Nutritional myodegeneration (NMD), more commonly known as white muscle disease, is a disorder that affects various animals, including horses. In equids, the condition primarily occurs in newborn foals, although adult horses can also develop it. [1][2]

The condition results in degeneration in the skeletal and cardiac muscle most often due to inadequate levels of selenium in the body. It also occurs less commonly in horses that are deficient in vitamin E. [1][2]

Selenium and vitamin E are important antioxidant nutrients for horses. Antioxidants are molecules that neutralize free radicals, which are unstable molecules that can damage cells.

Common signs of white muscle disease include weakness, poor coordination, and difficulty standing, eating, and nursing. [1] Due to a loss of muscle function, respiration can be impaired, and respiratory failure may occur in foals.

If left untreated, nutritional myodegeneration can be fatal. [1] But with early diagnosis and treatment, some horses make a full recovery from NMS.

You can help prevent white muscle disease by ensuring that your horse has adequate levels of selenium and vitamin E in their diet.

Nutritional Myodegeneration in Horses

NMD causes premature cell death of skeletal and cardiac muscles, resulting in the development of white scar tissue in muscles.

It is referred to as white muscle disease because affected muscles affected are paler in color, and can become completely white in advanced cases. [1][2]

NMD is a disease that most commonly presents in newborn foals, although it can also occur in adult horses. [1][2] 82% of nutrition-related muscle disease in horses occur in animals less than four years of age. [3]

White muscle disease can occur in foals that did not receive sufficient selenium from their mother during gestation. Broodmares that are deficient in selenium may not transfer enough of this nutrient to the placenta of the developing fetus. [1]

This disease may also be caused by a lack of vitamin E in the broodmare’s colostrum, which is the first milk produced by a mare after they deliver a foal.

Adult horses can develop the condition from chronic or prolonged low dietary intake of selenium. [1] Vitamin E deficiency can also contribute to NMD in adult horses but is believed to play less of a role than selenium deficiency. [1]

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Importance of Dietary Selenium

Selenium is an essential trace mineral that plays an important role in muscle function and development. It serves as an antioxidant, protecting cells from free radical damage.

A typical adult horse that weighs 500 kg (1100 lb) requires a minimum of 1 mg per day of selenium to avoid deficiency. According to the NRC, the optimal intake to support the immune system is between 2 to 3 mg daily. [9]

Horses that are heavily exercised, stressed or ill may also have higher needs for selenium to support recovery and immune function.

Antioxidant Status

Selenium is a component of glutathione peroxidase (GSH-Px), an antioxidant enzyme that neutralizes highly reactive chemicals in the body.

Antioxidants prevent damage from reactive oxygen species, which are natural compounds produced during the breakdown (metabolization) of fatty acids for energy.

If the horse does not have enough selenium in its body to support glutathione peroxidase activity, cell damage can accumulate at a faster rate and lead to muscle problems.

Vitamin E is another important antioxidant, preventing fatty acids peroxidation – a process by which free radicals damage fats in the body. [3]

Highly active muscles are usually most severely affected by nutritional myodegeneration. When muscles are worked, the production of reactive oxygen species is increased and if the horse does not have adequate antioxidant protections, these muscles will experience damage.

Muscles most often affected include: [3][7]

  • The diaphragm
  • Chest wall muscles
  • Gluteal muscles
  • The tongue
  • Masticatory (chewing) muscles
  • Muscular tissue of the heart

Selenium Content in Soil and Forage

NMD typically occurs in horses living in regions where the soil is deficient in selenium. Plants and grasses take up selenium from the groundwater and soil through their roots.

In areas with low selenium levels in the soil, the vegetation will also be deficient in this mineral. Selenium levels in feed crops should be above 0.1 mg/kg to prevent deficiency in grazing animals. [3]

Most forages in the coastal and Northern areas of North America have inadequate levels of selenium. Horses in these regions that are maintained exclusively on pasture and hay have a higher risk of deficiency. [8]

Selenium Map of Canada & the USA

The prevalence of white muscle disease is expected to increase due to the depletion of this nutrient in soils. [1][2]

Acid rain can also affect selenium levels in forages. Soil exposed to acid rain releases less selenium, resulting in lower selenium levels in crops grown in that soil. [3]

Signs of White Muscle Disease in Horses

Common signs of white muscle disease in foals include rapid heartbeat and difficulty standing up. Severely affected foals experience tying up of their muscles or azoturia.

The first sign of NMD in adult horses is often difficulty eating because this condition affects the muscles used for chewing food. [6] The muscles involved in movement and cardiac function are also affected in adult horses. [2]

NMD can also contribute to the following clinical signs and progressive health complications: [4]

  • Sudden recumbency (laying down)
  • High respiratory rate (Tachypnea)
  • Shortness of breath (Dyspnea)
  • Inability to stand
  • Weakness
  • Inability to swallow (Dysphagia)
  • Jaw clenching (Trismus)
  • Muscle fasciculations
  • Trembling
  • Stiffness
  • Inadequate suckle reflex
  • Muscle breakdown

Nutritional myodegeneration is also associated with the following metabolic abnormalities, which may be detected in laboratory tests.

  • Increased potassium in the blood [5]
  • Reduced amounts of the electrolytes sodium, calcium, and chloride in the blood [5]
  • Increased serum muscle enzymes [5]
  • Low glutathione peroxidase (GSH-PX)
  • Low to normal serum vitamin E levels
  • Darker than normal urine due to higher nitrogen excretion from the breakdown of muscle tissue

Severe forms of NMD can be fatal due to cardiovascular arrhythmia, cardiovascular collapse, and fluid accumulation in the lungs (pulmonary edema). In these cases, death may occur within hours of onset. [3]


Inadequate Selenium in Developing Foals

A study of eight newborn foals diagnosed with NMD found that seven had blood selenium levels less than 1.26 micromol/l. Only one foal had a normal selenium level of 2.8 micromol/l. [4]

The selenium status of the foal in utero depends entirely on the amount of selenium in the mare’s diet. Foals receive selenium via the placenta during gestation.

If the mare does not have enough selenium in her forage and is not being supplemented, she may not be able to supply her foal with enough of this mineral during gestation.

Also, mares with poor liver function or gastrointestinal issues affecting nutrient absorption may not provide adequate selenium to their developing foal.

One study found that mares who were diagnosed with ragwort poisoning (a cause of progressive liver cirrhosis) a year prior to delivering foals produced offspring with NMD. The foals were born with NMD despite the mares having received vitamin E and selenium supplements for a prolonged period prior to birthing. [3]

It’s also important to ensure that your broodmare has adequate vitamin E levels in her diet. Sufficient vitamin E and selenium intake in healthy mares during gestation can help prevent NMD in newborn foals. [3]

High Levels of Stress

Although NMD typically occurs in geographic areas with low selenium soil content, not all foals and horses that are deficient in selenium will develop the disease.

Individual factors such as exposure to psychological and environmental stressors as well as exercise load may contribute to the development of the disease. [3]

A case report described transport of horses to a new stable and the introduction into a new herd as possible triggering factors for NMD. It also identified colic as a potential trigger for the condition. [2]


Your veterinarian will diagnose NMD by collecting a blood sample from your horse and checking serum levels of selenium and vitamin E.

If your horse is showing other signs of the condition and is low in these nutrients, then NMD is highly likely. [1][2]

Diagnosis of white muscle disease also involves examining levels of muscle enzymes in the blood to determine the severity of the disease and the extent of the muscular damage.

Elevations in enzymes including creatine phosphokinase (CK/CPK) and aspartate aminotransferase (AST) can indicate muscle breakdown has occurred. [2][5]

A low level of the antioxidant enzyme glutathione peroxidase may also indicate NMD. [2]

An autopsy can confirm a diagnosis of NMD. On a post-mortem examination, the skeletal muscle of affected horses will appear pale or in some cases completely white. [2] This indicates the premature cell death of skeletal muscles. [4]

Ruling Out Other Conditions

NMD must be differentiated from other conditions that involve similar clinical signs. These conditions include widespread infection detectable in the blood (septicemia), deprivation of oxygen due to neonatal asphyxia, pneumonia, botulism, tetanus, trauma, or septic arthritis. [2]

Other muscle diseases including atypical myopathy and rhabdomyolysis must also be ruled out. Atypical myopathy is not associated with an inability to eat and drink, so horses that present with these signs are not likely to have this condition. [2]


If your horse or foal has been diagnosed with NMD, consult a veterinarian to determine the most effective treatment plan.

Treatment for the condition may include selenium injections, Vitamin E supplementation, supportive therapies and antibiotics for horses with infections.

Selenium Injections

Your veterinarian will typically administer an intramuscular selenium injection. Depending on the dose, selenium levels in the whole blood can reach adequate levels within 10 – 30 days. [11]

Injections with higher doses of selenium have been associated with more severe injection site reactions including swelling and fibrosis at the site of injection. [11]

It is important to note that a single selenium injection only maintains adequate selenium for a short period of time (roughly 6 months). [11] The diet will also need to provide adequate selenium on an ongoing basis to meet requirements.

Ensure that their diet is supplemented with organic selenium in the form of selenized yeast. [12]

Note that relying on mineral blocks with selenium added will not be sufficient to correct a selenium deficiency. [13]

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  • Organic selenium yeast
  • Natural Vitamin E
  • Optimal antioxidant status
  • Supports muscle function

Vitamin E supplements

If vitamin E levels are low on your horse’s blood tests, an oral vitamin E supplement will also be administered. Whether an oral supplement will improve vitamin E status depends on the dose and form. In one study, doses of ~ 3000 IU synthetic vitamin E increased vitamin E levels in blood and muscle of exercising horses but doses of ~ 800 IU did not. [14]

Your horse should be getting natural vitamin E such as D-alpha-Tocopherol acetate as opposed to synthetic vitamin E (ie: DL-alpha-Tocopherol acetate). The body absorbs and utilizes natural forms of vitamin E better than synthetic forms. [10]

Supportive Therapies

To provide appropriate care, foals and horses affected by NMD may need to be hospitalized in an equine veterinary clinic.

Foals with NMD are often uncoordinated, weak and have difficulty swallowing. They may need help to stand and nurse. A foal that cannot nurse properly may need to be fed from a bottle or via a nasogastric tube.

Your veterinarian will monitor your foal’s fluid and electrolyte balance carefully to prevent dehydration. Oral or intravenous fluids may be administered to foals that are unable to drink normally.


Foals that have developed respiratory problems or secondary aspiration pneumonia due to NMD typically require antibiotics to treat the infection.


The mortality rate from nutritional myodegeneration in foals and horses ranges from 30% to 45%. [3]

If foals with NMD are identified and treated promptly, the condition may be reversible. [3] The prognosis of NMD in adult horses is poor.

If the condition progresses to the point of the cardiac muscle around the heart becoming compromised, it is unlikely that an affected foal or horse will recover.


The following strategies can help prevent nutritional myodegeneration in your horse:

  • Ensure your horse’s diet provides balanced levels of vitamins and minerals. Omneity is a concentrated vitamin and mineral supplement that provides 2.4 mg of organic selenium and ~ 1000 IU vitamin E per typical serving.
  • If necessary, provide additional selenium and vitamin E, preferrably as organic selenium and natural vitamin E. Natural E/Organic Se is a pelleted supplement that can be provided in addition to Omneity.
  • Consult with an equine nutritionist to ensure your broodmare’s diet contains adequate levels of selenium and vitamin E. You can submit your horse’s diet for analysis online for free.
  • Monitor the antioxidant status of broodmares on selenium-deficient pastures by assessing blood selenium levels and plasma glutathione peroxidase concentrations. This is especially important if your mare has previously given birth to a foal with white muscle disease.
  • If you grow your own forage, monitor the selenium content of the soil. If levels are low, you may need to use fertilizer to increase the selenium content of the soil.
  • Have your hay analyzed to determine its selenium content. Supplement as necessary.
  • Have your veterinarian administer selenium injections to your horse if blood levels are low. Selenium injections should only be administered by a veterinarian to deliver an appropriate dose and monitor for side effects.



Nutritional myodegeneration or White Muscle Disease can occur in horses and newborn foals with inadequate serum selenium levels. [1][2] Vitamin E deficiency can also play a role in the development of NMD. [1][2]

Blood tests are used to diagnose NMD by assessing levels of selenium, vitamin E, glutathione peroxidase, and muscle enzymes. [1][2]

Not all horses with low serum selenium and/or vitamin E will develop the condition. Stress and illness are potential triggers for the condition by contributing to muscle cell damage. [3]

NMD can be fatal if unrecognized or untreated. Treatment for the condition includes restoring selenium and vitamin E levels to normal.

Supportive therapies such as antibiotics (if an infection is present) and intravenous fluids and electrolytes may be required to help horses recover from the condition. [1][2]

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  2. Ludvikova, EK. et al. Nutritional myodegeneration as a cause of dysphagia in adult horses: three case reports. Veterinarni Medicina. 2018.
  3. Delesalle C. et al. White muscle disease in foals: focus on selenium soil content. A case series. BMC Vet Res. 2017. View Summary
  4. Streeter RM. et al. Selenium deficiency associations with gender, breed, serum vitamin E and creatine kinase, clinical signs and diagnoses in horses of different age groups: a retrospective examination. 1996-2011. View Summary
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  12. Kienzle, E. and Zorn, N. Bioavailability of Minerals in the Horse. Europ Equine Nutr Health Congress. 2006.
  13. Pitel, M.O. et al. Influence of specific management practices on blood selenium, vitamin E, and beta-carotene concentrations in horses and risk of nutritional deficiency. J Vet Intern Med. 2020.View Summary
  14. Siciliano, P.D. et al. Effect of dietary vitamin E supplementation on the integrity of skeletal muscle in exercised horses. J Anim Sci. 1997. View Summary