Treating Founder (Chronic Lamintis) without Horseshoes, Section 17

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As Dr. Strasser has pointed out, a constantly maintained wild horse trim, coupled with plenty of exercise and constant freedom to move, is your best line of defense against laminitis.  She finds that all foundered horses have high heels and some degree of heel contraction.  Trimming as she advocates will spread the heels and enhance circulation enough to provide more reserve circulation to better withstand laminitis triggers.

Here are some laminitis triggers:

  1. Any systemic upset, such as fever, colic, or getting into something toxic, can trigger an attack.  Drinking too much water when hot is another way.  Obesity greatly increases the probability of founder.   Gorging on grain can do it.  Gorging on the new spring grass is another way.   Bedding on black walnut shavings is an example of a toxic trigger.  Over-use of steroids is another systemic trigger.  Many of these can be avoided.  Many of these seem to be related to digestion.  Retained placenta after foaling another trigger.  I have also heard of several incidents where vaccinations, particularly rabies, triggered laminitis.  We MAY be over-vaccinating, and there may well be a connection between "spring shots" and founder occuring more often in the spring.

  2. Some medical conditions can make a horse more likely to founder, such as low thyroid.  Low thyroid can result from a pituitary adenoma, or Cushings Disease--a slow-growing benign tumor, which leads to low thyroid, high cortisone levels in the blood, rain rot, pot belly, muscle loss, increased urine output, poor vision, and a propensity to founder.  Another sign is a long, curly coat slow to shed out.  The tumor grows slowly and the signs develop gradually.  The tests are ACTH and Dex suppression.  There is medication available to control it, but it is expensive.  (Permax, around $100/month, which makes them less likely to founder and reduces some of the other symptoms.) Dr. Eleanor Kellon reports getting similar results with Hormonise on Cushings horses, however, which contains vitex agnus-castus (chaste berry), and is available at Emerald Valley Botanicals:

    "I published the first article on use of Chaste tree berry (aka Vitex agnus castus, aka Monk's Pepper) in Horse Journal in December, 2000.  I agree the liquid extract has more predictable results.  Extracts are always much more potent, and hopefully manufacturers make at least some effort to purchase from the same sources, while powders are prone to lose potency over time and vary quite a bit from batch to batch.  I do have clients using berries that they grind fresh each day.  Takes a considerable amount, average of 2 oz for a full size horse.  The original HJ article spurred a larger trial by the Laminitis Trust in the UK.  See "

    There is a email list for discussing Equine Cushings:

    For more information on Cushings, Insulin Resistance, and Hypothyroidism from Dr. Kellon, Click HERE

    Some of the symptoms of protein backing up into the system  because poor hoof mechanism not allowing rapid hoof growth and protein utilization, as described in Dr. Strasser's book, mimic many of these signs, interestingly enough.

  3. Malnutrition is a subtle thing.  A horse can be 300 lbs. overweight and still have serious mineral deficiencies; in particular, magnesium.  I recently  checked with the agricultural lime dealers in my area, who tell me that the only lime available in my area is calcium carbonate.  To get dolomite in large quantities for spreading on large fields, you have to go to a quarry in Northern Ohio.  So even if you are keeping your fields limed, it is not enough.  Add 1 Tbsp. daily of food grade calcium carbonate and an equal amount offood grade magnesium oxide.  (The magnesium needs to be balanced with calcium to prevent calcium loss in the bones.)

  4. Mechanical triggers, such as overwork on hard roads, can be lessened by trimming in the short toe-low heel style I have been writing about here.  Road founder may have an chemical aspect as well--higher lactic acid levels due to over-exertion.

  5. Excessive iron in their drinking water can be a culprit.  I had mine drinking out of a dug well when I had the most trouble.  I have since hooked up the barn hydrant to a cistern, which gives them rainwater.  I had the water tested, and the cistern water is superior on just about every count to the well water.  (One caveat on cisterns and rain water, though--Linsey McLean of says that rain water is getting increasingly contaminated with nitrates and the "acid rain" problem.  There was a very slight trace of nitrates in my cistern water test, but the concrete holding tank must have counteracted any acidity, as the pH of the water was OK.  Linsey says nitrates inhibit thyroid activity. Anyone building a cistern should incorporate a drain so they can drain the water periodically and clean the tank...and put in filter boxes between the cistern and the downspout where you can run the water through sand, activated charcoal, etc., before it reaches the tank.  I did put in a drain, but I am sorry I did not insist on filter boxes when the cistern was built.)

    Dr. Dan Pitzen's article on the relationship between excess iron in the water and laminitis:

    Some Laminitis Problems in Horses May be Caused by Excessive Iron Intake

    by Dr. Dan Pitzen, PhD

    Thirteen years ago when routinely formulating rations for dairy cattle based on laboratory analysis of grain, forage, and water supplies, I observed a connection between iron intake and some health disorders. When the forage contained over 400 parts per million (ppm) of iron and/or the water supply contained over 0.3 ppm iron, cows often exhibited more sore feet problems, rough dull hair coats, silent estrus (heats), and increased susceptibility to infectious diseases. When supplemental sources of iron were removed, health and breeding usually improved in these herds.

    When in excess, iron is a prooxidant (free radical generator) that is damaging to body tissue and organs. The health of animals with a high iron intake usually responds to supplementation of higher than normal levels of antioxidant nutrients such as Vitamin E, selenium, zinc, and copper. As a mineral, iron binds with zinc and copper and reduces their absorption through the intestinal wall. Zinc and copper are essential for the growth of good quality hooves. Copper is essential for good tendons and ligaments.

    My observations were published in Feed Management magazine, June 1993, and Feed International, August 1996 in an article titled, "The Trouble With Iron (Prooxidant:Antioxidant Balancing)."

    In the last several years I have made similar observations regarding iron toxicity in horses, particularly as the primary cause of some incidences of laminitis (founder).

    In a series of 3000 hay samples analyzed in the Maddy Feed Lab one year, the average iron content was 431 ppm which is about 10 times greater than the NRC iron requirement of 40-50 ppm for horse rations. Approximately 10% of the hays tested contained over 1000 ppm iron. Only 0.1% of the hays contained less than 50 ppm. Oats contain about 85 ppm iron, molasses about 750 ppm and dicalcium phosphate supplies, as a major calcium and phosphorus source in horse feeds, contain 6,000 to 14,000 ppm of iron.

    The iron in water supplies is usually in a very available and reactive form especially in clear water. In rust colored water, the more apparent iron may not be as harmful since it is already oxidized. From my observation, areas of the country that commonly have iron in well water supplies seem to have a greater incidence of laminitis occurring.

    Usually the forage or water supply does not have to be changed to correct the associated problems. It is the total iron intake that is the problem. That total can be reduced by eliminating supplemental source of iron in the grain-sweet feeds formula and supplements, including phosphorus mineral sources high in iron content.

    I question that horses ever need to receive iron supplementation. I haven’t found any research showing a need and haven’t added any to horse and cattle rations for years. Anemia results from a deficiency of other nutrients such as copper, cobalt, Vitamin B12, and Folic Acid that are also present in the high iron "blood building" supplements.

    Since the prooxidant iron can damage muscle tissue, and since it increases the need for antioxidants such as Vitamin E and selenium, iron toxicity may also be a factor in some incidence of typing-up problems.

    Dr. Eleanor Kellon also has an interesting article on the relationship between too much iron, and laminitis and insulin resistance: 


    Eleanor M. Kellon, V.M.D.
    Equine Nutritional Solutions
    58 Maple Farm Road
    Ephrata, Pennsylvania, 17522 USA


    Hyperinsulinemia unrelated to recent high soluble carbohydrate feeding and disproportionate to blood glucose levels, indicating insulin resistance, is well known to occur in equine pituitary pars intermedia dysfunction (PPID, Cushing's disease), has been described in ponies and miniatures, and is receiving increasing attention as an underlying problem in horses prone to obesity and laminitis. In humans, several studies have identified iron overload as both a risk factor for the development of insulin resistance, and a consequence of insulin resistance. The purpose of this study was to determine if insulin resistant horses and ponies also show blood indices indicative of iron overload.

    Materials and Methods

    The insulin resistant (IR) study group was composed of adult horses and ponies from several breeds, known to be hyperinsulinemic. Horses with active infections or laminitis were excluded to avoid false elevations of ferritin (McLean, 1987; Smith et al, 1984). This group was further divided into horses receiving mineral supplementation, based on forage analysis (including a maximum Fe:Cu of 10:1 and Fe:Z of 3.3:1, Johnson et al, 2004) and those on unsupplemented diets. Controls were adult horses and ponies free of obvious disease. Hyperinsulinemic horses were on diets of low NSC forage only, or forage and beet pulp with small amounts of rice bran and flax. Control horses were on diets of forage only or forage plus concentrate or beet pulp. No horses in any group were receiving supplemental iron with the exception of what may have been added to commercial concentrate mixes. Serum iron, total iron binding capacity (TIBC) and ferritin were analyzed by the Comparative Hematology Laboratory at Kansas State Veterinary Medical Center by methods previously published by the founder of that laboratory (Smith et al, 1984). Transferrin saturation index (TSI) was calculated by the equation:   TSI = (serum iron/TIBC) x 100.  Data was analyzed by ANOVA and Student's T.


    Serum iron, TIBC, and ferritin values in control horses were similar to those previously reported for normal horses and well within the observed ranges used by the testing laboratory. There was no significant difference between groups for TIBC. There was no significant difference between IR balanced and unbalanced diets for serum iron (P = 0.12), or between IR balanced diets and normal (P = 0.22), but a significant difference between IR unbalanced and normal (P = 0.0031). For TSI and ferritin, there were no significant differences between IR horses on balanced diets and normal controls, but highly significant differences (P<0.0001) between IR on unbalanced diets and both the control and IR on balanced diets.


    Serum Values

    IR – balanced diets

    IR – unbalanced diets


    Iron ug/dl

    155 +/- 38.3  N = 10

    181 +/- 48.9*  N = 32

    135 +/- 40.0    N = 18

    TIBC ug/dl

    381 +/- 73.6a  N = 10

    347 +/- 65.2a  N = 32

     351 +/- 60.1a   N = 18

    TSI %

    40.3 +/- 5.29a  N = 10

    53.1 +/- 14.5b  N = 32

     36.5 +/- 5.33a  N = 18

    Ferritin ng/ml

    116 +/- 57.8a  N = 10

    313 +/- 99.9b  N = 38

     139 +/- 43.9a   N = 27

    ·        Significant difference from controls but not when compared to IR on balanced diet
    a,b Different superscripts represent significant differences within a row (P<0.05)


    Risk factors for equine insulin resistance have not been completed identified but likely represent an interaction between genetic predisposition, underlying disease states and the environment. Since genetic factors are beyond our control and drug therapy for PPID does not necessarily lead to resolution of IR, identifying external factors has the potential to improve control. The role of iron overload as a risk factor for IR (Fernandez-Real et al, 2002; Jehn et al, 2004), and therapeutic effect of lowering body iron levels (Fargion, 2005; Piperno, 2004), has been documented in man. Ferritin has been shown to be highly correlated with hepatic iron stores in horses (Smith et al, 1984). This study has documented a highly significant elevation of body iron in insulin resistant horses on uncontrolled mineral intakes. This elevation is believed to be real, and not the result of occult inflammation, since transferrin saturation in these horses was also elevated and serum iron was not depressed (McLean et al, 1987). Animals on mineral balanced diets had normal TSI and ferritin levels, and improvement in their insulin resistance, but since other measures were undertaken concurrently (e.g. reduction in NSC of the diet), the effect of the mineral balancing per se could not be determined.  More extensive prospective and intention to treat studies are necessary to clarify the role iron might play in equine IR

    Fargion S, Dongiovanni P, Guzzo A, Colombo S, Valenti L, Fracanzani AL, 2005. Iron and insulin resistance. Aliment Pharmacol Ther, Nov;22 Suppl 2:61-3.
    Fernandez-Real JM, Lopez-Bermejo A, Ricart W, 2002. Cross-talk between iron metabolism and diabetes. Diabetes, 51(8):2348-2354.
    Jehn M, Clark JM, Guallar E, 2004. Serum ferritin and risk of metabolic syndrome in U.S. Adults. Diabetes Care, Oct;27(10):2422-8.
    Johnson PJ, Messer NT, Kellon E, 2004. Treatment of Equine Metabolic Syndrome. Comp Cont Ed, Feb;26(2), 122-30.
    McLean LM, Hall ME, Bell JE, 1987. Evaluation of serum iron, total iron binding capacity, unbound iron binding capacity, percent saturation and serum ferritin in the equine. Proceedings of the 10th Equine Nutrition and Physiology Society Symposium, Ft. Collins, Colorado, USA, 443-446.
    Piperno A, Vergani A, Salvioni A, Trombini P, Vigano M, Riva A, Zoppo A, Boari G, Mancia G, 2004. Effect of venesections and restricted diets in patients with the insulin resistant hepatic iron overload syndrome. Liver Int, Oct;24(5):471-6.

    Smith JE, Moore K, Cipriano JE, Mooris PG, 1984. Serum ferritin as a measure of stored iron in horses. J Nutr, 114:677-81.

    Just how safe IS your horse's drinking water?  The best nutritional program will still be undermined by polluted drinking water.  For a comprehensive water quality test from Lehman's Hardware, that fabulous place full of 19th century stuff catering to non-electric living, CLICK HERE   (Go to "Water Dept., then to "Water Filters," and finally to "Water tests.")

    (You can also find treadle sewing machines, hand pumps, kerosene lamps and refrigerators, wood stoves, sleigh bells, and so much more at Lehman's!  My favorite place to go shopping, in the heart of Holmes County, Ohio's Amish area!  To get OUT of their site, doubleclick on the BACK button rapidly.)

  6. Pregnant mares:  Extra calcium taken immediately before and after foaling can help prevent retained placenta, and many other stresses related to delivery. Retained placenta is a common cause of laminitis. An oral calcium gel, one dose given within 24 hours before foaling, and a second dose within 24 hours after foaling, can help prevent: prolapsed uterus, long labor, mastitus, ketosis, retained placenta, hypocalcemia relapses. This is a prescription drug available through vets, and has been mainly marketed for cattle.

  1. I have gotten some feedback that DMG and/or MSM may be of some preventative value as well.  The connection between lactic acid build-up, DMG and laminitis warrants more investigation.  However, this is not a substitute for mechanically restoring full hoof mechanism with a correct trim and enough movement.  The letter below mentions the 4-point trim not working alone, but I have no idea if it really was an optimum trim.  Further, people on the naturalhorsetrim list have been reporting getting harder hooves and faster hoof growth after adding MSM to their horses' diets.

    From Diane Kowallek --
    ".... my pony continued to founder....He would founder on less than a minute of grass... So I went to the library and picked up every book they had on lameness and diseases and horse care.  They all said the same thing, which was basically nothing. But then one old old book said that when a horse founders, he gets a tremendous amount of lactic acid buildup in his system... I had just gone through an equine supply catalog and under the description of DMG, it said it reduced lactic acid buildup...The results were great.  The next spring, he was able to graze for 30 minutes without any problems.  If I pushed it past that, he would get a pulse in his front feet, but within less than 24 hours, it would be gone.  Once the spring grass was gone, he was able to graze for an hour... I ran out of DMG and decided not to get any more, because I thought maybe it was the 4 point trim that did the trick.  Within two weeks, he was lame.  Within a week of going back on it, he was fine.  Unfortunately, I got lazy and didn't give it to him all winter, and this spring was his worst.   I've got him back on DMG and he is gradually getting better.  My vet said he has heard of MSM working on several ponies.  Last year I told several people on the internet about DMG and they all wrote back and said it helped their horses."

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