Sunlight Deficiency: A Review of the Literature

Cynthia Good Mojab
Issue 117, March/April 2003

Woman breastfeedingMaking informed decisions about complex and controversial health issues, such as vitamin D supplementation of breastfed infants, is inherently challenging. When evaluating information, mothers may wish to consider the goals, potential biases, and sources of funding of health organizations, researchers, healthcare providers, and vitamin manufacturers; the depth, breadth, and limitations of the information on which public health policies are based; whether a recommendation might be out of date or applicable in only some situations; whether any conflicts of interest might be involved; and whether the organization or individual making the recommendation is in full compliance with the letter-and spirit-of the WHO/UNICEF International Code of Marketing of Breast-Milk Substitutes. 1, 2 A review of the related scientific literature, though essential, is just the beginning.

What Is Vitamin D?
Vitamin D is actually not a vitamin at all, but a steroid hormone produced in the body after direct exposure of the skin to ultraviolet B (UVB) radiation in sunlight. Vitamin D plays a critical role in the maintenance of proper blood calcium and phosphorous concentrations, and in bone mineralization by stimulating the absorption of calcium and phosphorous in the small intestine. It also acts as a chemical messenger in a wide variety of other biological responses.3

What Is Vitamin D Deficiency and What Are Its Consequences? In the absence of underlying organic causes, such as prematurity or liver or kidney disease, vitamin D deficiency is sunlight deficiency. Vitamin D deficiency can lead to bone disease: osteomalacia in adults, rickets in infants and children. Research has shown that higher latitude and lower vitamin D levels are related to several cancers, type 1 diabetes, and other diseases.4-6

How Do People Get Enough Vitamin D?
The direct, casual exposure of skin to sunlight is the most common and the biologically normal way that human beings attain sufficient levels of vitamin D. However, sunlight exposure for many people around the world has been reduced by industrialization, urbanization, migration, concern about skin cancer, and social inequities. Because only a few foods naturally contain significant levels of vitamin D (e.g., the oils and livers of some fatty fish), it would be unusual for people to obtain adequate vitamin D from their diet alone without supplementation or enrichment.7

The skin has a large capacity to produce vitamin D. Exposure of the entire adult body to the smallest amount of UVB radiation that produces transient, just perceptible skin reddening is comparable to taking an oral dose of 10,000 to 25,000 IU of vitamin D.8, 9 Therefore, sufficient levels of vitamin D can be developed from partial exposure of the body to sunlight well before sunburn occurs.

Levels of vitamin D vary seasonally among people exposed to sunlight at higher latitudes, where UVB radiation is higher in the summer and lower in the winter.10, 11 With inadequate summer exposure, vitamin D deficiency and insufficiency can result, particularly during the winter.12, 13 However, with adequate exposure to sunlight in the summer, vitamin D can be stored in the body for winter use.14 The lower vitamin D stores of the spring can be replenished with exposure to the higher UVB radiation of summer sunlight.

How Do Nurslings Get Enough Vitamin D?
The natural sources of vitamin D for nurslings are primarily the stores they developed prenatally (for newborns) and the vitamin D they produce with exposure of their skin to sunlight; a smaller additional contribution is from human milk.15, 16 The concentration of fat-soluble vitamin D in human milk varies from 5 to 136 IU/L, depending on how its activity is measured and on maternal vitamin D status during lactation.17-19 This concentration provides less than the 200 to 400 IU/day commonly recommended for infants under one year of age.20 However, human milk should not be considered “deficient” in vitamin D, because the biologically normal means of obtaining sufficient vitamin D in humans is via sunlight exposure, not diet.21-23

The neonate’s stores of vitamin D depend on maternal vitamin D status during pregnancy.24, 25 A study of exclusively breastfed infants in Tampere, Finland (61° N) in winter showed that, without UVB exposure or vitamin D supplementation, vitamin D stores of fetal origin were depleted by eight weeks of age.26 Although these vitamin D-depleted infants had serum levels of vitamin D at which rickets can occur, none had active or biochemical rickets. The concentration of vitamin D in human milk increases significantly with what are currently considered pharmacological doses of vitamin D supplements.27, 28 Administration of 2,000 IU-but not 1,000 IU-to lactating mothers in another study normalized the 25-hydroxyvitamin D levels of their infants in winter.29 Supplementation with over 1,000 IU/d is currently considered to greatly exceed normal maternal vitamin D needs (200 IU/d).30

Studies have shown that children can store enough vitamin D to avoid deficiency for several months when they are exposed to only a few hours of summer sunlight.31-33 Exclusively breastfed Caucasian infants under six months of age (39° N; Cincinnati, Ohio, US) are expected to achieve adequate vitamin D status when exposed to sunlight for 30 minutes per week (diaper only) or two hours per week (fully clothed without a hat). 34 The sunlight exposure needed by darkly pigmented infants is poorly understood.35 Studies of the influence of skin pigmentation on the cutaneous production of vitamin D in adults have shown conflicting results.36, 37 However, a study by Brazerol and colleagues showed that darkly and lightly pigmented adults were equally capable of producing vitamin D when episodes of UVB exposure occurred periodically over time (i.e., biweekly for six weeks in their study).38

Who Is at Risk for Vitamin D Deficiency?
Anyone with inadequate exposure to UVB radiation in sunlight is at risk for vitamin D deficiency. Risk factors for nurslings and their mothers overlap and interact, and include indoor confinement during the day (e.g., due to exclusively indoor daycare, unsafe neighborhoods, custom),39 living at higher latitudes (e.g., essentially no vitamin D is produced with sun exposure from November to February in Boston [42° N] and from mid-October to mid-April in Edmonton, Canada [52º N]),40, 41 darker skin pigmentation,42-45 living in urban areas with pollution and/or buildings that block sunlight,46-48 sunscreen use,49-51 seasonal variations resulting in less ultraviolet radiation (e.g., late winter and early spring in the northern hemisphere),52, 53 covering much or all of the body when outside (e.g., due to custom, fear of skin cancer, cold climate),54-57 increased birth order (e.g., a mother’s sixth child has a higher risk of vitamin D deficiency than does her first child),58, 59 the replacement of human milk with foods low in calcium,60-64 the replacement of human milk with foods that reduce calcium absorption (e.g., grains and some green leaves containing phylates, oxalates, tannates, and phosphates; cereals grown in soil high in strontium),65-67 and exposure to lead (due to lead’s inhibition of vitamin D synthesis).68, 69

What Is Rickets?
Vitamin D-deficiency rickets is a disease of childhood caused by lack of sunlight exposure. Rickets can also be caused by calcium deficiency and underlying disease. The symptoms of rickets vary with age of onset and include bone deformities and fractures, muscle weakness, developmental delays, short stature, failure to thrive, respiratory distress, tetany, and, rarely, heart failure.70 Rickets that develops in breastfed infants during the first six months of life is likely to be related to maternal vitamin D and/or calcium deficiency during pregnancy, which is often asymptomatic.71, 72 Among younger infants, rickets has been reported among formula-fed infants and breastfed infants receiving vitamin D supplementation.73 In that report, no correlation was found between season of birth, breast- or formula feeding, or routine vitamin D supplementation, suggesting that maternal vitamin D status was the direct cause of rickets in that population (i.e., Asian infants living in the United Kingdom).74 In a study of African children older than six months, vitamin D deficiency appeared unlikely to be the primary cause of rickets; insufficient dietary calcium probably interacted with genetic, hormonal, and other nutritional factors to cause rickets in susceptible children.75 Many children affected by early childhood rickets come from poor socioeconomic conditions and sometimes show signs of general malnutrition.76

How Common Is Rickets in Nurslings?
There are currently no national data on the prevalence of rickets in the US,77 though case reports and descriptive studies clearly indicate that rickets is not a disease of the past. At the start of the 20th century, rickets was epidemic in industrialized cities of northern Europe and North America. Through the use of vitamin D supplementation and the fortification of cow’s milk, it was virtually eliminated in most developed countries by the 1960s. Rickets in breastfed infants has been documented among at-risk populations in northern Europe, North America, and former Soviet countries since the 1970s.78 In some developing countries it remains a serious health problem.79-82 Overt rickets is more common in children 6 to 36 months of age than in infants under 6 months of age.83-86 Findings of bone deformities suggestive of rickets are very rare in full-term or premature neonates.87

What are Current Recommendations for Preventing Vitamin D Deficiency in Nurslings?
Public health policies regarding vitamin D supplementation vary globally, reflecting different incidences of and risk factors for vitamin D deficiency, cultural practices, and financial resources.88 No global consensus exists on whether or how to screen nurslings or mothers for vitamin D deficiency or on how to prevent vitamin D deficiency among nurslings. Recommendations for prevention vary, from supplementing all breastfed infants (universal supplementation) to supplementing only at-risk infants (conditional supplementation) to exposing infants to regular small doses of sunshine. (See sidebar, “Recommendations Around the World.”)

The American Academy of Pediatrics’ policy on vitamin D supplementation for breastfed infants has been in development and discussion for two years.89 It is now before the AAP Board of Directors for consideration. If approved, it will become official AAP policy once it is published in the journal Pediatrics. In Breastfeeding and the Use of Human Milk, the AAP currently states that vitamin D may be needed for infants younger than six months whose mothers are vitamin D-deficient or for infants who are not exposed to adequate sunlight.90 However, it seems likely that the AAP will soon recommend universal supplementation for breastfed infants beginning sometime during the first six months of life.91, 92

Some policy makers, researchers, healthcare providers, and mothers in Western or Westernized countries may prefer vitamin D supplementation of all breastfed infants (rather than vitamin D supplementation of only those infants at risk of vitamin D deficiency), in part, because of culturally based discomfort with processes-such as UVB exposure-that are natural, irregular, and not easily measured.93-96 Whether recommendations are universal or conditional, breastfeeding mothers have the right to talk with their healthcare providers about their and their nurslings’ specific risks of vitamin D deficiency and about whether conducting blood tests to determine their and their children’s actual vitamin D status would be appropriate.

Are there Any Risks of Vitamin D Supplementation?
Prophylactic vitamin D supplementation is demonstrably useful for infants at risk of vitamin D deficiency. No known risks of supplementation exist with 200 to 400 IU/day. Supplementation and fortification with vitamin D has been used for decades in many countries. According to the Canadian Department of National Health and Welfare, “It seems probable that the widely accepted figure of 10 µg (400 IU) per day considerably exceeds the true requirements of the great majority of infants, but that amount can be recommended as an effective and safe prophylactic level of intake from all sources.”97 Vitamin D intoxication can occur with excessive intake of dietary vitamin D (i.e., more than 40,000 IU/day for many months in normal adults), but not with endogenous production via sun exposure.98

Many potential risks of vitamin D supplementation, however, have not been investigated. No one knows whether vitamin D supplementation has any deleterious physiological effects on the infant, such as aspiration when supplementation is not tolerated, harmful alterations of the infant gut, or increased rates of infection.99 When studies of health outcomes based on infant feeding routinely fail to define “exclusive breastfeeding” clearly and consistently or even to include truly exclusive breastfeeding (nothing other than human milk fed to the infant directly from the mother’s breasts), it is impossible to know the full effects of vitamin D or other supplementation on infant health and development.100, 101 When studies have differentiated between health outcomes for exclusively and partially breastfed babies, significant differences between the two groups have been shown. For example, in a study by Coutsoudis and colleagues, partially breastfed infants of HIV-positive mothers had a greater risk of becoming HIV-positive than exclusively breastfed infants (who had a risk similar to never-breastfed infants).102

In addition, the effects of universal recommendation of vitamin D supplementation on breastfeeding beliefs and behaviors (e.g., use of other supplements, premature introduction of other foods, weaning) have not been studied. No one knows how vitamin D supplementation affects the likelihood of other types of supplementation. Some breastfeeding mothers may see no difference between the feeding of a vitamin D supplement and the feeding of a small amount of another liquid or food. Some breastfeeding mothers may see universal supplementation as evidence that breastfeeding is inadequate. The importance of exclusive breastfeeding in the first six months of life, however, is well supported.103 If mothers-or other caregivers-see no difference between vitamin drops and other supplementation or believe that human milk is inadequate because supplements are recommended for all breastfed infants, then recommendations of universal vitamin D supplementation could indirectly serve to increase the risk of illness and disease for many infants, including those not at risk for vitamin D deficiency.

Disturbingly, vitamin D supplements are produced by formula manufacturers in some countries (e.g., D-Vi-Sol by Mead Johnson in Canada). Formula manufacturers commonly violate the International Code of Marketing of Breast-Milk Substitutes by engaging in unethical marketing practices, such as advertising formula directly to the general public.104 Mead Johnson’s marketing of D-Vi-Sol includes advertising of its formula.105, 106 Formula advertising has been shown to decrease the duration and exclusivity of breastfeeding.107 Therefore, in countries with no legislation enforcing the Code, such as the US, and in which formula companies manufacture vitamin supplements, a universal recommendation of vitamin D supplements for breastfed infants will result in the routine exposure of large numbers of breastfeeding mothers to formula advertising-with a concomitant increased risk of additional supplementation, premature weaning, and deleterious health consequences for infants and mothers.

Are there Any Risks of Producing Vitamin D via Sun Exposure?
Chronic, excessive sun exposure is strongly associated with a marked increase in the incidence of skin cancer in fair-skinned populations worldwide, as well as with the development of cataracts regardless of skin pigmentation.108 Skin cancer is the most common form of cancer in the US.109 More than a million cases of basal- and squamous-cell skin cancer and more than 53,000 cases of malignant melanoma are diagnosed in the US each year.110 Malignant melanoma occurs ten times more frequently in Caucasians than in African Americans.111 Risk factors for skin cancer include fair to light skin complexion, a family and/or personal history of skin cancer, chronic exposure to the sun, a history of sunburns during childhood, atypical moles, a large number of moles, and freckles (an indicator of sun sensitivity and sun damage).112 No research exists examining the relationship between the risk of skin cancer and a lifetime of minimal levels of sun exposure just sufficient for the endogenous production of adequate levels of vitamin D. Therefore, there currently is no evidence that such levels of sun exposure increase the lifetime risk of skin cancer.

The American Academy of Pediatrics recommends that infants under six months of age be kept out of direct sunlight.113 However, the Global Solar UV Index: A Practical Guide, a joint recommendation of the World Health Organization, World Meteorological Organization, United Environment Programme, and International Commission on Non-Ionizing Radiation Protection, states: “Small amounts of UV radiation are beneficial for people and essential in the production of vitamin D.”114 According to UNICEF, cases of vitamin D deficiency that occur outside of temperate regions with weak sunlight “are the result of the overprotection of certain individuals from the sun. “The best prevention is to change these habits, and health professionals must insist on the need to be in sunlight.”115

What is the Greater Context of Sunlight Deficiency?
The many social causes and health consequences of sunlight deficiency cannot be fully ameliorated through vitamin D supplementation. While supplements are an invaluable tool for preventing rickets in at-risk infants, they do not, for example, protect nurslings from other negative effects that poverty, pollution, unsafe neighborhoods, and crowded inner cities have on the health and development of all infants living in those contexts. Nor do they prevent the negative health consequences of inadequate sunlight on mental health (e.g., seasonal onset and remission of depressive episodes) and women’s reproductive systems (e.g., irregularities of the menstrual cycle and premenstrual syndrome).116-118

When rickets occurs in breastfed infants, it indicates that something is very wrong with the context in which breastfeeding is happening, not with breastfeeding itself. Social and environmental problems in that context warrant assessment, further research, and amelioration. Breastfeeding is the foundation of normal health and development, the original paradigm for nourishing and nurturing young human beings. Health policies and healthcare systems must first and foremost protect breastfeeding. Otherwise, they will ultimately serve to undermine the health they seek to enhance.

NOTES
1. C. Good Mojab, “Breastfeeding Resource List,” in Breastfeeding Annual International 2001, D. Michels, ed. (Washington, DC: Platypus Media, 2001), 202-203.
2. International Code of Marketing of Breast-Milk Substitutes (Geneva, Switzerland: World Health Organization, 1981).
3. M. Holick, “Noncalcemic Actions of 1,25-Dihydroxyvitamin D3 and Clinical Applications,” Bone 17, no. 2 (suppl.) (1995): 107S-111S.
4. M. Holick, “Sunlight ‘D’ilemma: Risk of Skin Cancer or Bone Disease and Muscle Weakness,” Lancet 357 (2001): 4-6.
5. E. Hyppönen et al., “Intake of Vitamin D and Risk of Type 1 Diabetes: A Birth-Cohort Study,” Lancet 358, no. 9292 (2001): 1500-1503.
6. M. Holick, “Evolution, Biological Functions, and Recommended Dietary Allowance for Vitamin D,” in Vitamin D: Physiology, Molecular Biology, and Clinical Applications, M. Holick, ed. (Totawa, NJ: Humana Press, 1999), 1-16.
7. Ibid.
8. M. Holick, “Environmental Factors that Influence the Cutaneous Production of Vitamin D,” Am J Clin Nutr 61 (suppl.) (1995): 638S-645S.
9. W. Brazerol et al., “Serial Ultraviolet B Exposure and Serum 25 Hydroxyvitamin D Response in Young Adult American Blacks and Whites: No Racial Difference,” J Am Coll Nutr 7, no. 2 (1988): 111-118.
10. A. Webb et al., “Influence of Season and Latitude on the Cutaneous Synthesis of Vitamin D3: Exposure to Winter Sunlight in Boston and Edmonton will not Promote Vitamin D3 Synthesis in Human Skin,” J Clin Endocrinol Metab 67 (1988): 373-378.
11. M. McKenna, “Differences in Vitamin D Status between Countries in Young Adults and the Elderly,” Am J Med 93 (1992): 69-77.
12. D. Rucker et al., “Vitamin D Insufficiency in a Population of Healthy Western Canadians,” Can Med Assoc J 166, no. 12 (2002): 1517-1524.
13. V. Tangpricha et al., “Vitamin D Insufficiency among Free-Living Healthy Young Adults,” Am J Med 112 (2002): 659-662.
14. M. Holick, “Vitamin D and Bone Health,” J Nutr 126 (1996): 1159S-1164S.
15. H. Makin et al., “Vitamin D and Its Metabolites in Human Breast Milk,” Arch Dis Child 58 (1983): 750-753.
16. M. Ala-Houhala, “25-Hydroxyvitain D Levels during Breast-Feeding with or without Maternal or Infantile Supplementation of Vitamin D,” J Pediatr Gastroent Nutr 4, no. 2 (1985): 220-226.
17. B. Specker et al., “Effect of Race and Normal Maternal Diet on Breast Milk Vitamin D Concentrations,” Pediatr Res 18 (1984): 213A.
18. B. Hollis et al., “Vitamin D and Its Metabolites in Human and Bovine Milk,” J Nutr 111, no. 7 (1981): 1240-1248.
19. N. Butte et al., Nutrient Adequacy of Exclusive Breastfeeding for the Term Infant during the First Six Months of Life (Geneva: World Health Organization, 2002), 27.
20. See Note 6.
21. See Note 6.
22. See Note 15.
23. See Note 16.
24. B. Pal and N. Shaw, “Rickets Resurgence in the United Kingdom: Improving Antenatal Management in Asians,” J Pediatr 139, no. 2 (2001): 337-338.
25. J. Daaboul et al., “Vitamin D Deficiency in Pregnant and Breast-Feeding Women and Their Infants,” J Perinatol 1997; 17: 10-14.
26. See Note 16.
27. F. Greer et al., “Effects of Maternal Ultraviolet B Irradiation on the Vitamin D Content of Human Milk,” J Pediatr 105, no. 3 (1984): 431-422.
28. B. Hollis et al., “The Effects of Oral Vitamin D Supplementation and Ultraviolet Phototherapy on the Antirachitic Sterol Content of Human Milk,” Calcif Tissue Int 34 (suppl.) (1982): 582.
29. M. Ala-Houhala et al., “Maternal Compared with Infant Vitamin D Supplementation,” Arch Dis Child 61 (1986): 1159-1163.
30. See Note 6.
31. See Note 6.
32. E. Poskitt et al., “Diet, Sunlight, and 25-Hydroxyvitamin D in Healthy Children and Adults,” Br Med J 1 (1979): 221-223.
33. B. Specker et al., “Sunshine Exposure and Serum 25-Hydroxyvitamin D Concentrations in Exclusively Breastfed Infants,” J Pediatr 107 (1985): 372-376.
34. Ibid.
35. See Note 33.
36. C. Lo et al., “Indian and Pakistani Immigrants Have the Same Capacity as Caucasians to Produce Vitamin D in Response to Ultraviolet Radiation,” Am J Clin Nutr 44 (1986): 683-685.
37. T. Clemens et al., “Increased Skin Pigment Reduces the Capacity of the Skin to Synthesize Vitamin D,” Lancet 1 (1982): 74-76.
38. See Note 9.
39. See Note 33.
40. See Note 8.
41. A. Webb et al., “Influence of Season and Latitude on the Cutaneous Synthesis of Vitamin D3: Exposure to Winter Sunlight in Boston and Edmonton Will Not Promote Vitamin D3 Synthesis in Human Skin,” J. Clin Endocrinol Metab 67 (1988): 373-378.
42. S. Grover and R. Morley, “Vitamin D Deficiency in Veiled or Dark-Skinned Pregnant Women,” MJA 175 (2001): 251-252.
43. K. Feldman et al., “Nutritional Rickets,” Am Fam Physician 42 (1990): 1311-1318.
44. I. Sills et al., “Vitamin D Deficiency Rickets: Reports of Its Demise Are Exaggerated,” Clin Pediatr 33 (1994): 491-493.
45. M. Pugliese et al., “Nutritional Rickets in Suburbia,” J Amer College Nutr 17, no. 6 (1998): 637-641.
46. See Note 8.
47. See Note 43.
48. See Note 44.
49. See Note 6.
50. L. Matsuoka et al., “Sunscreens Suppress Cutaneous Vitamin D3 Synthesis,” J Clin Endocrinol Metab 64, no. 6 (1987): 1165-1168.
51. L. Matsuoka et al., “Chronic Sunscreen Use Decreases Circulating Concentrations of 25-Hydroxyvitamin D,” Arch Dermatol 124, no. 12 (1988): 1802-1804.
52. See Note 8.
53. See Note 41.
54. See Note 42.
55. See Note 43.
56. See Note 44.
57. See Note 45.
58. See Note 45.
59. L. Muhe et al., “Case-Control Study of the Role of Nutritional Rickets in the Risk of Developing Pneumonia in Ethiopian Children,” Lancet 349 (1997): 1801-1804.
60. See Note 43.
61. See Note 44.
62. See Note 59.
63. T. Thacher et al., “A Comparison of Calcium, Vitamin D, or Both for Nutritional Rickets in Nigerian Children,” New Engl J Med 341, no. 8 (1999): 563-568.
64. N. Carvalho et al., “Severe Nutritional Deficiencies in Toddlers Resulting from Health Food Milk Alternatives,” Pediatrics 107, no. 4 (2001): E46.
65. See Note 63.
66. I. Robertson et al., “The Role of Cereals in the Etiology of Nutritional Rickets: The Lesson of the Irish National Nutrition Survey 1943-8,” Br J Nutr 48 (1981): 17-22.
67. S. Özgür et al., “Rickets and Soil Strontium,” Arch Dis Child 75 (1996): 524-526.
68. Why Barns Are Red: Health Risks from Lead and Their Prevention (Toronto, Ontario: Metropolitan Toronto Teach Health Units and the South Riverdale Community Health Center, 1995).
69. M. Berglund et al., “Metal-Bone Interactions,” Toxicol Lett 112-113 (2000): 219-225.
70. M. Garabédian and H. Ben-Mekhbi, “Rickets and Vitamin D Deficiency,” in Vitamin D: Physiology, Molecular Biology, and Clinical Applications, M. Holick, ed. (Totawa, NJ: Humana Press, 1999), 273-286.
71. See Note 24.
72. See Note 63.
73. See Note 24.
74. See Note 24.
75. See Note 63.
76. D. Fraser, “The Physiological Economy of Vitamin D,” Lancet 1 (1983): 969-972.
77. K. Scanlon, ed., Final Report, Vitamin D Expert Panel Meeting, Atlanta, GA, Oct. 11-12, 2001; see www.cdc.gov/nccdphp/dnpa/nutrition/pdf/Vitamin_D_Expert_Panel_Meeting.pdf
78. See Note 70.
79. See Note 63.
80. See Note 67.
81. X. Ma, “Epidemiology of Rickets in China,” J Pract Pediatr 1 (1986): 323.
82. M. Rafii, “Rickets in Breast-Fed Infants below Six Months of Age without Vitamin D Supplementation,” Arch Irn Med 4, no. 2 (2001): 93-95.
83. See Note 70.
84. See Note 43.
85. See Note 44.
86. See Note 45.
87. See Note 70.
88. C. Good Mojab, “Sunlight Deficiency and Breastfeeding,” Breastfeeding Abstracts 22, no. 1 (2002): 3-4.
89. Lawrence M. Gartner, MD, FAAP, Chairperson, American Academy of Pediatrics Section on Breastfeeding, personal communication, December 6, 2002.
90. American Academy of Pediatrics, “Breastfeeding and the Use of Human Milk,” Pediatrics 100, no. 6 (1997): 1035-1039.
91. See Note 77.
92. M. Elias, “Breast-Fed Babies May Need Extra Vitamin D: Doctors Seeing More Cases of Bone Disease,” USA Today, October 21, 2002; see www.USAToday.com/USAtonline/20021021/4550577s.htm
93. C. Good Mojab, “The Cultural Art of Breastfeeding,” Leaven 36, no. 5 (2000): 87-91.
94. R. Dana, Multicultural Assessment Perspectives for Professional Psychology (Needham Heights, MA: Allyn & Bacon, 1993).
95. F. Kluckholn and F. Strodtbeck, Variations in Value Orientations (Homewood, IL: Dorsey, 1961).
96. H. Triandis, Culture and Social Behavior (New York: McGraw-Hill, 1994).
97. Bureau of Nutritional Sciences, Department of National Health and Welfare, Recommended Nutrient Intakes for Canadians (Ottawa: Health and Welfare Canada, 1983).
98. R. Vieth, “Vitamin D Supplementation, 25-Hydroxyvitamin D Concentrations, and Safety,” Am J Clin Nutr 69, no. 5 (1999): 842-856.
99. See Note 77.
100. M. Labbok, “What is the Definition of Breastfeeding?” Breastfeeding Abstracts 19, no. 3 (2000): 19-21.
101. M. S. Kramer and R. Kakuma, “Optimal Duration of Exclusive Breastfeeding (Cochrane Review),” in The Cochrane Library, no. 4, 2002 (Oxford: Update Software).
102. A. Coutsoudis et al., “Method of Feeding and Transmission of HIV-1 from Mothers to Children by 15 Months of Age: Prospective Cohort Study from Durban, South Africa,” AIDS 15, no. 3 (2001): 379-387.
103. See Note 101.
104. See Note 2.105. See Note 77.
106. Mead Johnson Canada Website Information on D-Vi-Sol, www.meadjohnson.ca/i1/Divisol.htm
107. C. Howard et al., “Office Prenatal Formula Advertising and Its Effects on Breastfeeding Patterns,” Obstetric Gynecology 95, no. 2 (2000): 296-303.
108. Global Solar UV Index: A Practical Guide (Geneva, Switzerland: World Health Organization, 2002).
109. Skin Cancer: Preventing America’s Most Common Cancer (Atlanta, GA: Centers for Disease Control 2001); see www.cdc.gov/Cancer/Nscpep/Skinpdfs/Sknaag01.pdf
110. Cancer Facts and Figures 2002 (Atlanta, GA: American Cancer Society, 2002); see www.cancer.org/Downloads/STT/Cancerfacts&Figures2002TM.pdf
111. Ibid.
112. See Note 109.
113. American Academy of Pediatrics, “Ultraviolet Light: A Hazard to Children (RE9913),” Pediatrics 104, no. 2 (1999): 328-333.
114. See Note 108.
115. UNICEF, “Vitamin D: Rickets in Children and Osteomalacia in Pregnant Women,” The Prescriber: Guidelines on the Rational Use of Drugs in Basic Health Services 8 (Dec. 1993): 11.
116. M. Rao et al., “The Influence of Phototherapy on Serotonin and Melatonin in Nonseasonal Depression,” Pharmacopsychiatry 23 (1990): 155-158.
117. B. Perry et al., “Morning vs. Evening Bright Light Treatment of Late Luteal Phase Dysphoric Disorders,” Am J Psych 146 (1991): 9.
118. Diagnostic and Statistical Manual of Mental Disorders (Washington, DC: American Psychiatric Association, 1994): 389-390.

Cynthia Good Mojab, MS (clinical psychology), IBCLC, RLC, is Research Associate in the Publications Department of La Leche League International and Senior Editor at Platypus Media. She is the co-author of Breastfeeding at a Glance: Facts, Figures, and Trivia about Lactation (Platypus Media, 2001). Her publications can be accessed from her website, Ammawell home.attbi.com/~ammawell, which provides breastfeeding and parenting information.