Circulating 25-Hydroxyvitamin D Levels in Fully Breastfed Infants on Oral Vitamin D Supplementation
Carol L.Wagner, Cindy Howard, Thomas C. Hulsey, Ruth A. Lawrence, Sarah N. Taylor, HeatherWill, Myla Ebeling, Jay Hutson, and BruceW. Hollis
International Journal of Endocrinology
Volume 2010, Article 235035.

Objective: To examine the effectiveness of oral vitamin D3 (400 IU) supplementation on the nutritional vitamin D status of breastfeeding infants.

Design: As part of a larger ongoing vitamin D RCT trial of lactating women, infants of mothers assigned to control received 1 drop of 400 IU vitamin D3/day starting at one month of age. Infant 25(OH)D levels (mean ± S.D.) were measured by RIA at visits 1, 4, and 7.

Results: The infant mean ± S.D. 25(OH)D at baseline was 16.0 ± 9.3 ng/mL (range 1.0–40.8; n = 33); 24 (72.7%) had baseline levels <20 ng/mL (consistent with deficiency). The mean levels increased to 43.6 ± 14.1 (range 18.2–69.7) at 4 months and remained relatively unchanged at month 7: 42.5 ± 12.1 ng/mL (range 18.9–67.2). The change in values between 1 and 4 months and 1 and 7 months was statistically significant (P = .0001), and despite a decrease in dose per kilogram, values were not significantly different between months 4 and 7 (P = .66).

Conclusions: Oral vitamin D3 supplementation as an oil emulsion was associated with significant and sustained increases in 25(OH)D from baseline in fully breastfeeding infants through 7 months.

Vitamin D deficiency in exclusively breast-fed infants
S. Balasubramanian & R. Ganesh
Indian J Med Res 127, March 2008, pp 250-255

Exclusive breast-feeding is recommended up to 6 months of age with all its beneficial effects on child survival. Several studies have concluded that adequate intake of vitamin D cannot be met with human milk as the sole source of vitamin D. As breast-feeding rates increase, the incidence of vitamin D deficiency rickets is also expected to rise. One of the potential sources of vitamin D synthesis is in the skin from the ultraviolet rays of sunlight. Risk factors for developing vitamin D deficiency and rickets include low maternal levels of vitamin D, indoor confinement during the day, living at higher altitudes, living in urban areas with tall buildings, air pollution, darker skin pigmentation, use of sunscreen and covering much or all of the body when outside. In a study of 50 cases of hypocalcaemia reported from an urban tertiary care children’s hospital in Chennai, 13 exclusively breast-fed infants presented with hypocalcaemia due to vitamin D deficiency and most of them with seizures. None of them had received vitamin D supplementation and all their mothers had biochemical evidence for vitamin D deficiency. This review discusses the rising incidence of vitamin D deficiency in infancy and the need to consider and implement methods to prevent the same by supplementation and increased exposure to sunlight without the hazards of ultraviolet rays on the skin.

Vitamin D deficiency in healthy breastfed term infants at 3 months & their mothers in India:
Seasonal variation & determinants
Vandana Jain, Nandita Gupta, Mani Kalaivani, Anurag Jain, Aditi Sinha & Ramesh Agarwal
Indian J Med Res 133, March 2011, pp 267-273

Background & objectives: Vitamin D deficiency with a resurgence of rickets and tetany are increasingly being reported in young infants from temperate regions, African Americans and also from India. The data on vitamin D status of healthy term breastfed Indian infants and mothers are scant. Therefore, we undertook this study to determine the prevalence of vitamin D deficiency and insufficiency [serum 25 hydroxyvitamin D (25OHD) < 15 ng/ml and 15-20 ng/ml, respectively] among healthy term breastfed 3 month old infants and their mothers, evaluate for clinical and radiological rickets in those infants having 25OHD < 10 ng/ml, and check for seasonal variation and predictors of infants’ vitamin D status. Methods: A total of 98 infants aged 2.5 to 3.5 months, born at term with appropriate weight and their mothers were enrolled; 47 in winter (November- January) and 51 in summer (April-June). Details of infants’ feeding, vitamin D supplementation, sunlight exposure and mothers’ calcium and vitamin D intake were recorded. Serum calcium, phosphate, alkaline phosphatase, 25 hydroxyvitamin D (25OHD) and parathormone were estimated.
Results: Vitamin D deficiency was found in 66.7 per cent of infants and 81.1 per cent of mothers; and insufficiency in an additional 19.8 per cent of infants and 11.6 per cent of mothers. Radiological rickets was present in 30.3 per cent of infants with 25OHD < 10 ng/ml. 25OHD did not show seasonal variation in infants but maternal concentrations were higher in summer [11.3 (2.5 - 31) ng/ml] compared to winter [5.9 (2.5-25) ng/ml, P=0.003]. Intake of vitamin supplement, sunlight exposure and mother’s 25OHD were predictors of infants’ 25OHD levels.
Interpretation & conclusions:
Prevalence of vitamin D deficiency and insufficiency was found to be high in breastfed infants and their mothers, with radiological rickets in a third of infants with 25OHD < 10 ng/ml in this study. Studies with large sample need to be done in different parts of the country to confirm these findings.

Prevention of Rickets and Vitamin D Deficiency in Infants, Children, and Adolescents
Carol L. Wagner, MD, Frank R. Greer, MD, and the Section on Breastfeeding and Committee on Nutrition
Pediatrics 2008;122:1142–1152

Rickets in infants attributable to inadequate vitamin D intake and decreased exposure to sunlight continues to be reported in the United States. There are also concerns for vitamin D deficiency in older children and adolescents. Because there are limited natural dietary sources of vitamin D and adequate sunshine exposure for the cutaneous synthesis of vitamin D is not easily determined for a given individual and may increase the risk of skin cancer, the recommendations to ensure adequate vitamin D status have been revised to include all infants, including those who are exclusively breastfed and older children and adolescents. It is now recommended that all infants and children, including adolescents, have a minimum daily intake of 400 IU of vitamin D beginning soon after birth. The current recommendation replaces the previous recommendation of a minimum daily intake of 200 IU/day of vitamin D supplementation beginning in the first 2 months after birth and continuing through adolescence. These revised guidelines for vitamin D intake for healthy infants, children, and adolescents are based on evidence from new clinical trials and the historical precedence of safely giving 400 IU of vitamin D per day in the pediatric and adolescent population. New evidence supports a potential role for vitamin D in maintaining innate immunity and preventing diseases such as diabetes and cancer. The new data may eventually refine what constitutes vitamin D sufficiency or deficiency.

Hypovitaminosis D and Hypocalcemic Seizures in Infancy
P Mehrotra, RK Marwaha, S Aneja, Anju Seth, B M Singla, Ganie Ashraf, B Sharma, Aparna Sastry & N Tandon
Indian Pediatrics, Volume 47-July 17, 2010

Background: Hypocalcemia accounts for a majority of seizures in infants reporting to the emergency ward of our hospital.
Objective: To evaluate the role of Vitamin D deficiency in the etiology of hypocalcemic seizures in infancy.
Design and Setting: Cross sectional hospital based study, from April 2006-March 2007.
Subjects: 60 infants with hypocalcemic seizures and their mothers (study group) and 60 healthy breastfed infants with their lactating mothers (control group).
Measurements:
Vitamin D [25(OH) D] and intact parathormone levels.
Results: High prevalence of hypovitaminosis D [25(OH)D levels <10 ng/mL] was observed in study mothers (85%), control mothers (50%), study infants (90%), and control infants (41.7%). Mean serum 25(OH) D values in study mothers and their infants (6.54 ± 5.32 ng/mL and 4.92 ± 4.62 ng/mL) were significantly lower than those of mother infant pairs (9.06 ± 4.78 ng/mL and 9.03 ± 4.63 ng/mL) in the control group (P<0.001). A strong positive correlation of 25(OH) D levels between mothers and their infants was seen in both the study and control populations (P<0.001). Of the 54 study infants who had 25(OH)D levels <10ng/ mL, 48 (89%) were born to mothers who also had 25(OH) D levels <10ng/mL.
Conclusions: Vitamin D deficiency is a major cause of hypocalcemic seizures in infants. Infants born to vitamin D deficient mothers are at a significantly higher risk to develop hypocalcemic seizures.


The impact of atmospheric pollution on vitamin D status of
infants and toddlers in Delhi, India
K S Agarwal, M Z Mughal, P Upadhyay, J L Berry, E B Mawer, J M Puliyel
Arch Dis Child 2002;87:111–113

Aims: To compare the vitamin D status of 34 children, 9–24 months old, living in an area of Delhi renowned for high levels of atmospheric pollution (Mori Gate), with a comparable age matched group of children from a less polluted (Gurgaon) area of the city.
Methods: Serum concentrations of calcium, alkaline phosphatase (ALP), parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), and 1,25-dihydroxyvitamin D (1,25(OH)2 D) were measured. Haze scores, regarded as a surrogate marker of solar UVB radiation reaching ground level, were measured in both areas.
Results: Mean 25(OH)D of children in the Mori Gate area was 12.4 (7) ng/ml, compared with 27.1 (7) ng/ml in children living in the Gurgaon area (p < 0.001). The median ALP (p < 0.05) and mean PTH (p < 0.001) concentrations were higher in children living in the Mori Gate area than in the Gurgaon area. The mean haze score in the Mori Gate area (2.1 (0.5)) was significantly lower (p < 0.05) than in the Gurgaon area (2.7 (0.4)), indicating less solar UVB reaching the ground in Mori Gate.
Conclusion: We suggest that children living in areas of high atmospheric pollution are at risk of developing vitamin D deficiency rickets and should be offered vitamin D supplements.

Resurrection of vitamin D deficiency and rickets
Michael F. Holick
The Journal of Clinical Investigation, Volume 116, Number 8, August 2006.

Rickets has, however, made an unfortunate comeback. The major cause of rickets in the United States is a lack of appreciation that human milk contains very little if any vitamin D to satisfy the infant’s requirement. African American women are often vitamin D deficient, and women who always wear sun protection and only take a prenatal multivitamin are also at a high risk of vitamin D insufficiency. If they provide breast milk to their infant as the sole source of nutrition, the infant will become vitamin D deficient. If the infant is not exposed to sunlight or does not receive a vitamin D supplement, the infant will inevitably develop rickets. However, the skeletal manifestations of rickets represent only the tip of the vitamin D deficiency iceberg. Vitamin D deficiency in utero and during the first year of life has devastating consequences and may imprint on the child’s life chronic diseases that will shorten his/her life span. In utero, vitamin D deficiency results in reduced intrauterine long bone growth and slightly shorter gestation. This has been linked to increased risk of osteoporosis and fractures later in life. Children born and raised at latitudes below 35° for the first 10 years have a 50% reduced risk of developing multiple sclerosis later in life. Neonates who are vitamin D deficient during the first year of life are 2.4-fold more likely to develop type 1 diabetes compared with children who received 2,000 IU of vitamin D3/day. It has been suggested that the increased risk of developing schizophrenia may be initiated in utero and during childhood due to vitamin D deficiency. Muscle function, innate immunity, cellular growth and maturation, immunomodulation, insulin secretion, as well as regulation of calcium, phosphorus, and bone metabolism are all affected or controlled by vitamin D. Thus, ensuring that women during pregnancy are vitamin D sufficient and that newborns either be immediately evaluated for their vitamin D status by measuring 25(OH)D levels in cord blood or given vitamin D prophylactically should be a high priority. Vitamin D deficiency should be immediately treated with at least 1,000 IU of vitamin D2 or vitamin D3/day for the first week of life.