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Role of red meat in the diet for children and adolescents.


* Optimal nutrition during the first years of life is crucial for optimal growth and development and, possibly, the prevention of chronic disease of adulthood.

* Iron-deficiency anaemia in childhood and adolescence is associated with serious adverse outcomes that may not be reversible, making detection and early treatment an imperative.

* Zinc plays a major role in cellular growth.

* Vitamin A is essential for the functioning of the eyes and the immune system.

* Vitamin A is necessary for membrane stability, and zinc is essential for mobilisation of the beta-carotene. Vitamin A deficiency contributes to anaemia by immobilising iron in the reticuloendothelial system, reducing haemopoiesis and increasing susceptibility to infections.

* Like iron, iodine appears to be involved in myelin production and, hence, nerve conduction.

* Meat is a core food in the diet for children and adolescents because it provides significant amounts of these micronutrients.


Over the first few years of postnatal life, an infant's body undergoes dramatic changes not only in physical attributes, but also in developmental milestones. By three years of age, an infant's head circumference and hence brain size will have reached 80% of what it will potentially achieve in adulthood, and its length will also have doubled in size. Therefore, it is not surprising that any adverse events occurring during these periods may have a negative impact upon psychomotor development.

In 1968, Dobbing (1) suggested that there were vulnerable periods of neurological development that coincided with times of maximal brain growth. These periods begin during foetal development at around the 25th week of gestation and continue for the first two years of postnatal life. Nutrient deficiencies occurring during these vulnerable periods may well have an impact upon brain growth and, hence, neurological and psychomotor development. (1) These nutrient deficits have subsequently been shown to result in more functional deficiencies rather than physical abnormalities. Not only is optimal nutrition essential for achieving optimal physical and psychosocial development, but it also appears to have significant disease implications for later in adult life. Barker and his epidemiology group in the UK proposed that not only intrauterine malnutrition, but also poor weight gain in the first year of life, was associated with an increased incidence of cardiovascular disease (particularly in adults aged >50 years), hypertension and glucose intolerance during adulthood. (2) Their retrospective, epidemiological report has been supported by several studies on the Netherlands famine during World War II, which affected women during early, mid and late stages of gestation. (3,4) Subsequently, animal and prospective human studies have suggested that either under- or over-nutrition in utero can be associated with epigenetic changes as well as intrauterine adverse programming of organ function. (5)

Development of functional activity may be associated with myelination. Many nerve fibres are covered with a whitish, fatty, segmented sheath called the myelin sheath. Myelin protects and electrically insulates fibres from one another and increases the speed of transmission of the nerve impulses. Myelinated fibres conduct nerve impulses rapidly, whereas unmyelinated fibres tend to conduct quite slowly. This acceleration of nerve conduction is essential for the function of the body and survival. In humans, the myelin sheath begins to appear around the fourth month of foetal development and first appears in the spinal cord before spreading to the higher centres of the brain. It is assumed that this myelination precedes functional activity. This paper considers micronutrient deficiency in the context of myelination and other developmental features to highlight the need for micronutrients which can be delivered in the diet through red meat.


Vitamin and mineral deficiency touches the lives of perhaps a third or more of the world's population, with many of these deficiencies overlapping and impacting upon each other. Up to 50% of children with vitamin and mineral deficiencies suffer from multiple deficiencies with resultant immeasurable burdens upon the individual, upon health services and upon education systems globally. (6) There is ample evidence that undernutrition can impact upon a child's development, but it is often difficult to separate macronutrient deficiency from that of isolated or combined micronutrient deficiency.


Iron is one of the best-understood micronutrients with respect to its role in the nervous system. Iron-deficiency anaemia affects an estimated 1-2 billion people worldwide. (7) In developing countries, over 50% of pregnant women are anaemic, (8,9) as are 46-66% of children under four years of age, with half attributed to iron deficiency (ID). (10) It has been estimated that 50-80% of children in Asia are iron deficient. (6) Even in developed Western countries such as the USA and Australia, the incidence of ID can be as high as 20% in young children and adolescents. (11,12) Common gestational conditions, such as intrauterine growth restriction or prematurity, expose infants to ID in the late foetal or neonatal period. Given the number of infants potentially affected, adverse effects of early ID on the developing brain are worrisome on both the individual and societal level.

Iron is essential for brain development. Brain iron is stored preferentially in the extra pyramidal tracts and is laid down in the first 12 months of life. Once the blood-brain barrier closes, very little iron can be deposited in the brain and, hence, an adequate dietary intake of iron is essential during this critical period. Iron also appears to be an integral part of the synthesis, uptake and degradation of the neurotransmitter dopamine, with iron-deficient animals having been shown to have dopamine deficiency. (13,14) With respect to myelination, iron is directly involved as a cofactor for cholesterol and lipid biosynthesis, and indirectly through its involvement in oxidative metabolism (that is highest in the brain in the oligodendrocytes). (15-17) The oligodendrocytes are the iron-containing cells in the brain, and their only known function is myelin production. The oligodendrocytes also contain transferrin and ferritin, both of which are essential for normal iron homeostasis. The ferritin in the oligodendrocytes is in the form of H-ferritin. This is the heavy-chain form, which is associated with high iron usage and low iron storage. (18) H-chain ferritin is only seen in the oligodendrocytes in early development at the time of maximal myelin deposition. Hence, it is very clear that iron deprivation occurring during this time period may have an adverse effect upon myelination. A number of studies have demonstrated this, and have also suggested that deficiencies occurring during these vulnerable periods of development result in permanent disability. (13,19,20) It has been shown that ID does have a negative effect upon nerve conduction, with studies of auditory-evoked potentials showing an increase in central conduction time. (21,22) Several studies have now shown that iron-deficient anaemic 6- to 24-month-old infants can score lower on tests of mental development compared with non-iron-deficient controls (13,19,20) and are at risk for poorer cognitive, motor, social-emotional and neurophysiological development at least in the short term. Furthermore, at least one study has shown that these deficits appear to be permanent. (19) These infants appeared to have reproducible deficits in body balance and coordination and in language skills, which could be interpreted as implying problems with nerve conduction and hence myelination.


Zinc is also an essential nutrient for human health. Zinc plays a major role in cellular growth, where it is crucial in the enzyme systems necessary for the production of RNA and DNA. In the brain, zinc binds with proteins and is involved with both structure and function. Severe zinc deficiency in animals has been associated with significant malformations such as anencephaly and microcephaly, and with functional deficits such as short-term memory deficits and behavioural problems. (23) In humans, cerebella dysfunction, behavioural and emotional disturbances have all been described. (23) In spite of the proven benefits of adequate zinc nutrition, approximately 2 billion people still remain at risk of zinc deficiency. (6) When zinc is provided as a supplement to children in lower-income countries, it reduces the frequency and severity of diarrhoea, pneumonia, and possibly malaria. Moreover, studies have shown that children who receive zinc supplements have lower death rates. (6)

Vitamin A

Vitamin A deficiency continues to compromise the immune systems of approximately 40% of the developing world's children under five years of age, leading to the early deaths of an estimated 1 million young children each year. (6) The term 'vitamin A' is a generic label for beta-ionone derivatives other than provitamin A carotenoids. The latter is a generic term for all carotenoids that have the biologic activity of beta-carotene. Beta-carotene ultimately is converted to retinol, which is essential for normal retinal development in the human eye. Vitamin A is necessary for membrane stability, and zinc is essential for mobilisation of the beta-carotene. Vitamin A deficiency contributes to anaemia by immobilising iron in the reticuloendothelial system, reducing haemopoiesis and increasing susceptibility to infections. Vitamin A is essential for the functioning of the eyes as well as the immune system.

Vitamin A deficiency is associated with impaired humoral and cellular immune function, keratinisation of the respiratory epithelium and decreased mucus secretion, which weaken barriers to infection. (24) In developing countries, acute respiratory infections, mostly in the form of pneumonia, are the leading cause of death in children under five year of age. (23) In developing countries, it is estimated that up to 20 million children require hospitalisation as a result of pneumonia, with approximately 3.8 million of them having a fatal outcome. (23) In vitamin A deficiency, linear stunting is common, xerophthalmia can occur and visual dysfunction can be the outcome. Vitamin A supplementation to children has shown a 23% reduction in childhood mortality irrespective of the cause of the mortality. (6) In the developing world, trials indicate that improving the vitamin A status of preschool age children can reduce childhood mortality by 20% to 56%, and also, that supplementation of women of child-bearing age can reduce maternal mortality by 40% to 50%. (6)


Iodine deficiency is a worldwide public health problem with an incidence of congenital hypothyroidism of 1:3000 to 1:4000 live births. (6) Iodine deficiency is estimated to have lowered the intellectual capacity of almost all of the nations reviewed by as much as 10-15%. (6) In developed nations there has been a recent and disturbing increase in iodine deficiency, with as many as 25% of children and women of child-bearing age being deficient. (6) This increase has coincided with the declining dietary intake of iodized salt and also the elimination of iodophor-based cleaning compounds in commercial dairies. (25) Impaired physical and mental development is common. (26) Foetal iodine deficiency in the first and early second trimester of pregnancy results in retardation and deaf mutism, whereas in the early postnatal period, the main abnormalities are growth stunting and somatic abnormalities. (27) The hearing loss can be variable, depending on the age of onset, and can also be associated with dysarthria and other disorders of speech. Physical deficits seen include lower limb spasticity, rigidity and bradykinesia. The critical stage of foetal development for iodine appears to be around the 14th week of foetal life. Magnetic resonance imagery scans taken in severely effected individuals reveal normal brain structure apart from cystic lesions in the globus pallidus. (28) Like iron, iodine appears to be involved in myelin production and, hence, nerve conduction. This appears to be supported in animal model research where rats fed upon an iodine-deficient diet were found to have alterations in myelin basic protein immunoreactivity and hence function. (29)


Early childhood

Toddlers and preschoolers often have limited food habits; yet energy and iron demands for growth are relatively high. Iron stores can be affected by prolonged breastfeeding, delayed introduction of solids and excessive use of cow's milk. (30) In Australia, iron intakes appear to be low in the diets of very young children, with the National Nutrition Survey of 1995/1996 showing one-third of 2- to 3-year-olds having intakes below the recommended dietary intake (RDI), and some 10% below 70% RDI. About 20% of adolescent boys and 50% of adolescent girls also did not meet the RDI for iron on the day of the survey, with some 25% of girls aged 12-18 years having intakes below 70% RDI compared with 6-8% of boys of this age (31) Studies to estimate the extent of the problem of ID in children and adolescents in Australia have only been performed on relatively small groups of Australian children to date, but the results indicate that significant numbers of children (up to 35%), particularly young children, may be iron depleted. Children from a number of Aboriginal communities appear to be particularly at risk for ID. (32,33)


Statistics on the prevalence of ID in Australian teenagers are limited. There has been no recent national assessment of iron status in Australian adolescents. However, if the results obtained from two surveys of adolescent girls and young women in West Australia (34,35) and data from a National Survey from the mid-1980s (36) can be generalised to the current adolescents and young adult population, low iron stores or ID without anaemia could be relatively common in female adolescents and young women in Australia. An adequate supply of iron is critical during adolescence to maintain haemoglobin levels but also to increase the total iron mass during this period of rapid growth. Iron requirements for boys increase during the growth spurt as new muscle is laid down. With the slowing of growth, at the end of puberty, iron requirements decline. Although girls develop less extra muscle tissue than boys, menarche increases the need for iron, and this increased need continues throughout reproductive life. (37) The adolescent girl is therefore at risk for developing ID due to the combined effects of continuing growth, menstrual iron losses and a low intake of dietary iron.


Meat plays a central role in the diet, providing a significant contribution to the intakes of 10 key nutrients: energy, protein, vitamin A, vitamin B1, vitamin B2, niacin, vitamin B6, vitamin B12, iron and zinc. In young children, an over-dependence on milk may put young children at increased risk of poor iron status, owing to its displacement of iron-rich or iron-enhancing foods from the diet. This risk becomes nonsignificant when moderate to high amounts of iron-rich or iron-enhancing foods (e.g. meat and fruit, respectively) are also consumed. A study performed on infants in the UK has shown that the addition of meat powder to a weaning food has a marked enhancing effect on the absorption of iron, (38) which reinforces the fact that lean red meat is not only an appropriate weaning food but should be considered an essential food during the critical stages of brain development Dietary diversification involves promotion of a diet with a wider variety of naturally iron-containing foods, especially red meat, poultry and fish. These foods have a high content of highly bioavailable haem iron, and thus are most appropriate for infants and children on weaning. Despite their widespread availability, foods from this group are not always used or may be diluted before use (e.g. meat is rich in iron but meat broth is not). Given the information above, however, it is reasonable to argue that meat is a core food in the diet for children and adolescents because it provides significant amounts of essential micronutrients.


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2 Baker DJP. Fetal origins of coronary heart disease. Br Med J 1995; 311: 171-4.

3 Ravelli GP, Stein ZA, Susser MW. Obesity in young men after famine exposure in utero and early infancy. N Engl J Med 1976; 295: 349-53.

4 Painter RC, de Rooij SR, Bossuyt PM et al. Early onset of coronary artery disease after prenatal exposure to the Dutch famine. Am J Clin Nutr 2006; 84: 322-7.

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6 Progress for Children. A Report Card on Nutrition. UNICEF. 2006. Available from URL:

7 Stoltzfus RJ. Defining iron-deficiency anemia in public health terms: a time for reflection. J Nutr 2001; 131: 565S-7S.

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9 Administrative Committee on Coordination Sub-Committee on Nutrition (ACC/SCN). Fourth Report on the World Nutrition Situation. Geneva: ACC/SCN in collaboration with IFPRI, 2000.

10 Stoltzfus RJ, Mullany L, Black RE. Iron deficiency anaemia. In: Ezzati M, Lopez AD, Rodgers A et al., eds, Comparative Quantification of Health Risks. Global and Regional Burden of Disease Attributable to Selected Major Risk Factors. Geneva: WHO, 2004; 163-209.

11 Looker AC, Dallman PR, Carroll MD, Gunter EW, Johnson CL. Prevalence of iron deficiency in the United States. JAMA 1997; 277: 973-6.

12 Brewster DR. Iron deficiency in minority groups in Australia. J Paediatr Child Health 2004; 40: 422-3.

13 Lozoff B, Georgieff K. Iron deficiency and brain development. Semin Pediatr Neurol 2006; 13: 158-65.

14 Dallman PR, Spirito RA. Brain iron in the rat: extremely slow turnover in normal rats may explain long lasting effects of early iron deficiency. J Nutr 1977; 107: 1075-81.

15 Bradbury MW. Transport of iron in the blood-brain barrier-cerebrospinal fluid system. J Neurochem 1997; 69: 443-54.

16 Gerber MR, Connor JR. Do oligodendrocytes mediate iron regulation in the human brain? Ann Neurol 1989; 26: 95-8.

17 Connor JR. Iron acquisition and expression of iron regulatory proteins in the developing brain. Dev Neurosci 1994; 16: 233-47.

18 Connor JR, Menzies SL. Relationship of iron to oligodendrocytes and myelination. Glia 1996; 17: 83-93.

19 Walter T, De Andraca I, Chadud P, Perales CG. Iron deficiency anemia: adverse effects on infant psychomotor development. Pediatrics 1989; 84: 7-17.

20 Lozoff B, Jimenez E, Wolf AW. Long term developmental outcome of infants with iron deficiency. N Engl J Med 1991; 325: 687-94.

21 Roncagliolo M, Garrido M, Walter T, Peirano P, Lozoff B. Evidence of altered CNS development in infants with iron deficiency anaemia at 6 months. Delayed maturation of auditory brainstem responses. Am J Clin Nutr 1998; 68: 683-90.

22 Li YY, Wang HM, Wang WG. The effect of iron deficiency anemia on the auditory brainstem response in infant. Natl Med J China 1994; 74: 367-9.

23 Rudan I, Tomaskovic L, Boschi-Pinto C, Campbell H (on behalf of WHO Child Health Epidomiology Reference Group). Bulletin of the World Health Organization (Print ISSN 0042-9686): Global Estimate of the Incidence of Clinical Pneumonia Among Children Under Five Years of Age. (Cited 30 March 2005.) Available from URL:

24 Ross A. Chapter 9. In: Sommer A, West K, eds. Vitamin A Deficiency: Health, Survival and Vision. New York: Oxford University Press, 1996; 251-73.

25 Li M, Eastman CJ, Waite KV et al. Are Australian children iodine deficient? Results of the Australian National Iodine Nutrition Study. Med J Aust 2006; 184: 165-9.

26 Delange F. The role of iodine in brain development. Proc Nutr Soc 2000; 59: 75-9.

27 Delange F. Optimal iodine nutrition during pregnancy, lactation and the neonatal period. Int J Endocrinol Metab 2004; 2: 1-12.

28 Farquharson J, Cockburn F, Patrick WA, Jamieson EC, Logan RW. Infant cerebral cortex phospholipid fatty-acid composition and diet. Lancet 1992; 340: 810-13.

29 Martinez-Galan JR, Pedraza P, Santacana M, Escobar del ray F, Morreale de Escobar G, Ruiz-Marcos A. Myelin basic protein immunoreactivity in the internal capsule of neoantes from rats on a low iodine intake or methylmercaptoimidiazole (MMI). Brain Res Dev Brain Res 1997; 101: 249-56.

30 Jiang T, Jeter JM, Nelson SE, Ziegker EE. Intestinal blood loss during cow milk feeding in older infants: quantitative measurements. Arch Pediatr Adolesc 2000; 154: 673-8.

31 Baghurst KI, Record SJ, Leppard P. Red meat consumption in Australia: intakes, nutrient contribution and changes over time. Aust J Nutr Diet 2000; 57 (Suppl. 4): S1-36.

32 Harris MF, Cameron B, Florin S. Iron deficiency in Bourke children. Aust Paediatr J 1988; 24: 45-7.

33 Holt AR, Spargo RM, Iveson JB, Faulkner GS, Cheek DB. Serum and plasma zinc, copper and iron concentrations in Aboriginal communities of north Western Australia. Am J Clin Nutr 1980; 33: 119-32.

34 Rangan AM, Blight GD, Binns CW. Factors affecting iron status in 15-30 year old female students. Asia Pac J Clin Nutr 1997; 6: 291-5.

35 Sadler S, Blight G. Iron status and dietary iron intake of young women. Proc Nutr Soc Aust 1996; 20: 216.

36 English RM, Bennett SA. Iron status of Australian children. Med J Aust 1990; 152: 582-6.

37 Wharton B, Wharton P. Nutrition in adolescence nutrition and health. 1987; 4: 195-203. National Health and Medical Research Council 101.

38 Hallberg L, Hoppe M, Andersson M, Hulthen L. The role of meat to improve the critical iron balance during weaning. Pediatrics 2003; 111: 864-70.

This section considers the key stages of growth and development through to ageing, with a consideration of how red meat in the diet may contribute to meeting nutritional needs at these stages. Cleghorn focuses on the role of micronutrients in childhood nutrition and the need to deliver these through diet. Smith and Mann discuss the possibility that diet may affect the severity of acne during adolescence. Nowson outlines the nutritional challenges in meeting nutritional requirements for the elderly and discusses a number of ways forward


Discipline of Paediatrics & Child Health, University of Queensland, Brisbane, Queensland, Australia
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Title Annotation:Section 3: The role of red meat in meeting nutritional challenges during the life stages
Author:Cleghorn, Geoffrey
Publication:Nutrition & Dietetics: The Journal of the Dietitians Association of Australia
Date:Sep 1, 2007
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