Vitamins–tiny organic compounds with a huge impact on the health and well-being of your horse. Sometimes gleaned from the diet, sometimes manufactured within the digestive tract, vitamins have the power to promote and regulate virtually all of the body’s normal functions, and they need be present only in minute amounts.
There is still much we don’t know about vitamins, and much that is misunderstood. One of the most common misconceptions about vitamins is that “if some is good, more is better.” Horses can become vitamin-deficient, and these deficiencies can have devastating effects on a horse’s normal functions, but equally dangerous are toxicities from an “overdose”–a real possibility with some (but not all) of the vitamins. Further, different species have different vitamin requirements, so assumptions extrapolated from human medicine might not necessarily apply to horses. Vitamin requirements don’t really vary with the amount of work a horse does, either; the pleasure horse and high-performance athlete have almost identical needs. And while we frequently succumb to marketing ploys designed to convince us that our horses are in need of supplemental vitamins in their diet, the reality is that horses usually receive an excellent daily dose of the vitamins they require–those they cannot manufacture for themselves–from their forage (pasture or hay).
Researchers have classified vitamins into two categories that affect how the vitamins are absorbed, stored, and excreted by the body: fat-soluble and water-soluble. Vitamins A,D, E, and K are fat-soluble vitamins, which tend to be stored in the body (and thus can build up toxicities if there is an excess), while the B vitamins and vitamin C are water-soluble, meaning that any excess not used quickly by the body tends to be excreted rather than stored.
Vitamins also can be classified according to their source. Under normal conditions, the horse quite efficiently produces his own vitamins C, D, and niacin (one of the B-complex vitamins) from other organic molecules he ingests, and the beneficial microbes living in his cecum and large intestine, as part of their symbiotic bargain, produce all of the other B vitamins, as well as vitamin K. Only vitamins A and E are not produced within the horse’s body and must be sourced from vegetable matter in the diet.
As a rule, vitamin excesses or deficiencies extreme enough actually to cause symptoms are rare in horses. That’s not to say, however, that every diet provides absolutely optimum levels of vitamins; it’s quite possible for a horse to be receiving enough vitamins for maintenance metabolism, but not for maximum beneficial health effects. For example, a real vitamin E deficiency only occurs when a horse takes in less than 10-15 International Units (IU) per kilogram of his body weight in the dry diet; this is a level that is easily exceeded by most feeds.
Studies have demonstrated that a higher level of vitamin A, along the lines of 50-100 IU/kg (more than is delivered by most feeds), might increase a horse’s resistance to infections and to exertion-induced muscle damage. This is a case where some supplementation might produce a beneficial effect over and above what’s required nutritionally; biotin, which we’ll discuss in more depth later, is another vitamin that often is fed in excess of the amounts a horse strictly requires to live. But it’s important to realize that in some cases, such effects might be more old horseman’s lore than fact; research is still ongoing, and each vitamin must be considered individually before you do any supplementing.
Should I Supplement?
Vitamin supplementation might be beneficial in cases like the following:
- For horses on a high-grain, low-forage diet (such as youngsters in heavy race training), or for those on very poor-quality forage, or eating hay that is more than a year old. Vitamins tend to break down over time in stored feed; for example, there is a 9.5% loss of vitamin A activity in hay every month.
- For horses receiving prolonged antibiotic treatment for illness or infection. Broad-spectrum antibiotics inhibit the growth of the beneficial cecal and intestinal bacteria, which inhibits their production of B vitamins and vitamin K.
- For horses in high-stress situations, such as frequent traveling, showing, or racing.
- For horses which are eating poorly–for example, those recovering from surgery or illness.
- For horses which are anemic–although the source of the anemia should be determined and treated.
Vitamins can decompose when exposed to sunlight, heat, air, or the processes that feeds go through in commercial packaging (such as grinding or cooking). Losses during long-term feed storage are greatest for vitamins A, D, K, and thiamin (B1); A is the most crucial of these since it is sourced completely from the diet.
Furthermore, some vitamins are incompatible with each other or with minerals that might also be in the feed. For example, most vitamins are prone to oxidative destruction by iron, copper, sulfates, sulfides, phosphates, and carbonates, all of which could be present in a feed or a vitamin/mineral supplement. The B vitamin thiamin (B1) is incompatible with riboflavin (B2), and both are incompatible with cobalamin (B12) in the presence of light. So, feed manufacturers might go to great lengths to protect the vitamins’ activity and efficacy by coating them with gelatin, wax, sugar, or ethylcellulose–harmless, fortunately, to the horse in the amounts required. These compounds might make up a large part of the composition of a powdered or pelleted vitamin/mineral supplement. (It’s very difficult to cover vitamins with any sort of protective coating in a liquid format, so many of the liquid supplements rich in B vitamins, iron, and copper, sold as “blood builders,” actually could have very little active vitamin content.)
Following is a profile on the function of each of the vitamins important to the horse, beginning with the fat-soluble vitamins.
Vitamin A, also called retinol, is important for the maintenance of good vision, particularly at night. It is also an important factor in bone and muscle growth of young horses, in reproduction, and in healthy skin. Horses must satisfy all of their daily vitamin A requirements from their diets; fortunately, green forages and yellow vegetables (such as carrots) are an excellent source of vitamin A’s main precursor, beta-carotene, which is broken down by enzymes in the small intestine. The converted vitamin A is then stored in the liver, which can retain a three- to six-month supply, releasing it back into the bloodstream as the horse’s body requires or excreting it if there is an excess.
Not all of the carotenoid pigments the horse takes in on a daily basis are converted to vitamin A; some are absorbed intact and transported to body tissue such as the fat, skin, and ovaries for use and storage. (In the ovaries, beta-carotene has been shown to be involved in the control of progesterone secretion by the corpus luteum, making it a key player in the control of ovulation, embryo implantation, and the maintenance of pregnancy.) A deficiency of beta-carotene interferes with these functions, and interestingly, cannot be corrected by feeding more vitamin A, as the conversion doesn’t seem to be wholly reversible.
General signs of a vitamin A deficiency include a depressed appetite, weight loss, a dull hair coat, night blindness (distinguishable from periodic opthalmia, or moon blindness, by characteristically cloudy corneas), excessive tearing of the eyes, anemia, and even convulsive seizures. Long-term deficiencies can cause abortion in broodmares, and stallions might suffer decreased libido and soft, flabby testicles. Under normal conditions, the only way a horse can develop a vitamin A deficiency is if he is deprived of hay or pasture for more than six months (allowing time to deplete the stores in the liver). But if horses are going to be fed on very old hay or poor pasture for an extended period of time, vitamin A supplementation is a good idea.
Like all of the fat-soluble vitamins, vitamin A is poorly transported across the placenta. Thus, foals are born vitamin A deficient. Provided the mare’s diet has sufficient beta-carotene, she will provide vitamin A to her foal in her colostrum, but if the foal’s colostrum intake is insufficient, the deficiency will persist. Vitamin A deficient foals can suffer from diarrhea, although they are not usually night-blind.
Horses also can experience vitamin A toxicity, although as a rule it only occurs when an owner over-supplements the diet. In one study where foals were deliberately fed vitamin A in quantities exceeding 20,000 IU/kg, the results included stunted growth, scaly skin, increased bone size, bone fragility, and decreased blood clotting, leading to internal hemorrhages. There has been no demonstrated benefit to horses by feeding more than 2,000 to 3,000 IU/kg per day.
Vitamin D is the “sunshine vitamin,” created through chemical reactions of ultraviolet rays from the sun with 7-dehydrocholesterol (synthesized in the horse’s skin) and ergosterol (in the dead leaves of plants). The chlorophyll in living plants blocks out ultraviolet rays, and it is only after plants have been cut and exposed to sunlight (as in sun-cured hay) that vitamin D begins to be present. Its function, unlike that of vitamin A, is simple and clear-cut; it assists in maintaining plasma calcium concentrations by interacting with parathyroid hormone (PTH) and calcitonin. This has the effect of increasing the absorption of both calcium and phosphorus in the intestine, with an indirect impact on bone mineralization. A vitamin D deficiency results in rickets in the young of most species (including humans); the bones become soft and bendable, resulting in bowed legs and emaciation, and in severe cases, the affected animal will be reluctant to stand. Rickets per se have not been observed in horses with vitamin D deficiencies. Pony foals deprived of sunlight for five months did demonstrate decreased bone strength, and slower growth and feed intake, as well as irregular growth plates (visible on radiographs).
Most horses are unlikely ever to need vitamin D supplementation. Hay contains approximately 2,000 IU/kg of vitamin D when it is freshly baled, although like all vitamins, it degrades over time, at a rate of about 7.5% per month. Hay that is more than a year old might not, therefore, meet a horse’s vitamin D needs, but as long as the horse receives a few hours of sunlight a day, this should be of no consequence.
However, stabled horses who are not allowed access to direct sunlight for months on end should be provided in their diets a level of 800 IU/kg (in the total diet) for growth, pregnancy, and lactation, or 300 IU/kg for normal maintenance.
Vitamin D toxicity is the most common of all vitamin “overdoses.” It occurs as a result of indiscriminate supplementation (either oral or injectable). Excess vitamin D is stored in the liver, and the effects are cumulative, becoming more obvious after a period of several weeks. They include calcium deposits that collect in the heart valves and walls, the walls of large blood vessels, and the kidney, diaphragm, salivary glands, and gastric mucosa. The result is decreased exercise tolerance, weight loss, stiffness, a decrease in spontaneous activity (with flexor tendons and suspensories often sensitive to palpation), an increased resting heart rate, the development of heart murmurs, and increased water intake and urination. Toxicosis can be confirmed by elevated plasma concentrations (over 5 ng/ml).
Versatile vitamin E enhances immune function, is essential for cellular respiration, is involved in DNA synthesis, reduces the signs of zinc deficiency (more about this in a future issue), and improves the absorption and storage of vitamin A, among other effects. But most importantly, vitamin E and the mineral selenium are partners in protecting the horse’s body tissues–especially cell membranes, enzymes, and other intracellular compounds–from the damaging effects of oxidation. Inadequate amounts of either one in the horse’s system assure that there will be considerable free-radical damage to the tissues.
Vitamin E is the only vitamin other than A that horses must get from their diets. Green growing forage contains good amounts of vitamin E, but from 30-80% of the vitamin’s activity is lost during the process of cutting and baling hay, and nearly all of the vitamin E is destroyed in high-moisture feeds, such as haylage. Because not all horses are lucky enough to have good pasture year-around, commercial grain rations usually are fortified with stable forms of vitamin E.
Signs of deficiency (which usually are grouped with selenium deficiency) include muscle wastage and malformation (sometimes called “white muscle disease” in foals), subcutaneous edema, infertility, a stiff, stilted, “base-wide” gait, a swollen tongue, and inflammation of fatty tissues (or steatitis) by insoluble pigments (often called “yellow-fat disease”), especially in foals. A mild deficiency of vitamin E might only produce a decrease in the horse’s immune response, and in foals a slower growth rate.
Horses easily can suffer from selenium excesses (selenium has the lowest toxicity level of any mineral important to the equine diet), but vitamin E is relatively non-toxic. No clinical signs of vitamin E toxicosis have been produced, but because very high levels of vitamin E can interfere with the absorption of other fat-soluble vitamins, a conservative maximum level of 1,000 IU/kg in the diet generally is recommended.
Vitamin K’s primary function is as an activator for blood clotting factors, although it also participates in the activation of other proteins throughout the body. There are several forms of vitamin K that occur in nature, some in green leafy plants, and others manufactured by the horse’s cecal bacteria. While the natural forms of vitamin K are fat-soluble, they are converted to a water-soluble format before they are stored in the horse’s liver. As a result, vitamin K is easily excreted in the urine and so the body does not tend to retain a large supply. However, the combination of vitamin K ingested in pasture or hay, and that produced in the cecum, is considered adequate for any horse’s needs under almost all circumstances.
One exception is a vitamin K deficiency induced by sweet clover poisoning. An anticoagulant called dicoumarol (chemically related to warfarin) sometimes occurs in moldy sweet clover hay or haylage. If the moldy hay is ingested over a period of several weeks, the horse’s synthesis of vitamin K-dependent clotting factors is impaired. The problem occurs most often in cattle, but has been reported in horses and sheep; if untreated, mortality (and the risk of abortion in broodmares) can be high.
Vitamin K deficiencies also can result from anything that compromises the gut flora–such as severe colic or diarrhea, abdominal surgery, or antibacterial drugs. Chronic liver disease also can be a factor. And because newborn foals are deficient at birth, vitamin K injections often are recommended to prevent hemorrhagic diseases. A long-term vitamin K deficiency decreases blood coagulation; bleeding from the nose is frequently one of the first signs in horses. Hematomas and/or internal bleeding also can occur, and if sufficient blood is lost, the horse will have pale mucous membranes, a rapid and irregular heartbeat, and be depressed and weak.
Toxicosis of vitamin K is rare, although injections of the water-soluble form can be dangerous, causing acute renal failure and death. Oral forms of the vitamin appear to be innocuous, fortunately. No ideal levels of vitamin K have been established for the horse, but in a case where supplementation is called for (for example, after a course of antibiotics or after a serious colic), the usual recommendation is for three to five mg/kg of body weight/day, mixed into the feed, for a week or more.
Water-Soluble Vitamins: Thiamin (Vitamin B1)
Thiamin plays an important role in carbohydrate metabolism and in nerve transmission and stimulation. While horses receive good concentrations of thiamin from their intestinal bacteria, several studies have determined that they also require some from their diets. Fortunately, most green forage is an excellent source of thiamin (and indeed, all of the “B-complex” vitamins), as is brewer’s yeast.
Thiamin deficiency can occur when horses eat bracken ferns (which contain a compound that inhibits its absorption), but is otherwise uncommon. In studies where it has been artificially produced, horses showed signs of anorexia, loss of coordination, skipped heartbeats, and unusually cold hooves, ears, and muzzles.
Thiamin toxicity is very unlikely; dietary intakes of up to 1,000 times the recommended amount have been safely administered to horses without any ill effects. However, if doses of 1,000 to 2,000 mg of thiamin are injected, they can produce a slowed pulse rate and a mild tranquilizing effect (a result that has been disputed in some research). Certainly thiamin has the reputation, in some circles, of being a tranquilizer, but it is important to keep in mind that large doses of this vitamin have produced convulsions, labored breathing, and death by respiratory paralysis in dogs, mice, and rabbits. High doses of thiamin also have been suspected, on occasion, to cause the opposite effect in horses–over-excitation.
Riboflavin (Vitamin B2)
Fresh forage and yeast supplements are two good sources of riboflavin, a vitamin also synthesized by the gut flora. Oxidative energy metabolism depends on riboflavin, and deficiencies (which have not been documented naturally, but have been induced in experimental situations) compromise the tissues most in need of oxygen during strenuous exercise. Other signs of a riboflavin deficiency include decreased feed intake, scaly skin and a dull hair coat, inflammation of the lips and tongue, colon ulcers, diarrhea, anestrus (lack of heat periods in the mare), and a rear-end muscular weakness. Irritation to the eyes also results, with increased tearing, sensitivity to light, and inflammation of the surrounding tissues.
Some years ago, riboflavin was thought to be involved with periodic opthalmia (moon blindness); more recent research, however, has absolved it of this responsibility, pointing the finger instead at infection by the parasite onchocerca cervicalis, or an aggravated immune response.
Horses tolerate high levels of riboflavin very well, and no signs of toxicity have been documented.
Niacin (Nicotinic Acid) And Pantothenic Acid
Niacin is considered a B vitamin, but has no numerical designation. It does share qualities of the other B vitamins, however, being important in the regulation of energy metabolism, especially the processing of carbohydrates, amino acids, and fats. And because it, like the other members of the B family, is involved in biochemical reactions in the body, the symptoms of its deficiency tend to resemble those described for the other B vitamins. Actual niacin deficiencies–or excesses, for that matter–have not been described in horses. Another B vitamin, pantothenic acid (formerly designated vitamin B3), also is involved in the metabolism of carbohydrates, fats, and proteins, and it is widely available in virtually all vegetable matter.
Pyroxidine (Vitamin B6)
Amino acid metabolism is the main function for pyroxidine, but it also is involved in glycogen utilization, the synthesis of epinephrine (adrenaline) and norepinephrine, and in the metabolism of fats. Again, no signs of deficiency or excess have been documented in the horse because it is widely available in the diet and is manufactured by the intestinal flora, although in humans, high doses of pyroxidine administered on a daily basis have produced signs of sensory nervous system dysfunctions. Dietary levels of up to 50 times the nutritional requirement are considered safe for horses.
Most horsepeople are familiar with biotin as a supplement for hooves, but fewer know that it is considered one of the B-complex vitamins. Its primary role is as a co-enzyme in several crucial, but complex, chemical reactions related to metabolism, including the synthesis of glycerol for body fats, RNA, and DNA. Although the intestinal flora produce biotin, researchers debate whether that amount is adequate for a horse’s daily needs; biotin deficiencies in fish, mink, foxes, pigs, and turkeys have been reported, and intriguingly, the symptoms that result often include skin, footpad, and/or periople lesions that provide a ready comparison to the thin, shelly hooves many horses grow.
Unfortunately, no one has established an optimal level of biotin. The amounts included in most of the popular hoof supplements (from 10-30 mg or more) are well above what is considered the base requirement. Fortunately, high levels of biotin are well-tolerated, making biotin supplementation a relatively harmless therapy, even if its results vary from horse to horse and could take six to nine months to become obvious.
Cobalamin (Vitamin B12) And Folacin
Both of these vitamins are needed for the synthesis of red blood cells, and a deficiency of either will result in anemia. While folacin can be found in green forage, B12 is unique among vitamins in that it is synthesized in nature only by microorganisms. In addition to its role in red blood cell synthesis, B12 also is required for the production of propionate, a major energy source derived from the fermentation of carbohydrates. So, although the gut flora seem to produce ample B12, the vitamin often is administered to high-performance horses to enhance performance, treat or prevent anemia, and stimulate the appetite.
So far, there is no evidence to support the belief that supplemental B12 does any of these things, although severely anemic or heavily parasitized horses do appear to respond to it. (It should be pointed out that it is likely far more valuable to treat this type of horse through deworming and a proper diet than through B12 injections, which only increase plasma concentrations of the vitamin for a short period of time.)
Vitamin C (Ascorbic Acid)
Most of us are familiar with vitamin C, but have heard very little of its function or requirement by horses. It is an antioxidant, which protects fats, proteins, and membranes from free radicals. In addition, it enhances the formation of bone and teeth, aids in the utilization of several of the B vitamins as well as cholesterol and glucose, and improves the intestinal absorption of iron. On top of this, it’s a component of the connective tissue collagen and several amino acids.
Humans are one of the few species which, because of the lack of a crucial enzyme, do not synthesize their own vitamin C from glucose in their livers. For species including the horse, vitamin C does not need to be taken in daily from the diet, and in fact there is no demonstrated dietary requirement of this vitamin for horses (which is just as well, since most equines aren’t big on citrus fruits).
The effects of a vitamin C deficiency do not occur in horses, although it is suspected that horses over the age of 20 years, or those which have been ill or stressed, sometimes can suffer low plasma concentrations of ascorbic acid, which could be associated with wound infections, bleeding from the nose, and an increased susceptibility to disease. Some cases of infertility in both mares and stallions have been reported to improve with the supplementation of vitamin C, but this has yet to be confirmed by research.
In any case, oral vitamin C has been shown to be poorly absorbed by the horse, and intramuscular injections of the vitamin tend to cause marked tissue irritation. Intravenous administration has been tried, but the body so efficiently eliminates this water-soluble compound that plasma concentrations only remained elevated for a few hours. The form that is sometimes included in feeds, on the off chance it might have some beneficial effect, is ascorbyl palmitate, which horses (but few other species) can absorb fairly well. Next month, we’ll explore the vitamin’s partner in nutrition–minerals.
Article by Karen Briggs