or not. As above, the goal of the trim should be to make the external structures conform to the interior. A physiologically correct trim is a work of art which sculpts/molds the hoof to the proper configuration.  Common problems such as flares, cracks, white line stretching, flat soles/distal descent, navicular irritation, underrun heels and coffin joint disease all have a major component of incorrect trimming.

On the other hand, nutrition plays a huge role in hoof quality. Poor nutrition can sabotage trimming efforts to restore hoof form. An example I see often is the long toe, underrun heel foot. This is the equivalent of you trying to walk in shoes two sizes too big in the toe but with the back half of the heel missing.

A long toe always creates tearing forces on the laminae. When the tissue is weak to begin with, toe flaring and laminar damage is worsened. Similarly, poor horn quality means heels will collapse forward more easily.

This is a quick rundown of key nutrients and their effects:

  • Protein: The hoof is over 90% protein. The amino acid methionine is particularly important because sulfur-sulfur bonds impart significant strength and sulfur amino acid levels are dropping in many forages.
  • Zinc: Deficiency has been linked to slow growth, thin walls, weak white line connections, weak horn
  • Copper: Inadequate copper or low copper+zinc has been associated with solar hemorrhage, thrush, cracks, abscesses, soft horn
  • Biotin: Supports normal growth rate and improves connections

These are only some of the more familiar big players. Because of the high metabolic rate of cells forming the hoof wall, virtually every vitamin and mineral has a role to play. However, more is not better and the key to growing healthy feet is identifying and correcting deficiencies and imbalances in the individual diet.

Good hoof supplements do exactly that, and so would a general “balancer” or vitamin/mineral supplement that actually matched the profile of vitamins and minerals your horse needs in his diet without providing too much of things he doesn’t need added.

A correct diet will eliminate the need for a hoof supplement – but it won’t substitute for a good physiological trim.  Get both of these right and you’re on your way to healthy feet.

Eleanor Kellon, VMD








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Reconditioning the Older Horse

Horses have tremendous athletic potential but they did not evolve to do most things we ask of them and conditioning is necessary.  On the flip side, periods without work lead to deconditioning and care should be taken to get the horse back in shape gradually. This is especially true for seniors.

by Iva Balk, from Pixabay

Many people don’t realize how much a horse loses fitness when not worked. For example, highly conditioned fit Arabians put in stalls with their only exercise being 30 minutes on a mechanical walker twice a day lost approximately 1% of the bone mineral content of the third metacarpal (cannon bone) every two weeks over a 12 week period. Cardiac changes with deconditioning were monitored for 12 weeks in intensely trained 3 and 4-year-old Standardbreds.  Heart size and function remained unchanged for the first 4 weeks, after which there was steady decline which was continuing at week 12. Skeletal muscle enzymatic efficiency, glycogen stores and mitochondrial numbers also decrease.

Horses on continuous turnout that are very active would have less dramatic declines but will still lose condition. Older horses also have to deal with age-related changes which include:

  • Sarcopenia (loss of muscle mass). This is worse in horses with PPID (Cushing’s disease) but also occurs with age
  • Decreased bone mineral density
  • Development of central core lesions in tendons
  • Reduced number of chondrocytes, the cells which produce joint cartilage
  • Altered heart function

Although you  may hear mention of lung function decreasing with age, this is actually one area where there are no age-related changes. However, horses with chronic lung disease do accumulate irreversible lung damage over time. Even without lung damage, older horses may seem to be working harder to breathe than younger ones at the same workload simply because it is harder for them to perform the work.

If this makes you inclined to want to retire your older horse, don’t!  Exercise actually combats many of the effects of aging. Even arthritis benefits from exercise. The exception is tendon/ligament strength. Because of this limitation, it’s very important to condition the older horse in a way that avoids fatigue.

The type and duration of exercise is not a reliable indicator of its intensity – how hard it is for the horse to perform it. Heart rate (pulse) is best for that. A heart rate of up to 80 immediately after  exercise is light work; up to 120 moderate work; over 120 hard work with 200-220 being maximal intensity. An overweight older horse doing a steep hill can easily reach the upper intensities. You have to check to tell. Keep exercise for the older horse in the moderate range. As he gets more fit, he will be able to do more at that heart rate.

Heart rate recovery is an excellent indicator of how fit the horse is for the work he just did. If he recovers to resting rate in 15 minutes, he’s fit for that level. If it takes 30 minutes, you are working in the safe training zone. If over 30 minutes, the work level is too high to be safe.

In my experience, older horses typically show rather dramatic responses to the correct nutritional support.  A sound diet with adequate quality protein, balanced minerals, salt, vitamin E and omega-3 is the foundation. Beyond that, these are my go-to support for the older horse:

  • Jiaogulan. This is an adaptogen free of the harsh cardiac stimulating effects of Ginsengs that supports exercise capacity by enhancing blood supply to the muscles and encouraging growth of new vessels, via nitric oxide production which also benefits tendon and ligament health.
  • Acetyl-L-carnitine.  The combination of antioxidant effects and support for energy generation and mitochondrial synthesis makes this the perfect exercise complement. i
  • L-leucine.  Highly anabolic amino acid, essential for maintaining and building muscle bulk. Very helpful in overcoming temporary exercise-related muscle discomfort.
  • Joint nutraceuticals (glucosamine, chondroitin, hyaluronate) plus MSM and herbal support.  Maintaining homeostasis between forces of breakdown and repair is one of the biggest challenges in older horses. I have found a combination of effective dose nutraceuticals with targeted herbals works best.

Condition your seniors carefully with full spectrum support and you will be able to enjoy their experience and wisdom for many years, while helping them maintain their best health at the same time.

Eleanor Kellon, VMD

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Pasture Associated Laminitis

Everyone loves Spring, but as a horse owner you may be anxious about the possibility of pasture associated laminitis [PAL] if you let your horse graze those tantalizing luscious new growths of pasture. How great is the risk?  Can you avoid it?

Green goodness or potential disaster?

There are plenty of articles out there that warn about the dangers of high fructan in Spring pastures triggering laminitis. Many of them are written by people who want to sell you a product to control hind gut acidosis. They will tell you in the fructan theory that laminitis is caused by fermentation of fructans to lactate causing acidosis in the hind gut and damage to the lining which allows entry of dangerous bacterial products into the blood stream.  So far, so good.

What they don’t tell you is that this scenario has only occurred in an experimental setting with huge doses of 5 to 7.25 pounds of pure chickory root fructan given to horses by stomach tube in a single dose.  Lower doses do not cause a problem and do not damage the intestinal lining. A horse grazing a high, 7.5% fructan North American pasture would have to eat all day to take in only 1.65 pounds of fructan. [Based on a 500 kg horse eating 2% of body weight, dry matter,]

They also don’t tell you that a horse with hind gut acidosis severe enough to damage the mucosa and cause laminitis would also be obviously ill with fever, septicemia, colic and severe diarrhea.  There’s no such thing as a little bit septicemic. The dose of fructan matters. The horse’s digestive tract can handle wide variations in pH without becoming damaged.  There has never been a naturally occurring case of laminitis linked to pasture fructan levels.

There’s much more at stake here than wasting money on an inappropriate supplement. If you don’t understand what is really the driving force behind PAL you may have a false sense of security, putting the horse or pony at risk.

PAL has been studied by multiple researchers and the overwhelming conclusion is that it is related to elevated insulin levels in endocrine disorders, caused by the response to starch and/or sugar – not fructan.

It is very important for owners to understand what puts a horse at risk of PAL or even laminitis from an inappropriate diet with no pasture access. PAL is linked to elevated insulin responses. The classical appearance of a horse or pony at risk is one that is overweight with an obvious fatty crest on the neck but many metabolically abnormal horses have a normal weight. A horse that is older may also develop PPID (Cushing’s disease) and change from one that always tolerated pasture well to one that is now at risk of laminitis.

If you suspect your horse is at risk, speak with your veterinarian and pursue testing. For further details, visit

Eleanor M. Kellon, VMD

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Mares Transitioning to the Breeding Season

Horses are long day seasonal breeders, with both males and females showing seasonal variability in reproductive function but it is much more obvious for the mares. Most mares have suppressed ovarian activity which begins in the fall and ends in early spring but they do not immediate begin normal cycles.  The interval between normal cycling and cessation of cycling is called the transition period and lasts approximately 6 to 10 weeks.


 Cycling resumes under the influence of increasing day length

Here in the continental United States, the transition period usually begins between March and April but may be delayed by older age, low body weight, very cold weather or poor nutrition. An increasing plane of nutrition, such as grazing spring pastures, seems to hasten cycling and fertility.

During the transition period there will be 2 to 5 “waves” of developing follicles which are either resorbed or remain as large follicles which fail to ovulate. Most mares show no outward sign of cycling or receptivity to the stallion during the transition phase. Others may show estrus but at irregular intervals that are either longer or shorter than normal.

There is really no treatment available or necessary for the transition period in most mares. If you would like to breed your mare, an experienced reproductive veterinarian will be able to follow the follicles by palpation and/or ultrasound to know when your mare is truly ovulating and ready to be bred.

Mares that typically show wide swings in behavior with their cycles will begin to show this pattern during the transition period. It may even be exaggerated when follicles reach a large size but fail to ovulate (anovulatory).

Some mares with metabolic syndrome have the most difficulty of all. The large anovulatory follicles can cause severe colicy pain.  Insulin may rise and is not controlled well by diet. Crests typically enlarge and harden at the same time.  Some mares have mammary development and may lactate. The mare can even progress to becoming laminitic.

Tincture of time will resolve any transition period issues for most mares. However, when irregular cycling, pain, behavior swings and anovulatory follicles persist Vitex agnus-castus can help support the natural transition to a normal hormonal balance.

Vitex agnus-castus (Chastetree, Chasteberry) fruits/berries act like adaptogens for the reproductive system, helping the mare’s body maintain normal function in both the brain and the ovaries. Unlike common hormonal drugs, it does not interfere with function but assists her to progress to natural, balanced activity. Studies have shown Chasteberry extracts help maintain normal levels of dopamine and the hormones LH and FSH.

The transition period is a temporary interval of disarray during which the mare’s hormones progress to a more orderly normal cycle. Mares that remain highly symptomatic or do not appear to be leveling out can be helped to achieve homeostasis with Vitex agnus-castus. Using a 5X extract allows you to feed a much smaller volume. Most average size horses will respond to a dose of 3 to 6 grams.

Eleanor Kellon, VMD



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(Some of) The Worst Persistent Myths Out There

Horses can’t get all the salt they need from a lick because they don’t have rough tongues.

Cows do have rougher tongues but that has nothing to do with getting salt from a lick/block.  If their tongues were rough enough to actually scrape salt off a block they would cut skin easily. They don’t.  All animals get salt from a block when their saliva melts it – just like licking a  lollipop. Cows don’t always get all they need either. It’s a matter of requirement versus how much time they spend licking. Since the horse will rarely take all they need at one time, shifts of body sodium and water can occur to correct imbalances in the blood and they lose the drive to eat salt but the tissues remain somewhat dehydrated. This puts them at increased risk of severe dehydration.

Oats are safe for EMS horses.

You  may hear the rationale that all the fiber from the hulls makes them safe, or being a “whole grain”. These things apply to humans, where the standard against which all other foods are assigned a glycemic index is white bread. With horses, the standard is oats. The glucose response to feeding oats is assigned a value of 100 and everything else assigned a rating relative to that. Only corn and sweet feed are slightly higher.

Letting a hot horse drink all they want will cause colic or laminitis.

Most old myths have a kernel of truth in them but this one is an exception. It’s also not true that water can’t be cold. Horses should be properly cooled down with walking to prevent muscle spasms and cold hosed to drop the body temperature but they must be allowed to drink all the water they want during this process. Horses that have their water restricted often end up not consuming enough to replace their losses. The reason is the same as described above for salt intake.Shifts of sodium and water between body tissues and blood restore the blood at the expense of  dehydrating the tissues.

A horse has to get at least a little bit of a bagged feed to get the vitamins and minerals he needs.

That many people think this is a tribute to the marketing of horse feeds, but it’s simply not true. A horse can get all the vitamins, minerals, protein and calories needed from their basic diet. Even horses that are getting bagged feeds are obtaining most of their nutrients from the hay, not the feed. “A little bit”, or anything less than the full recommended amount on the bag, also means you only get a little bit of the formulated amount of nutrients. If a feed has 50 mg of copper in 5  pounds, it will only have 10 mg in 1 pound – which is 1/10 of the bare minimum recommended intake. What is often true is that diets including no grain or unsupplemented grains may have deficiencies. Some of these can be corrected by changing the composition of the diet. Others will require targeted supplementation. In any case, a little bit of a bagged feed won’t solve the problem.

Eleanor Kellon, VMD


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Acetyl-L-Carnitine – The Powerful, Versatile Nutrient You Never Heard Of

Acetyl-L-carnitine is a metabolite of L-carnitine, derived from the amino acid L-lysine in a series of reactions which require cofactors of methionine, zinc, iron, vitamin C, niacin and vitamin B6. It is synthesized in the horse’s liver, kidney and brain. Carnivores and omnivores have a rich dietary source of carnitine from animal products but herbivores like horses must make their own supply.

Active horses have higher carnitine requirements

Since there’s none in their diet, horses can obviously make enough L-carnitine to survive as a species but supplies may not be optimal for muscular demands, especially since lysine and methionine are the two most commonly deficient amino acids.  L-carnitine is essential for the aerobic  burning of fats because it acts as a carrier to bring the fatty acids  across the mitochondria membrane.  Only the volatile fatty acid acetate and the medium chain triglycerides don’t require the carnitine carrier.

In normal muscle metabolism, the acetyl-l-carnitine metabolite of L-carnitine naturally has even more important effects via activation of an enzyme called AMPK:

  • helps direct glucose into energy pathways and away from storage as glycogen
  • signals the cell to produce more mitochondria
  • assists burning of fatty acids
  • aids in inhibiting storage of fat
  • encourages increased blood supply to muscle

This basically mimics the normal effect of exercise on muscle, which makes the muscle level of L-carnitine drop and the level of acetyl-L-carnitine significantly increase.

The well documented effects of L-carnitine and acetyl-L-carnitine make it a logical possibility as a supplement for athletically active horses but it goes beyond just theory. Rivero et al [2002] showed support of the metabolic response to training with supplementation. Sato et al [2015] showed moderation of the serum muscle enzyme release that normally occurs in early training and less exercise-related muscle pain when supplementation was paired with the antioxidant astaxanthin.

Acetyl-L-carnitine is also well documented to protect the myelin sheath surrounding nerve axons and to help preserve normal sensory nerve function. In addition, acetyl-L-carnitine is important for normal semen quality.

L-carnitine and acetyl-L-carnitine can be interconverted by the body. When you  supplement one form, the other form also increases but higher levels will be achieved of the one supplemented.

Horses have been supplemented with dosages ranging from 10 to 100 mg/kg.  An easy to remember dosage which was used successfully in the Rivero study is 1 gram/100 lbs of body weight.

Acetyl-L-carnitine is a white crystalline solid that resembles snow. It has a mild odor similar to vinegar. Humans react differently to the taste. To me, it is “tart”. Horses very rarely object to having it added to their feed. Side effects are extremely rare. Mild bloating has been reported on occasion and disappears by splitting the daily dose between two meals.

Consider supplementation for stallions, horses just starting a training program and horses that may benefit from muscle or nerve support.

Eleanor Kellon, VMD



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All IR/EMS Horses Have Laminitis

The Equine Cushing’s and Insulin Resistance Group, now at, has been in existence for almost 20 years and currently has over 11,000 members. As you might expect, many members seek out the group when their horse/pony/mini/donkey/mule becomes obviously laminitic. Others report issues confirmed by blood work but state they have never had problems with laminitis. Unfortunately, they’re wrong.

Even when not obviously laminitic, EMS horses are typically subdued,     reluctant to move, slow to turn, and appear uncomfortable

Back in 2004, Johnson et al published an article entitled Endocrinopathic Laminitis in the Horse. They described a “remodeling” of the laminae [aka lamellae] that occurs in horses with hyperinsulinemia from EMS or PPID [Cushing’s disease]. Specifically, there is lengthening and thinning of the dermal laminae which leads to weakening and predisposes to separation with resultant white line widening, rotation and sinking.  This occurs without the basement membrane damage and white blood  cell infiltration characteristic of other causes of laminitis.

Of particular interest was the report these changes are clearly visible microscopically and on radiographs in horses not showing any obvious signs of pain, inflammation or lameness.

Johnson focused on a possible role for cortisol in these changes but more recent research has clearly shown that it is insulin elevation which is to blame. Exactly how this happens is still uncertain. There is growing evidence that insulin may be acting through the IGF-1 (insulin-like growth factor) receptors to cause increased cellular proliferation.

There is some discrepancy in published studies regarding whether or not dermal and epidermal tissues in the laminae express insulin receptors. If they do, high insulin may stimulate the changes seen via those receptors. In humans, epidermal keratinocytes stimulated with insulin show the same proliferation and elongation seen in the laminae.

It has also been shown that endocrinopathic laminitis, like human metabolic syndrome, is characterized by increased levels of the potent vasoconstrictor endothelin-1 which may be causing cellular proliferation via endothelin receptors with reduction in perfusion and delivery of oxygen/glucose to the laminae.  Positive responses to herbal and amino acid support for nitric oxide generation suggest this is part of the mechanism.  Hypoxia [low oxygen tension] itself also causes migration and proliferation of keratinocytes via release of HIF-1 [hypoxia inducible factor]. The imbalance between vasodilating nitric oxide and vasoconstricting endothelin-1 is directly caused by high insulin levels within the blood vessels.

Regardless of the exact mechanism, the important thing to realize is that these changes are occurring in every horse with elevated insulin, whether they are recognized to be in pain or not. Low level lameness is easy to miss because the pain is symmetrical (no head bob). More subtle signs include less spontaneous activity, reluctance to make sharp turns, preference for soft ground, muscle tension in the forearms, back and hindquarters, more rigid head carriage (high or low) and a subdued attitude. These horses can easily be pushed over the edge into more severe pain by dietary indiscretions or even cold weather.

The good news is that meticulous attention to dietary simple carbohydrates, calories/weight, mineral balancing and additional nutritional support as needed is very successful in controlling insulin and restoring your horse’s love of life.

This is the same horse as above after being on an IR appropriate diet.

If you suspect your horse has high insulin, get a diagnosis and take correct action. Don’t allow hoof damage to progress to the point of being crippling.

Eleanor Kellon, VMD


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