Absorption of Minerals
Minerals are elements. Animals cannot compose minerals. The only way to obtain the right amount of minerals, is by adapting absorption rate. Since absorption rate can never be over 100%, all animals need less minerals than their natural foods contain. After all, they have evolved based on those foods. They normally have to absorb little of the available minerals. And when the available food contains less minerals, they simply increase mineral absorption rate.
The same goes for humans. If our food contains much iron, absorption rate is decreased. If our food contains little iron, absorption rate is increased.
Because excessive anything is harmful.
Excessive minerals, like iron, zinc, cobalt, manganese, copper etc. is pro-oxidative (1), damaging nutrients, arteries (2) messenger-substances, cell-DNA (3) and enzymes (4), increases hart attack risk, and can cause diabetes (5), colon cancer (6) Parkinson's disease (7) and infertility. (8) And also; too much of one mineral decreases levels of other minerals / trace elements. (9)
Scientific analyses showed that healthy subjects were very capable of controlling iron absorption to prevent development of iron overload, even if the diet was fortified with iron and even if meat (containing much iron) intake was high. (10)
(But certainly not everybody will be able to sufficiently decrease absorption rate though)
So why would the body absorb so little calcium?
Maybe because we only need very little calcium?
Scientists do not think so. They think we need more calcium (and iron etc.) because absorption rate is low (because our food contains much). Thus we consume more, but guess what?
Absorption rate further decreases, and they think we therefore have to increase mineral consumption to compensate this lower absorption rate. And thus absorption rate further decreases etc. etc. Until we consume so much that the body is unable to sufficiently further decrease absorption rate, and too much is absorbed.
And we think we are so intelligent.
Abstracts of most sources can be found at The National Library of Medicine
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(2) Lee, T.S. et al, Iron-deficient diet reduces atherosclerosis lesions in ApoE-deficient mice Circuation 1999 / 99 (9) / 1222-1229. , Patel, R.P. et al, Formation of oxysterols during oxidation of low density lipoprotein by peroxynitrite, myoglobine, and copper. J. Lipid. Res. 1996 / 37 (11) / 2361-2371. , Dzeletovic, S. et al, Time course of oxysterol formation during in vitro oxidation of low density lipoprotein. Chem. Phys. Lipids 1995 / 78 (2) / 119-128. , Herbert, V. et al, Iron worsenes high cholesterol-related coronary artery disease. Am. J. Clin. Nutr. 1994 / 60 (2) / 299-300.
(3) Oikawa, S. et al, Distinct mechanisms of site-specific DNA damage induced by endogenous reductants in the presence of iron (III) and copper (II). Biochem. Biophys. Acta 1998 / 1399 (1) / 19-30.
(4) Sok, D.E., Oxidative inactivation of brain alkaline phosphatase responsible for hydrolysis of phosphocholine. J. Neurochem. 1999 / 72 (1) / 355-362.
(5) Burke, W. et al, Hemachromatosis : genetics helps to define a multifactorial disease. Clin. Genet. 1998 / 54 (1) / 1-9. , Crawford, R.D., Proposed role for a combination of citric acid and ascorbic acid in the production of dietary iron overload : a fundamental cause of disease Bichem. Mol. Med. 1995 / 54 (1) / 1-11. , Britton, R.S. et al, Pathophysiology of iron toxicity. Adv. Exp. Med. Biol. 1994 / 356 / 239-253. , Phatak, P.D. et al, Management of hereditary hemachromotosis. Blood Rev. 1994 / 8 (4) / 193-198.
(6) Sawa, T. et al, Lipid peroxyl radicals from oxidized oils and heme-iron :implication of a high fat diet in colon carcinogenesis. Cancer Epidemiol. Biomarkers Rev. 1998 / 7 (11) / 1007-1012.
(7) Jellinger, K.A., The role of iron in neurodegeneration : prospects for pharmacotherapy of Parkinson's disease. Drugs. Aging. 1999 / 14 (2) / 115-140. , Spencer, J.P. et al, Conjugates of catecholamines with cysteine and GSH in Parkinson's disease : possible mechanisms of formation involving reactive oxygen species. J. Neurochem. 1998 / 71 (5) / 2112-2122. , Snyder, R.D. et al, Enhancement of cytotoxicity and and clastogenicity of L-dopa and dopamine by manganese and copper. Mutat. Res. 1998 / 405 (1) / 1-8. , Vescovi, A. et al, Interactions of manganes with human brain glutathione-S-transferase. Toxicology 1989 / 57 (2) / 183-191.
(8) Olsen, P.A. et al, Effects of supplementation of organic and inorganic combinations of copper, cobalt, manganese, and zinc above nutrient requirement levels on postpartum two-year-old cows. J. Anim. Sci. 1999 / 77 (3) / 522-532.
(9) Scharl, M., B.Elsenhaus ,K.Schuman; In Welchem Maße nutzen Nickel und Eisen die selben intestinalen Resorptionswege. in : Köhrle ,J. ,Mineralstoffe und Spuren elemente. Wissenschaftliche Verlagsgesellschaft mbH Stuttgart 1998. / 195-197. , Ortega, R.M. et al, Supplementation with iron and folate during gestation : influence on the zinc status in the mother and on the zinc content in the maternal milk. (Spanish) Med. Clin. (Barc.) 1998 / 111 (8) / 281-285. , Shackelford, M.E., Mineral interactions in rats fed AIN-76A diets with excess calcium. Fd. Chem. Toxic. 1994 / 32 (3) / 255-263. , Taper, L.J. et al, Zinc and copper retention during pregnancy : the adequacy of prenatal diets with and without dietary supplementation. Am. J. Clin. Nutr. 1985 / 41 / 1184-1192. , Reinstein, N.H. et al, Zinc-copper interactions in the pregnant rat : fetal outcome and maternal and fetal zinc, copper and iron. J. Nutr. 1984 / 114 (7) / 1266-1279. , Mukherjee, M.D. et al, Maternal zinc, iron, folic acid and protein nutriture and outcome of human pregnancy. Am. J. Clin. Nutr. 1984 / 40 / 496-507. , Meadows, N.J. et al, Zinc in pregnancy. Maternal and Child Health 1984 / 150 (9) / 152-153.
(10) Hallberg L, et al, Iron stores in man in relation to diet and iron requirements. Eur J Clin Nutr 1998 / 52 (9) / 623-631.
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