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Breastmilk and Vitamin D Adequacy
Breastfeeding in the park assures
adequate vitamin D
Infant feeding interventions for all babies when needed only by a vulnerable few raises some important issues. Risks and benefits need cautious weighing. Long and short-term effects must be monitored and new information must constantly be assessed. Perhaps distrust of the public's capabilities or because a quick fix is easier to control, public education is often ignored as an effective means of achieving optimal health practices. Partiality of a universal public policy must also be critically assessed. Hence the case of vitamin D supplementation remains a controversial recommendation. The recommendation of unqualified vitamin D supplementation (see box) for Canadian infants would imply that all exclusively breastfeeding infants are at risk for developing vitamin D deficiency. Yet on examining the scientific literature on vitamin D only a small minority of infants are noted to be at risk. |
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Reported reviews of the prevalence of Vitamin D deficiency rickets also suggest otherwise. A six-year review4 of all cases at the Calcium and Bone Clinic of the Hospital for Sick Children in Toronto identified 17 cases (from January 1988 to December 1993). Parents had sought medical attention because of bowing of the lower limbs. On examination all the children had radiographic and clinical evidence of rickets. All the children presented were of African or Asian origin consumed no cow's milks were not taken outdoors regularly and if taken outdoors would be covered up. The mothers reported that they did not drink milk or consumed vitamin supplements during pregnancy. Similar findings5 are reported in other reviews. The Children's Hospital of New Jersey and UMD, Newark, reported only nine cases over a three-year period. All children were dark skinned, were breastfed and had restricted exposure to sunlight. The susceptibility to vitamin D deficiency rickets, of dark-skinned infants in populations who have immigrated from tropical climates to cold northern climates has long been recognized. Higher levels of melanin, a natural sun screen, requires more exposed sunlight than white skinned populations to produce the same amount of vitamin D. And in white-skinned infants the application of sunscreen blocks the synthesis of vitamin D after ultraviolet radiation. When infants are then also confined to the indoors throughout cold winters or are fully covered, the possibility of inadequate exposure to ultraviolet light and inadequate maternal storage increase the risk of vitamin D deficiency. |
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When vitamin D's structure and its ability to cure bone disease such as rickets and osteomalacia was first determined in the early 1900s it was classified as a vitamin since small amounts had been found to be present in some foods such as butter. Soon after, however, it was discovered that exposure to ultraviolet light also supplied vitamin D and could heal vitamin D-deficiency bone disease. Since only very few foods contain vitamin D, generally vitamin D status is maintained by exposure to sunlight. Even though intake as a dietary nutrient is not significant, the mistaken classification of an orally ingested "vitamin" persists. Vitamin D or properly termed cholecalciferol, formed in the skin is the precursor to the biologically active form 1,25(OH)2D, a steroid hormone that is synthesized via a number of steps in the liver and the kidney. It is this final form 1,25(OH)2D of "vitamin" D that performs the important calcium utilization function. Also because of its hormonal nature important questions have been raised about additional regulatory functions vitamin D may have. The relationship of vitamin D status to the etiology of heart disease, cancer and other chronic diseases have also been raised in the literature. |
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Infants meet their vitamin D requirements through stored concentrations obtained across the placenta before birth. Breastfeeding makes a small contribution and the majority of an infant's vitamin D requirement is met by exposure to sunlight. The development of deficiency after birth is without fail related to limited exposure to ultraviolet light and generally doesn't manifest itself until after 6 months of age.
Is the prevention of vitamin D deficiency by the means of dietary supplementation rational? Even though this "artificial route" of oral vitamin D has been demonstrated to offset the symptoms of vitamin D deficiency rickets, and the decline of rickets in the population has been attributed to public health measures of milk fortification, the evidence for this is not clear. In the biological realm, no vertebrates maintain their vitamin D status through nutritional sources and thus the important question remains does the long-term ingestion of dietary vitamin D have any deleterious effects? Evidence from animal studies suggests that there may be an association with the development of chronic vascular disease. Fraser6 in his careful review of the subject concludes "for this reason alone it is prudent that vitamin D should be obtained from the environment by careful exposure of the skin to solar ultraviolet light rather than from the artificial source of dietary supplements."
Prolonged exposure to sunlight will cause sunburn but will not produce excess vitamin D, a natural protective mechanism. Vitamin D toxicity is a 20th century disease. It occurs when oral vitamin D is taken for a prolonged period of weeks or months such as in the therapeutic treatment of tuberculosis, rheumatoid arthritis or hypothyroidism. The potent action of orally administered vitamin D can be demonstrated by the fact that it is used as an effective commercial rodenticide, capable of killing rats and mice in 24 to 48 hours7. One proposed mechanism8 of toxicity associated with consumed vitamin D is that the precursor of 25(OH)2D takes up all the binding sites on the vitamin D binding protein, displacing the functional form of the hormone and changing the normal status between receptor sites and 1,25(OH)2D. |
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In response to the controversial recommendation that all breastfed infants be supplemented with oral forms of vitamin D and not just those considered at "risk", we say this is unnecessary. Long term risks of artificial topping up the vitamin D levels for the majority of infants, where no risk and no cases have been reported may in fact do as yet undetermined harm. In its natural and functional form "vitamin" D is a powerful hormone. The artificial ingestion may have subtle and long-term effects as yet unknown. Should we be subjecting newborns to these uncertainties superfluously? References: 2. Mohrbacher, N., Stock, J. The Breastfeeding Answer Book. La Leche League International, revised edition, pp 515, 516, 1997 BACK 3. American Academy of Pediatrics, Breastfeeding and the Use of Human Milk. Pediatr 100:1035-1039, 1997 BACK 4. Binet, A. et al. Persistence of Vitamin D-deficiency Rickets in Toronto in the 1990s. Canadian Journal of Public Health 87:227-230,1996 BACK 5. Sills, I. et al. Vitamin D Deficiency Rickets. Clinical Pediatrics 8:491-493, 1994 BACK 6. Fraser, D.R. Vitamin D. The Lancet 345:104-107, 1995 BACK 7. Greaves, J.H. Some properties of calciferol as a rodenticide. J Hygiene 73:341-351, 1974 BACK 8. Vieth, R. The mechanisms of vitamin D toxicity. Bone and Mineral 11:267-272, 1990 BACK
Also: Specker, B.L. et al. Effect of Race and Diet on Human-Milk Vitamin D and 25 Hydroxyvitamin D. Am J Dis Children. 139:1134-1137,1985 Specker, B.L. et al. Sunshine exposure and serum 25 hydroxyvitamin D concentrations in exclusively breastfed infants. J Pediatr 107:372-376, 1985 Specker, B.L. Cyclical serum 25-hydroxyvitamin D concentrations paralleling sunshine exposure in exclusively breastfed infants. J Pediatr 110:744-747, 1987 |
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