“SUNLIGHT DEFICIENCY AND BREASTFEEDING” by Cynthia Good Mohab MS, IBLC

“SUNLIGHT DEFICIENCY AND BREASTFEEDING” by Cynthia Good Mohab MS, IBLC

from BREASTFEEDING ABSTRACTS, November 2002, Volume 22, Number 1, pp. 3-4.

In the absence of underlying organic causes (e.g., liver or kidney disease, prematurity), vitamin D deficiency is sunlight deficiency. “Vitamin D” is actually a steroid hormone produced in the body from a pro-steroid which is formed upon direct exposure of the skin to ultraviolet B (UVB) radiation in sunlight. Migration, industrialization, urbanization, social inequities, and concern about skin cancer have reduced sunlight exposure for many people globally. Nonetheless, direct, casual exposure of the skin to sunlight is the biologically normal, most common, and most important means of attaining sufficient levels of vitamin D for humans; dietary intake becomes important only with inadequate endogenous production and depletion of body stores. Only a few foods naturally contain significant levels of vitamin D (e.g., the liver and oils of some fatty fish). Without supplementation or enrichment, it would be unusual for people of any age to obtain sufficient vitamin D solely from their diet (1).

The Original Paradigm

The biologically normal sources of vitamin D for nurslings are primarily prenatal stores (for the neonate) and sunlight, with a smaller contribution made by human milk (2,3). Research has shown that without postnatal sunlight exposure, vitamin D stores of fetal origin were depleted by eight weeks in exclusively breastfed infants (Tampere, Finland [61°N] in winter)(2). However, studies in children have shown that only a few hours total of summer sunlight produces enough vitamin D to avoid deficiency for several months (1,4,5). In a study of exclusively breastfed Caucasian infants under six months of age (39°N; Cincinnati, Ohio, USA), 30 minutes/week (diaper only) or 2 hours/week (fully clothed without a hat) of sunlight exposure appeared sufficient to prevent deficiency (5). Exclusively breastfed Caucasian infants exposed to sunlight may not require vitamin D supplementation during the first six months of life, in spite of seasonal variations of UVB exposure, particularly if their mothers had sufficient sunlight exposure or took prenatal vitamins during pregnancy (6,7). Darkly pigmented infants may require three to six times the sunlight exposure of lightly pigmented infants to produce the same amount of vitamin D (8).

When infants and their mothers are exposed to biologically normal amounts of sunlight, human milk must be assumed to contain biologically normal amounts of vitamin D. However, human milk from mothers with vitamin D serum levels currently considered within the normal range for adults provides much less vitamin D than the 200 to 400 IU/day commonly recommended for infants in the first year of life (1). A variety of studies have shown that mature human milk contains approximately 5 to 136 IU/L of fat-soluble vitamin D, depending on how its activity is measured and on maternal vitamin D status (9,10,11). The concentration of vitamin D in human milk increases with higher maternal stores, which depend on sunlight exposure, skin pigmentation, latitude, season, and—in the absence of sufficient UVB exposure—on dietary vitamin D (12). The concentration of vitamin D in human milk increases significantly with what are currently considered pharmacological doses of vitamin D supplements (13,14). Yet administration of 1,000 IU to lactating mothers (Tampere, Finland [61°N] in winter) did not normalize the 25-hydroxyvitamin D levels of their infants (15). Breastfed infants require sufficient sunlight exposure or supplementation to avoid vitamin D deficiency.

Prevalence of Rickets

Vitamin D deficiency in childhood can cause rickets whose signs and symptoms include bone deformities and fractures, muscle weakness, developmental delays, short stature, failure to thrive, respiratory distress, tetany, and heart failure (16). The effects of subclinical rickets are unknown. Vitamin D deficiency in the first few months after birth is relatively rare, but has occurred congenitally in infants of mothers who were severely vitamin D deficient during pregnancy (17,18). Overt rickets appears more frequently in children 6 to 36 months of age than in infants under 6 months and its clinical presentation varies with age of onset (16).

Rickets was epidemic in the industrialized cities of North America and northern Europe at the turn of the 20th century. By the 1960s, it had been virtually eliminated in most developed countries through the use of vitamin D supplementation and cow’s milk fortification. Rickets remains a serious health problem in some developing countries (e.g., 40.7 percent of children in China; 23 percent of children in the Ulas Health Centre Region of Turkey (19, 20,21,22)). Due to the convergence of a variety of risk factors, it is actually most common in those regions of the world where sunlight is plentiful (e.g., the Indian subcontinent, Egypt, Ethiopia, Libya, Morocco, Tunisia (23,24,25,26)). Since the 1970s vitamin D deficiency rickets in breastfed infants has been documented among at-risk populations in North America, northern Europe, and former Soviet countries (16).

Many factors (e.g., genetic, hormonal, nutritional, cultural) interact to cause rickets in susceptible children. Maternal vitamin D deficiency during pregnancy, which is often asymptomatic, results in insufficiently developed fetal stores of vitamin D (17,18). Environmental risk factors for vitamin D deficiency in the breastfed infant interact with each other and overlap significantly with those of maternal deficiency. These include: indoor confinement during daylight hours; living at high latitudes; living in urban areas with buildings and/or pollution that block sunlight; darker skin pigmentation; sunscreen use; seasonal variations; covering much or all of the body when outside (e.g., due to cold climate, custom, fear of skin cancer); increased birth order; exposure to lead (27), and the replacement of human milk with foods low in calcium or foods that reduce calcium absorption. In the presence of these risk factors, other risk factors include not consuming vitamin D fortified cow’s milk, other vitamin D fortified foods, or vitamin D supplements.

Complexity and Controversy

There is no global consensus on whether or how to screen infants, children, or pregnant women for vitamin D deficiency or on how to best prevent vitamin D deficiency in breastfed infants and children. Recommendations for preventing vitamin D deficiency in breastfed infants include universal supplementation, supplementation of at-risk breastfed infants, and habitual small doses of sunshine; some regions with plentiful sunshine have not yet developed recommendations (28,29,30,31,32). Recommendations for supplementation of at-risk infants can be difficult to interpret and apply (e.g., the difficulty of defining “dark skin”). The exact assessment of UVB exposure is difficult. Research showing a relationship between sun exposure and an increased risk of skin cancer has led some agencies to recommend avoidance of all sunlight exposure. The determination of the exact amount of regular, brief, and nonerythemal sunlight exposure needed just to produce sufficient vitamin D in specific infants and children depends on many factors.

There are no known risks of orally supplementing infants and children with 200 to 400 IU/day. Vitamin D supplementation and fortification have been used in many countries for decades. However, that does not mean that supplementation is not problematic or without risk. The prevention of vitamin D deficiency through the routine supplementation of all breastfed infants under six months of age may be seen by some as evidence that breastfeeding is inadequate. However, continued reports of rickets among exclusively breastfed babies may also undermine efforts to increase breastfeeding initiation rates and rates of exclusive breastfeeding. Many questions related to vitamin D supplementation in breastfed infants remain unasked—and unanswered—in the scientific literature:

• Does vitamin D supplementation have any deleterious physiologic effects on the infant?
• How does vitamin D supplementation of breastfed infants at various dosages, ages, and latitudes affect the prevalence of vitamin D deficiency rickets among at-risk infants?
• Does a universal recommendation of vitamin D supplementation affect breastfeeding beliefs and behavior (e.g., use of other supplements, premature introduction of other foods, weaning)?
• How does direct sun exposure that is no greater than that needed to produce sufficient vitamin D in the breastfed infant affect the infant’s lifetime risk of skin cancer?
• What means of preventing maternal vitamin D deficiency would be most effective in reducing the risk of early vitamin D deficiency in infants?

Given the varying incidences, combinations of risk factors for vitamin D deficiency, cultural practices, and financial resources that occur across the globe, one uniform recommendation for prevention is unlikely to successfully meet the needs of infants living in different areas of the world. International organizations like La Leche League International and UNICEF acknowledge that vitamin D supplementation is necessary when sunlight exposure is inadequate and that some infants have a higher risk of vitamin D deficiency than others(32,33). Research on this complex, global, controversial, and interdisciplinary issue is incomplete and must be expanded.

Cynthia Good Mojab is Research Associate in the Publications Department of La Leche League International and Senior Editor at Platypus Media. She is an independent researcher, author, and speaker in the areas of psychology, culture, and the family, particularly in relation to breastfeeding.

REFERENCES

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2. Ala-Houhala, M. 25-Hydroxyvitamin D levels during breast-feeding with or without maternal or infantile supplementation of vitamin D. J Pediatr Gastroenterol Nutr 1985:4(2):220-26.

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6 . Greer, F. and S. Marshall. Bone mineral content, serum vitamin D metabolite concentrations, and ultraviolet B light exposure in infants fed human milk with and without vitamin D2 supplements. J Pediatr 1989; 114:204-12.

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8. Lo, C., P. Paris, and M. Holick. Indian and Pakistani immigrants have the same capacity as Caucasians to produce vitamin D in response to ultraviolet radiation. Am J Clin Nutr 1986; 44:683-85.

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14. Hollis, B., F. Greer, and R. Tsang. The effects of oral vitamin D supplementation and ultraviolet phototherapy on the antirachitic sterol content of human milk. Calcif Tissue Int (Suppl) 1982; 34:582.

15. Ala-Houhala, M. et al. Maternal compared with infant vitamin D supplementation. Arch Dis Child 1986; 61:1159-63.

16. Garabédian, M. and H. Ben-Mekhbi. Rickets and vitamin D deficiency. In Vitamin D: Physiology, Molecular Biology, and Clinical Applications ed. M. Holick. Humana Press: Totawa, NJ, 1999, 273-86.

17. Pal, B. and N. Shaw. Letters: Rickets resurgence in the United Kingdom: Improving antenatal management in Asians. J Pediatr 2001; 139(2):337-38.

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19. Özgür, S., H. Sümer, and G. Koçglu. Rickets and soil strontium. Arch Dis Child 1996; 75:524-26.

20. Ma, X. Epidemiology of rickets in China. J Pract Pediatr 1986; 1:323.

21. Rafii, M. Rickets in breast-fed infants below six months of age without vitamin D supplementation. Arch Irn Med 2001; 4(2):93-95.

22. Thacher, T., P. Fisher, J. Pettifor et al. A comparison of calcium, vitamin D, or both for nutritional rickets in Nigerian children. New Engl J Med 1999; 341(8)563-68.

23. Raghuramulu, N. and V. Reddy. Serum 25-hydroxyvitamin D levels in malnourished children with rickets. Arch Dis Child 1980; 55:285-87.

24. Lawson, D.E.M., T. J. Cole, S. I. Salem et al. Aetiology of rickets in Egyptian children. Hum Nutr Clin Nutr 1987; 41C:199-208.

25. Hojer, B., M. Gebre-Medhin, G. Sterky et al. Combined vitamin D deficiency rickets and protein energy malnutrition in Ethiopian infants. J Trop Pediatr 1977; 23:73-79.

26. Joint FAO/WHO Expert Committee on Nutrition. Seventh Report. Rickets. Rome: FAO, 1967, 31-34.

27. Metropolitan Toronto Teach Health Units and the South Riverdale Community Health Centre. Why Barns Are Red: Health Risks from Lead and Their Prevention. A Resouce Manual to Promote Public Awareness. Toronto, Ontario, 1995.

28. American Academy of Pediatrics Committee on Nutrition. Pediatric Nutrition Handbook. 4th ed. Elk Grove Village, IL: American Academy of Pediatrics, 1998, 275-76.

29. American Academy of Pediatrics. Breastfeeding and the use of human milk. Pediatrics 1997; 100(6):1035-39.

30. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary Reference Intakes for Calcium, Phosphorous, Magnesium, Vitamin D, and Fluoride. Washington, DC: National Academy Press, 1997, 264-66.

31. Vitamin D Expert Panel Meeting. October 11-12, 2001, Atlanta, Georgia. Final Report. url: http://www.cdc.gov/nccdphp/dnpa/nutrition/pdf/ Vitamin_D_Expert_Panel_Meeting.pdf

32. UNICEF. Vitamin D: Rickets in children and osteomalacia in pregnant women. In The Prescriber: Guidelines on the Rational Use of Drugs in Basic Health Services. December 1993; 8:11.

33. Mohrbacher, N. and J. Stock. THE BREASTFEEDING ANSWER BOOK (2d rev. ed., in press). Schaumburg, IL: La Leche League International, 606-7.

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