Copper Deficiency

What is Copper Deficiency?

Copper deficiency in humans is very rare, since this trace element is found in many foods (liver, fish, mollusks, cocoa powder, coconuts and nuts, mushrooms, legumes, wheat, plums). So in spite of the small absorption, it is not at all problematic to get your daily 2 mg of copper.

Copper is resorbed in the stomach and in the entire small intestine, then to connect with albumin and transported to the liver. So in a small amount is binding to Apocoeruloplasmin. Like Coeruloplasmin (a2-globulin), it is present in the transport of copper from the bloodstream to tissue. Copper promotes better iron resorption, participates in the accumulation of released iron in transferrin, and supports, among other things, the formation of myelin in nerve cells, the construction of bones and tissues, and the production of melanin. Various enzymes are dependent on copper, so necessary for the respiratory chain of mitochondria, cytochrome C oxidase and acting as a trap of radical superoxide dismutase.

Most of the copper that enters the liver is excreted in the bile; only a small amount of a person loses with urine, sweat and menstrual blood.

Symptoms of Copper Deficiency (Insufficiency)

A congenital form of copper deficiency is Menkes syndrome, a monosomal recessive hereditary disease that occurs with a decrease in enteral absorption of copper and already in the neonatal period leads to severe neurological damage.

One of the most common causes of copper deficiency in adulthood is prolonged parenteral nutrition without a sufficient amount of this trace element, and the replacement of zinc in high doses leads to a decrease in copper intake through the displacement of copper from the absorption sites on enterocytes. This principle is used in the treatment of Morbus Wilson. Other diseases leading to a decrease in the level of copper are disorders of resorption due to chronic inflammatory diseases of the intestines, celiac disease and other malabsorption syndromes, diseases with prolonged diarrhea, and gastroectomy in the background, sometimes with additional dumping syndrome. With the latter, a state of copper deficiency develops only after a few years. Significant copper losses can occur with nephrotic syndrome, depending on the height of proteinuria. Decreased serum copper levels are found in Wilson’s disease; even the copper that enters the liver cannot be transferred to Coeruloplasmin, so that it is deposited in hepatocytes and leads to toxic damage to liver cells. Determining copper based on a liver biopsy helps differentiate from true copper deficiency states.

Diseases and conditions with low serum copper levels

  • Prolonged diarrhea
  • Chronic inflammatory bowel disease
  • Celiac disease
  • Dumping syndrome
  • Former resections of the stomach and intestines
  • Prolonged parenteral nutrition without sufficient replacement
  • Vitamin C Deficiency
  • High Dose Zinc Therapy
  • Hyperhomocysteinemia
  • Prolonged use of proton pump blockers or H2-antagonists
  • Long-term steroid therapy
  • Nephrotic syndrome
  • Morbus wilson