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Jean E. Pierog R.N.,M.S. , NC

Copper and iodine are both essential to the human body. They are considered trace elements or minerals because the amounts needed by the body are minute. While there is an established RDA for iodine, there is insufficient data to determine copper’s RDA even though copper deficiency in animals has been demonstrated (Baar, 1994; Turnlund, 1994).


Copper has been used for over 2300 years as a therapeutic element for pulmonary and other diseases as prescribed by Hippocrates. It has been used in copper bracelets to help those with arthritis. The use of copper as a healing agent declined in the 1800’s when its treatments were deemed unsuccessful. In fact, today there’s more of a concern of copper toxicity due to the prevalence of copper in our environment such as the copper in our water pipes.

The body normally contains about 75-100 mg. of copper which is located throughout the tissues of our body, especially in the brain, heart and kidney (Bauman & Blazey, 1994; Haas, 1992). Infants, however, store up to 10 times the amount of copper that adults do and most of this is in the liver.

Although there is no established RDA for copper (the lowest dietary level required for healthy individuals), there is a recommended range suggested which is considered safe and adequate put out by the National Research Council of the United states. For adults, the range is 1.5-3.0 mg., for children the range is 1.5-2.5 mg. and for infants less than six months old the range is 0.4-0.6 mg (Turnland, 1994).

The food sources richest in copper are shellfish, liver and other organ meats, buckwheat and whole wheat, egg yolks, legumes, soybeans, avocados, raisins, nuts, oats, and whole grains. Oysters have five times as much copper as other foods (Haas, 1992). Chocolate, mushrooms, tomatoes, bananas, grapes and potatoes have intermediate amounts of copper. Cow’s milk is a very poor source of copper and in 1900 this was proven when animals kept on a whole milk diet developed anemia despite adequate amounts of iron supplements (Turnland, 1994).

Some nutritionists believe that copper deficiencies may be common due to soil depletion. In a study of 849 people living in Klevay, North Dakota, about 1/3 of them had a copper intake of less than 1 mg. a day (Baar, 1994). On the other hand, the use of copper plumbing increases the copper content of our drinking water.

It is generally recommended that people not take copper supplements because of the risk of toxicity. In addition, consuming any nutrient in large amounts is risky because trace elements are highly interactive with each other. The classic example of this is the relationship between copper and zinc; taking more copper can cause a zinc deficiency because they compete with each other for absorption in the stomach.

Other nutrients that are known to interact with copper are iron, molybdenum, ascorbic acid and carbohydrates. Iron, like zinc, has an inverse relationship with copper. That is, the more copper consumed, the less iron is absorbed and anemia can result. Molybdenum excess also causes copper deficiency and studies suggest that ingestion of more than 1500 mg. of Vitamin C per day causes impairment of copper absorption (Turnland, 1994). The relationship between carbohydrates and copper is less clearly understood in humans, but in rats a diet of sucrose and/or fructose causes copper depletion. Copper absorption is improved when protein and vegetables are eaten.

When copper is consumed, most of it is absorbed in the small intestine with a small amount absorbed in the stomach. Absorption occurs within 15 minutes and it is transferred across the gut wall by albumin into the liver where it is transformed into ceruloplasmin which is a copper protein complex. Ceruloplasmin is then released into the blood and it delivers copper to tissues throughout the body. Copper homeostasis is maintained by both the regulation of its absorption and by excreting it via bile in the gastrointestinal tract.

Copper has several important functions in the body. It serves as a catalyst in the formation of hemoglobin even though hemoglobin doesn’t actually contain copper. It is necessary for cell respiration because it is part of the cytochrome system. Copper as contained in the enzyme lysl oxidase is critical for the cross-linking of collagen and elastin which in turn are necessary for the creation of strong, flexible connective tissue. It therefore has a role in bone formation, skeletal mineralization and the integrity of the connective tissue in the cardiovascular system.

Copper plays a part in iron metabolism, but the exact mechanism is unclear. It is required for the formation of the myelin sheath that covers the neurons and is critical to normal neurotransmission functions. Copper assists the conversion of tyrosine to the pigment melanin, thereby giving hair, skin and eyes their coloring. Many enzymes contain copper, the most important being superoxide dismutase which is involved with oxygen free radical metabolism.

Other functions of copper are less clearly understood but it is known that there is a relationship of these to copper. These roles include cholesterol metabolism, thermal regulation, immune function, glucose metabolism and cardiac function.

Since 1928 it has been known that copper deficiency can lead to anemia and it is now linked to heart disease. Apparently copper deficient diets in people cause a rise in blood pressure and cholesterol, persons become glucose intolerant, the EKG is abnormal and they have difficulty dissolving blood clots (Baar, 1994).

Copper deficiency can also lead to anemia, leukopenia and neutropenia. Osteoporosis, arthritis, arterial disease, loss of pigmentation and neurological problems are also associated with low copper levels. Other deficiency states include reduced thyroid function, weakened immunity and skeletal defects. Although the above deficiency states are serious, there have been very few cases of outright copper deficiency reported and most of these have been accompanied by factors including malnutrition, malabsorption and excessive gastrointestinal losses (Turnland, 1994).

On the other hand, copper toxicity is probably more common than copper deficiency. Problems with copper toxicity include psychological depression and schizophrenia, senility, epilepsy, autism, anxiety states, poor memory, mental fatigue, and poor concentration. Additional problems include high blood pressure, PMS, pre-eclampsia and post-partum psychosis. Persons with chronic ailments such as Parkinson’s, TB, and hypertension have been found to have high blood copper levels.

If copper is ingested as an accidental poison, it can lead to nausea, vomiting and diarrhea and progress to coma, hepatic necrosis, cardiovascular collapse and death.

There are two well known genetic defects of copper metabolism: Menke’s disease and Wilson’s disease. Menke’s disease is a rare and fatal X-linked disorder of copper malabsorption in infants. Often fatal by 3 years of age, it is characterized by abnormal hair, mental retardation, seizures, temperature instability, artery abnormalities and maldistribution of copper. Wilson’s disease is an autosomal recessive disease of copper storage which allows copper to build up. It is associated with a low ceruloplasmin level and circulating levels of free copper accumulate in the liver, brain and cornea of the eye. There seems to be a defect in the breakdown and excretion of cerulosplasmin copper in the bile. If not treated early on with chelating agents such as penicillamine, it will result in neurologic damage, cirrhosis, hepatic failure and eventually death. In addition to chelation therapy, a diet low in copper and high in zinc is often prescribed.



Iodine in nutrition plays its largest role as the necessary constituent of thyroid hormones which affect growth and development. It is the main element of the thyroid hormones thyroxine, tetraiodothyronine (T4) and triiodothyronine (T3).

Iodine was discovered in 1811 when Courtois was making gunpowder. The iodine vaporized as a violet gas when some seaweed ash was being used for the gunpowder. In 1895, Baumann found iodine in the thyroid gland (Clugston & Hetzel, 1994). David Marine was the first to link iodine deficiency to the enlargement of the thyroid gland known as goiter in 1922. The thyroid gland enlarges in an effort to make more hormone. Marine and Kimball showed that goiter could be prevented and reduced by giving children small amounts of iodine.

The healthy human body contains about 15-25 mg. of iodine and about 70%-80% is found in the thyroid gland. Iodine is also found in the muscles, skin and bones and only one percent is in the blood. The two main thyroid hormones, T3 and T4, contain about one fourth of the thyroid iodine. The rest of the iodine in the thyroid is in the precursor molecules of these two hormones (Haas, 1992).

Iodine is taken into the body as iodides and is rapidly absorbed through the gut into the blood. The thyroid gland utilizes about 60 mcg (30%) a day to maintain a steady supply of thyroxine (which is 2/3 iodine). The normal daily requirement is 100-150 mcg per day. Any excess iodine is excreted via the kidneys in the urine and is not stored. Humans must therefore obtain iodine regularly from their diets.

The richest source of iodine are foods that come from the sea. Seaweeds, fish, and shellfish are excellent sources. The richest sources from fish are cod, sea bass, perch and haddock. Kelp is particularly high in iodine. Iodized salt, introduced in 1924 in Switzerland followed by Michigan (the goiter belt region), contains 76 mcg of iodine per gm of salt and is the most common source of modern day iodine consumption. In the American diet, besides salt, the most common sources of iodine are in dairy and processed foods. These sources contain "inadvertent" iodine as a result of iodine containing disinfectants used to clean milking machines, processing equipment and storage tanks (Deutsch & Morrill, 1993).

Other sources of iodine can be onions, peanuts, lettuce, mushrooms, spinach, pineapple, green peppers, whole wheat bread and cheddar cheese. These sources "can be" because they are dependent on the iodine content of the soil that they are grown. Animals grazing on iodine rich soil can also be good sources of iodine. The RDAs for iodine are: (Haas, 1992)

Adults- 150mcg/day

Children- 70-120 mcg/day

Infants- 4--50 mcg/day

Pregnant women- 175 mcg/day

Lactating women- 200 mcg/day

Some foods called goitrogens, can actually interfere with the formation of thyroglobulin and therefore produce goiter. These sources include cabbage, peanuts, soybeans, millet and cauliflower. Drugs like sulfa medicines can also be goitrogens.

Iodine is requisite for normal thyroid functioning which in turn regulates the metabolic energy of the body. The thyroid hormones set our BMR or basal metabolic rate. The thyroid is also responsible for cell respiration as well as the production of energy as ATP(Haas, 1992).

Thyroid hormone regulation is a very complex process involving the pituitary gland, the brain, the peripheral tissues and, of course, the thyroid. Thyroxine and triiodiothyronine are crucial for protein synthesis, growth and development and energy metabolism. Mental state, reproduction, nerve and bone development, speech and the skin, hair, nails and teeth are all affected by thyroid regulation. In addition, Vitamin A formation from carotene, cholesterol synthesis, carbohydrate absorption and the conversion of ribonucleic acid to protein are all influenced by the thyroid gland (Haas, 1992).

The major effect of iodine deficiency is to interfere with the production of thyroid hormones. Iodine deficiencies are common, especially in regions where the soil is iodine poor or in underdeveloped nations. It only takes a few months for iodine deficiency and thus goiter and/or hypothyroidism to occur. Goiter is linked to hypothyroidism which causes fatigue, weight gain (due to a lower metabolic rate) dry hair, diminished immune system, coldness, sluggishness and a decrease in sexual appetite. As the symptoms progress, a hyperactive, manic state occurs (which also occurs with hyperthyroidism) and iodine cannot reverse this progression (but may lessen or delay it).

Iodine deficiency disorders (IDD) are caused by iodine deficiency’s effect on growth and development. These disorders vary depending on the extent of the deficiency and the age at which it occurs. A severe deficiency during fetal life (the mother is deficient) causes cretinism which is mental and physical retardation. Iodine deficiency in children is typically associated with goiter formation as well as impaired school performance and lower IQs. Adulthood iodine deficiency may produce a barely noticeable effect to that of obvious goiter with the associated hypothyroid effects.

Excess iodine can slow or stop the production of thyroid hormone and can cause goiter (so goiter may be due to a deficiency or an excess state of iodine). Although unusual, an excess state can result from eating large amounts of iodine rich seaweed, too much iodized salt, or too many kelp tablets. The resulting goiter, however, can only be produced if iodine is consumed in excess on a regular basis.



Baar, Karen. "Trace Minerals: How Much Does a Body Need?" in San Jose Mercury News, November 2, 1994.

Balch, Phyllis and Balch, James. Prescription for Cooking and Dietary Wellness. p 40. Indiana: P.A.B. Publishing, Inc. 1992.

Bauman, Edward and Blazey, Griselda. Nutrition Educator Course. pp 226-227, 232. Cotati: Institute for Educational Therapy. 1994.

Clugston, Graeme and Hetzel, Basil. "Iodine" in Modern Nutrition in Health and Disease. 8th ed. vol. 2. Philadelphia: Lea & Febiger. pp 252- 262.

Deutsch, Ronald and Morrill, Judi. Realities of Nutrition. pp 387-389. Palo Alto: Bull Publishing Co. 1993.

Haas, Elson M. Staying Healthy With Nutrition. pp 190-197. California: Celestial Arts. 1992.

Murray, Michael T. The Healing Power of Foods. pp 8-70. California: Prima Publishing. 1993.

Turnland, Judith. "Copper" in Modern Nutrition in Health and Disease. 8th ed. vol. 2. Philadelphia: Lea & Febiger. pp 231-240.

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