Reference from the joint report of FAO/WHO expert consultation on Human Vitamin and Minerals verbatim.
3. Dallman, P.R. 1986. Biochemical basis for the manifestations of iron deficiency. Ann.
Rev. Nutr., 6: 13-40.
82. Egderton, V.R. 1972. Iron deficiency anemia and physical performance and activity of
rats. J. Nutr., 102: 381-400.
83. Finch, C.A. , 1976. Iron deficiency in the rat. Physiological and biochemical studies of
muscle dysfunction. J. Clin. Investig., 58: 447-53.
Studies in animals have clearly shown that iron deficiency has several negative effects on important functions in the body (3). Physical working capacity in rats has been shown to be significantly reduced in iron deficiency, that is especially valid for endurance activities (82, 83).
84. Scrimshaw, N.S. 1984. Functional consequences of iron deficiency in Human populations. J. Nutr. Sci. Vit., 30: 47-63.
This negative effect seems to be less related to the degree of anaemia than to impaired oxidative metabolism in the muscles with an increased formation of lactic acid, that in turn is due to a lack of iron-containing enzymes which are rate limiting for the oxidative metabolism (84).
85. Lozoff, B., Jimenez, E. & Wolf, A. 1991. Long-term developmental outcome of infants with iron deficiency. N. Engl. J. Med., 325: 687-694.
86. Youdim, M.B.H. 1988. Brain iron:Neurochemical and behavioural aspects. New York, Taylor & Francis.
87. Beard, J.L., Connor, J.R. & Jones, B.C. 1993. Iron in the brain. Nutr. Revs., 1: 157-170.
88. Pollitt, E. 1993. Iron deficiency and cognitive function. Ann. Rev. Nutr., 13: 521-37.
The relationship between iron deficiency and brain function is of great importance for the choice of strategy in combating iron deficiency (85-88). Several structures in the brain have a high iron content of the same magnitude as observed in the liver. Of great importance is the observation that the lower iron content of the brain in iron-deficient growing rats cannot be increased by giving iron later on. This fact strongly suggests that the supply of iron to brain cells takes place during an early phase of brain development and that, as such, early iron deficiency may lead to irreparable damage to brain cells.
84. Scrimshaw, N.S. 1984. Functional consequences of iron deficiency in Human populations. J. Nutr. Sci. Vit., 30: 47-63.
89. Brock, J.H. 1994. Iron in infection, immunity, inflammation and neoplasia. In: Brock JH et al., eds. Iron metabolism in health and disease. p. 353-389. London, W.B.Saunders
Company Ltd.
In humans about 10 percent of brain iron is present at birth; at the age of 10 years the brain has only reached half its normal iron content, and optimal amounts are first reached at the age of 20-30 years. In populations with long-standing iron deficiency, a reduction of physical working capacity has been demonstrated by several groups with improvement in working capacity after iron administration (84).
Iron deficiency also negatively influences the normal defence systems against infections. The cell-mediated immunologic response by the action of T lymphocytes is impaired as a result of a reduced formation of these cells. This in turn is due to a reduced DNA synthesis depending on the function of ribonucleotide reductase, which requires a continuous supply of iron for its function. The phagocytosis and killing of bacteria by the neutrophil leukocytes is an important component of the defence mechanism against infections.
These functions are impaired in iron deficiency. The killing function is based on the formation of free hydroxyl radicals within the leukocytes, the respiratory burst, and results from the activation of the iron-sulphur enzyme NADPH oxidase and probably also cytochrome b (a heme enzyme) (89).
The impairment of the immunologic defence against infections that was found in animals is also regularly found in humans. Administration of iron normalises these changes within 4–7 days. It has been difficult to demonstrate, however, that the prevalence of infections is higher or that their severity is more marked in iron-deficient subjects than in control subjects. This may well be ascribed to the difficulty in studying this problem with an adequate experimental design.
A relationship between iron deficiency and behaviour such as attention, memory, and learning, has been demonstrated in infants and small children by several groups. In the most recent well-controlled studies, no effect was noted from the administration of iron. Thisfinding is consistent with the observations in animals. Therapy-resistant behavioural impairment and the fact that there is an accumulation of iron during the whole period of brain growth should be considered strong arguments for the more active and effective combating of iron deficiency.
90. Bruner, A.B. 1996. Randomised study of cognitive effects of iron supplementation in non-anaemic iron-deficient adolescent girls. Lancet, 348: 992-96.
This is valid for women, especially during pregnancy, for infants and children, and up through the period of adolescence and early adulthood. In a recent well controlled study, administration of iron to non-anaemic but iron-deficient adolescent girls improved verbal learning and memory (90).
91. Rowland, T.W. 1988.The effect of iron therapy in the excersice capacity of non-anemic iron-deficient adolescent runners. Am. J. Dis. Child., 142: 165-169.
92. Ballin, A. 1992. Iron state in female adolescents. Am. J. Dis. Child., 146: 803-805.
93. Zhu ,Y.I. & Haas, J.D. 1997. Iron depletion without anemia and physical performance in young women. Am. J. Clin. Nutr., 66: 334-41.
Well-controlled studies in adolescent girls show that iron-deficiency without anaemia is associated with reduced physical endurance (91) and changes in mood and ability to concentrate (92). A recent careful study showed that there was a reduction in maximum oxygen consumption in non-anaemic women with iron deficiency that was unrelated to a decreased oxygen-transport capacity of the blood (93).
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