Vitamin E, which is plentiful in green pasture but perishes in hay under dry storage, may merit special attention as both a preventative and a therapeutic agent in horses.
The metabolic role of vitamin E is not completely understood. It appears to prevent free radical damage to tissues or lipid peroxidation (i.e. chemical breakdown of cell membranes). These processes can result in harmful effects in the body. Vitamin E also is important for the proper function of nerves and muscles, boosts the immune system and promotes an anti-inflammatory effect in the central nervous system. In contrast, deficiencies of this important vitamin may impair neuromuscular function.
Since the mid-1980s, Lynda Blythe, DVM, PhD (neuroscience), Associate Dean, Oregon State University, has been studying the role of vitamin E in animals. Through clinical trials she and other researchers have demonstrated the preventive and therapeutic effects of vitamin E. They also identified several disease risk factors for horses that do not have adequate levels of vitamin E.
One of those diseases is equine degenerative myeloencephalopathy (EDM). A degenerative nerve disease of the spinal cord and brain stem, EDM is a cause of ataxia (un-coordination) and weakness, i.e. "wobbles," especially during the first year of life. Clinical signs can be acute in onset or progress slowly from clumsiness to visible ataxia. If the horse does not deteriorate to the point where euthanasia is recommended progression of EDM usually stops by age two or three. However, horses with EDM usually cannot be ridden or used for breeding purposes.
Although the disease is not something foals are born with, EDM nevertheless may have a genetic predisposition. "EDM tends to run in families and occurs in almost every breed of horse," Dr. Blythe notes. Initially, her study at Oregon State University found that vitamin E levels in foals, offspring of an ataxic EDM-affected stallion, fell far below their control counterparts on the same pasture.
Another study conducted by Dr. Blythe of wobbler and control foals grazing on the same pasture found that when the wobbler foals started developing poor coordination and their vitamin E levels dropped at about six months of age, the disease could be largely reversed through supplementation of 6,000 IU per day of vitamin E. By the time the horses were two years old, their coordination appeared close to normal. "All markedly improved, while one or two had some residual neurological deficits," she says.
A University of Florida study examined the offspring of two stallions that produced EDM in 40 percent of their get. In repeat breedings the next year, the mares and their foals were supplemented with 1,500 IU a day of vitamin E: The following year, only 10 percent of their offspring were affected. In subsequent years, none of the supplemented offspring of those stallions had EDM.
As a result of these studies Dr. Blythe determined that foals should receive about 1500 to 2000 IU of vitamin E either through diet or diet plus supplements for prevention of EDM and 6000 to 9000 IU of vitamin E if affected.
Vitamin E deficiency also is linked to equine motor neuron disease (EMND), a rare, naturally occurring disease of the nerve cells that control skeletal muscles. Similar to Lou Gehrig's disease in humans, the affected horse can suffer from weight loss, excessive recumbency, trembling, muscle atrophy, constant weight shifting of the rear limbs, and abnormally low head carriage. They just appear weak all over, often tripping on obstacles or unable to rise.
Although the cause is unknown, Cornell researchers discovered that horses with EMND have low levels of vitamin E in tissues or blood, and that an absence of grazing for more than a year and poor quality hay is the most common identifiable environmental risk factor. "An inadequate intake of vitamin E may not be the only factor, but it is a predisposing cause," Dr. Blythe says. When vitamin E was increased via pasture diet or diet and supplements researchers noted dramatic clinical improvement in four of the five most acutely affected horses.
Hence, the current recommended protocol is for 2000 IU of Vitamin E for prevention of EMND and 6000 to 9000 IU for treatment.
Vitamin E may aid in the treatment of equine protozoal myeloencephalitis (EPM). A disease of the central nervous system, brain, and spinal cord, EPM is caused by a protozoal parasite. Onset can be extremely rapid, slow and insidious, or subtle. Clinical signs vary and can include weakness, lameness, incoordination, inability to move correctly (especially in the hindquarters), persistent recumbency, seizures, weight loss, blindness, loss of balance and disuse of a single limb.
Standard treatment includes administering anti-protozoal medications to kill the protozoa. There is some evidence that adding 7000 to 9000 IU of vitamin E aids recovery. "Vitamin E has been shown to protect muscles from some of the disuse atrophy process that occurs. Its role in aiding the immune system is really critical to destroying and clearing the protozoa from the horse's nervous system," Dr. Blythe says.
Not every horse needs vitamin E supplementation. Most healthy adult horses with access to green grass probably will get sufficient amounts of vitamin E from diet alone. In fact, blood levels of vitamin E and vitamin A rise and fall with the spring-summer to fall-winter cycles of pasture consumption. So, when is vitamin E supplementation necessary?
Vitamin E and Selenium
Selenium also acts as a cofactor in enzymes that protect against oxidative damage to tissues, so it is suggested that vitamin E and selenium are administered together in many cases. The spectrum of problems that arise with selenium deficiency are slightly different than those that stem from vitamin E deficiency, but the therapeutic and preventative merits overlap considerably with vitamin E. The difference is that selenium does not decay in stored feeds and it is thought that vitamin E specifically is necessary to prevent the neurologic syndromes.