How did We Discover that Trace Minerals were Necessary for Livestock?

How did we discover that trace minerals were necessary for livestock?

One of the textbooks I routinely use to answer questions about trace minerals is Minerals in Animal and Human Nutrition by Lee McDowell from the University of Florida. Dr. McDowell’s book is fascinating, because he gives the history of our knowledge of trace minerals and how scientists and livestock producers described symptoms of both deficiencies and toxicities. I think you might enjoy some of the history of trace mineral research.

Copper, Molybdenum, and Sulfur

  • The necessity of copper for cattle was first established in the 1930’s with the discovery in Florida that cattle that had a wasting disease were deficient in cobalt, iron and copper. Researchers in Northern Europe described this wasting disease by animals as having diarrhea, loss of appetite, and anemia.

  • In the late 1930’s, scientists in England described a severe scouring disease of cattle called “teart” that was caused by ingestion of forage with high levels of molybdenum. Later, scientists discovered that large doses of copper sulfate could prevent this condition. Still, later it was shown that molybdenum limited the retention of copper in the body especially in the presence of adequate amounts of inorganic sulfate in the diet. It was this discovery that led to numerous studies on the relationship among copper, molybdenum, and sulfate. We can summarize these interrelationships as: 

  1. Molybdenum, in the presence of sulfate, reduces the deposition of copper in organs and increases the excretion of copper in the urine.

  2. An increase of dietary copper reduces molybdenum deposition in the liver.

  3. When the copper to molybdenum ratio of forages in the presence of adequate sulfate was less than 2.8 to 1, then copper deficiency is evident. A copper to molybdenum ratio of no less than 4:1 has been proposed to ensure that the copper requirement will be met.

  4. High levels of dietary zinc and iron depress copper absorption and tend to increase the requirements. High dietary levels of zinc (100 ppm) reduce liver copper storage.

  5. Cattle can die from copper poisoning. These animals may experience nausea, vomiting, salivation, abdominal pain, convulsions, paralysis, and death. The usual cause is improperly formulated supplements or diets.


  • Zinc is widely distributed through the body, but animals have a limited ability to store zinc in a form that can be mobilized to prevent a deficiency, In cattle, the highest concentrations of zinc were found in the following order:
  1. pancreas
  2. liver
  3. pituitary gland
  4. kidney
  5. adrenal gland
  6. Additional reports have shown that the testicles and accessory sex glands contain high concentrations.
  • It is suspected that zinc was applied as an for skin lesions by several cultures, including the Egyptians.In 1960 scientists discovered that a skin disorder cattle could be cured with zinc therapy.
  • Loss of appetite is one of the first signs of the deficiency in calves followed by a bowing of the hind stiffness of the joints.

  • In lab animals, severe zinc deficiency during pregnancy has resulted in offspring with impaired learning ability.
  • Additional clinical signs of a zinc deficiency in cattle include:

  1. inflammation of the nose and mouth with submucous hemorrhages

  2. unthrifty appearance

  3. rough hair coats

  4. stiffness of the joints with swelling of the feet front of fetlocks

  5. cracks in skin of coronary bands around the hooves

  6. dry scaly skin on the ears

  • In grazing animals, a marginal zinc deficiency results in subnormal growth, fertility, low serum zinc values, resistance to infection and stress.


  • During the 1930’s, selenium was identified as the toxic element in some forages that caused animals to lose hair, nails and hooves. Selenium is now known to be required by food animals and humans. Consumption of feedstuffs containing both toxic and deficient concentrations of selenium presents a problem for grazing livestock.

  • Marco Polo in his travels in western China, (ca. 1295), described a syndrome resulting from the ingestion of seleniferous plants. He reported that when horses ate this poisonous plant, their hooves dropped off.
  • In 1860, an army surgeon in South Dakota also described a fatal disease in horses grazing near Fort Randall. The horses exhibited extreme tenderness and inflammation of the feet, accompanied by loss of hair from the mane and tail.

  • Some speculate that many horses of the U.S Calvary commanded by General Custer exhibited selenium toxicity during the summer of 1876.
  • Pioneers on the northern Great Plains in the 1890s also described selenium toxicity of their livestock. They associated the disease with alkali seeps and waters of high salt content. It became known as alkali disease.

  • In the 1950s, selenium was reported to be beneficial for livestock and shown to prevent liver necrosis in swine and muscular dystrophy in calves.
  • Selenium is closely linked to vitamin E. They both protect biological membranes from degeneration. Lack of these nutrients results in tissue breakdown.

  • Selenium deficiency in ruminants is called muscle disease and is a degeneration of striated muscles. Animals with it have a generalized weakness, stiffness and muscle deterioration. These animals have difficulty standing.
  • There are a couple of clinical patterns:

  1. The a congenital type of muscular dystrophy in which calves are stillborn or die within a few days of after sudden physical exertion such as nursing running. It is observed in calves between 1 and months of age.

  2. Poor reproductive performance is also a symptom of selenium deficiency and includes retained placenta. Work from Ohio showed that the incidence in retained placentas was reduced when cows were injected with a combination of selenium and vitamin E.
  • When consumed in sufficient amounts, it can cause toxicity. Alkali disease generally happens when animals graze forages with selenium in the range of 5 to 40 parts per million. Certain selenium mutating plants have between 100 and 9,000 parts per million of selenium.

  • Clinical signs of animals suffering from selenium toxicity are:
  1. have loss of appetite
  2. lack of thriftiness
  3. cirrhosis of the loss of hair
  4. lameness
  5. elongated hooves

Part V by John Paterson, MSU Extension Beef Specialist