11. Powanda MC. Clofibrate-induced alterations in Zinc, Iron and Copper metabolism. Biochem 1978;27(1):125-7.
12. Mark-Savage P, Keen CL, Hurley LS. Reduction by Copper supplementation of teratogenic effects of D-penicillamine. J Nutr
1983;113(3):501-10.
13. Loudianos G, Gitlin JD. Wilson’s disease. Semin Liver Dis 2000;20(3):353-64.
14. Kaji M, Ito M, Okuno T, Momoi T, Sasaki H, Yamanaka C, et al. Serum Copper and Zinc levels in epileptic children with valproate
treatment. Epilepsia 1992;33(3):555-7.
15. Baum MK, Javier JJ, Mantero-Atienza E, Beach RS, Fletcher MA, Saubedich HE, et al. Zidovudine-associated adverse reactions in
a longitudinal study of asymptomatic HIV-1-infected homosexual males. J Acquir Immune Defic Syndr 1991;4(12):1218-26.
16. Solecki TJ, Aviv A, Bogden JD. Effect of a chelating drug on balance and tissue distribution of four essential metals. Toxicology
1984;31(3-4):207-16.
17. Mehta SW, et al. Effect of estrogen on serum and tissue levels of Copper and Zinc. Adv Exp Med Biol 1989;258:155-62.
Comment [c15]: Authors?
18. Hoffman HN II, Phyliky RL. Fleming CR. Zinc-induced Copper deficiency. Gastroenterology 1998;94(2):508-12.
19. Fosmire GJ. Zinc toxicity. Am J Clin Nutr 1990;51(2):225-7.
20. Haschke F, Ziegler EE, Edwards BB, et al. Effect of Iron fortification of infant formula on trace mineral absorption. J Pediatr
Comment [c16]: Authors?
Gastroenterol Nutr 1986;5(5):768-73.
21. Vyskocil A, Viau C. Assessment of molybdenum toxicity in humans. J Appl Toxicol 1999;19(3):185-92.
22. Turnlund JR, Keyes WR, Hudson CA, et al. A stable-isotope study of Zinc, Copper, and Iron absorption and retention by young
Comment [c17]: Authors?
women fed Vitamin B-6 deficient diets. Am J Clin Nutr 1991;54(6):1059-64.
23. Kies C, Harms JM. Copper absorption as affected by supplemental Calcium, Magnesium, Manganese, Selenium and Potassium.
Adv Exp Med Biol 1989;258:45-58.
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Meschino Health Comprehensive Guide to Minerals
Iron
General Features
In a healthy adult, there are 3-5 mg of Iron. Of this, 60-70 percent is present in hemoglobin, 30 percent is stored, and
the remainder functions as a component of various substances, in particular the cytochrome enzymes of the electron
transport system and myoglobin which provides intracellular transfer and storage of oxygen within muscle cells.
As an essential component of hemoglobin, Iron binds oxygen when it passes through the blood vessels in the lungs,
which it later releases to the tissue. Thus, Iron plays a vital role in oxygen transport through the body.
In turn, oxygen's delivery to the cells of the body enables them to continuously generate ATP energy through aerobic
metabolism (electron transfer chain, also known as oxidative phosphorylation). As well, DNA synthesis, thyroid
hormone synthesis, synthesis of several neurotransmitters and healthy immune system function, all require adequate
Iron nutritional status. Iron deficiency is considered to be the most common nutritional deficiency in North American.
Even marginal deficiencies of Iron may result in fatigue, weakening of the immune system, impaired immune function
and impaired neurotransmitter and thyroid hormone synthesis.
Absorption and Metabolism
There are two forms of dietary Iron, heme Iron in the form of hemoglobin and myoglobin, and non-heme Iron. Heme
Iron is absorbed into the mucosal cells as the intact porphyrin complex (as occurs in animal foods) and is little af ected
by the composition of the meal. Hence, Iron absorption is generally about 25 percent, whereas non-heme Iron
absorption (from plant foods) is often only 5 percent. Non-heme Iron absorption is affected by meal composition.
Factors that increase non-heme Iron absorption include ascorbic acid, meat, fish and poultry, acid medium, calcium
(binds to phosphates and oxalates, allowing more Iron to be absorbed instead of bound to these common plant-based
components), intrinsic factor (enhances Iron absorption as well as being necessary for vitamin B12 absorption), and
increased Iron need (pregnancy, anemia, periods of growth, etc.).
Once absorbed from the intestinal tract into the mucosal cells of the gut, both heme and non-heme Iron form a
common Iron pool. Within the mucosal cell, Iron combines with apoferritin to form ferritin. Iron is then released to the
circulation in accordance with the body's needs. In times of need, transferrin in the blood is less saturated with Iron
and, as it passes through the gut blood vessels, Iron passes from the intestinal mucosal cells to transferrin.
Transferrin then transports it through the bloodstream to the target tissue.
If blood transferrin is already adequately saturated with Iron (one-third of its total Iron-binding capacity - TIBC), less
Iron is absorbed from the mucosal cells to transferrin and the remaining mucosal Iron cannot be absorbed. These
mucosal cells are sloughed of every two to three days and the Iron within them is excreted via the feces. This
elaborate system is in place to guard against an Iron overload, which carries serious health implications. It can,
however, become overwhelmed by excessive Iron intake leading to hemochromatosis where excessive Iron is stored
in the liver, heart, pancreas, skin and other organs. This leads to increased free radical damage to this tissue and is
linked to cancer, heart disease, arthritis, diabetes and possibly psychiatric illnesses.
Hereditary forms of hemochromatosis exist in which the body lacks the ability to limit Iron absorption from the gut and
stores greater than normal amounts. Chronic alcoholism can also lead to hemochromatosis.1
The evidence from many scientific studies suggest that high Iron levels (above 200 mcg per litre blood), may lead to an
increase in the risk of cardiovascular disease. The increased risk is thought to be due to increased oxidative (free
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Meschino Health Comprehensive Guide to Minerals
radical) damage to the heart, blood vessels and LDL-cholesterol. Once oxidized LDL-cholesterol is more inclined to
participate in the atherosclerotic process, narrowing arteries.2,3
On the other hand, adequate Iron levels are necessary as every second 2.5 million erythrocytes (RBC), 20,000 white
blood cells, and 5 million platelets are sent into the circulation. Each red blood cell contains over 250 million
hemoglobin molecules, which means that a single RBC can transport to the body more than a billion molecules of
oxygen from their entry point in the lungs.
RBCs have an average life span of 120 days. As they die, their Iron is recycled very ef iciently by the body. So
ef icient is the recycling system that very little Iron is excreted on a daily basis - less than 0.1 mg in the urine, 0.5 mg
from the intestine and even less by perspiration and sloughed skin. Most of the Iron present in feces represents
unabsorbed dietary Iron and exfoliated mucosal cells, to a lesser degree.1
Overall, men lose about 1 mg of Iron per day. Women lose about 1.8 mg per day on average, during their childbearing
years (blood loss during menstruation accounts for significantly more Iron loss than occurs in men).
Assuming Iron absorption is about 10 percent, men require 10 mg per day of Iron intake and women require 18 mg per
day of Iron intake to replenish the daily Iron losses.
Most men can achieve this level of intake, but many women fail to consume 18 mg of Iron per day from food and
consequently, Iron deficiency is more common in women.1
Recommended Daily Allowance (Iron)
Age Group
Dosage (mg)
0-6 mths
6
6–12 mths
10
1–10 yrs
10
Males 11–18 yrs
12
Males 19 yrs and older
10
Females 11–30
15 (up to 18)
Females 30 years and older
10
Pregnant females
30
Lactating females
15
Iron Deficiency
Iron deficiency is the most common nutrient deficiency in the United States. The groups at highest risk are infants
under 2 years of age, teenage girls, pregnant women, and the lower-income elderly. Studies have found evidence of
Iron deficiency in 30-50 percent of people in these groups. In fact, 35-58 percent of young, healthy women have Iron
deficiency. During pregnancy, the number is even higher.1,4 In elderly persons, Iron absorption is reduced due to less
gastric acidity.5
Iron deficiency can lead to anemia, excessive menstrual loss, learning disabilities, impaired immune function or
decreased energy levels and physical performance.1,4,6
Iron deficiency is the most common cause of anemia, however, anemia is the last stage of Iron deficiency (microcytic
hypochromic). A low level of serum ferritin is an early marker of sub-optimal Iron status. A deficiency is indicated by a
blood level of 12 mcg per litre or less. Normal range is 40-160 mcg per litre. A level of 30 mcg per litre or less should
demand at ention from a health practitioner.4,8
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Meschino Health Comprehensive Guide to Minerals
Marginal Iron deficiency can occur without anemia, producing such symptoms as fatigue, behavioural problems
(decreased alertness and at ention span), muscle weakness and increased susceptibility to infections.7
Supplementation, Studies and Clinical Applications