Neonatal Vitamin D Status at Birth at Latitude 32 Degrees 72': Evidence of Deficiency

L A Basile; S N Taylor; C L Wagner; L Quinones; B W Hollis


J Perinatol. 2007;27(9):568-571. 

In This Article

Abstract and Introduction


Objective: With vitamin D deficiency as a serious public health problem, vitamin D status at birth was measured in neonates at latitude 32°72' (southeastern United States).
Study Design: In umbilical cord blood, vitamin D status, demonstrated by circulating 25-hydroxyvitamin D, was measured and related to race and season of birth.
Result: The mean±standard deviation of 25-hydroxyvitamin D in 100 cord blood samples was 13.5±8.3 ng/ml for the cohort. African-American infants, with a mean±standard deviation of 10.5±6.0 ng/ml, demonstrated significantly lower vitamin D status than Caucasian infants, with a mean±standard deviation of 19.5±9.6 ng/ml (P<0.0001). By season, the mean 25-hydroxyvitamin D level at birth in November-March compared to April-October was 11.3 ng/ml lower in Caucasian infants (from 29.0 to 17.7 ng/ml) and 3 ng/ml lower in African-American infants (from 13.1 to 10.1 ng/ml).
Conclusion: The prevalence of vitamin D insufficiency is high in this cohort. African-American infants demonstrate significantly lower vitamin D status at birth than Caucasian infants. Seasonality, while significant in both groups, had a greater impact on the vitamin D status of Caucasian newborns.


Vitamin D deficiency has emerged as a serious public health problem that affects all ages and races, especially in those with darker pigmentation, owing to the importance of sunlight in generating vitamin D in the body. The most devastating physical manifestation of vitamin D deficiency in infants and children is nutritional rickets. Rickets was thought to be disappearing in the United States and Canada, but a 2004 review from the Centers for Disease Control and Prevention describes 166 cases of vitamin D-deficiency rickets in the literature from 1986 to 2003.[1] Of the 166 cases, 50 occurred in southern states.[1,2,3,4,5] In the southern states, all cases involved African-American infants diagnosed at 8-25 months of age.[1] Recognition of the persistence of rickets in the United States and Canada has sparked reinforcement of guidelines for vitamin D intake and investigation of the risk factors leading to the development of vitamin D-deficient rickets.[6,7,8,9]

Risk factors for the development of rickets in an infant include exclusive breastfeeding without vitamin supplementation, dark pigmentation, decreased sunlight exposure, winter season, increased latitude, maternal vitamin D deficiency and an infant serum 25-hydroxyvitamin D [25(OH)D] level <11 ng/ml, which commonly defines vitamin D deficiency in infants.[1,6,7,9] Studies consistently demonstrate that maternal vitamin D deficiency in pregnancy leads to infant vitamin D deficiency.[8,10,11] Newborn infants depend on the maternal supply of vitamin D during gestation, and, at birth, the infant's 25(OH)D level is 60-75% of the mother's level.[8,11,12,13] A study published by the CDC and our laboratory using the NHANES III database reveals a serious risk for newborn infants: 42.4% of African-American women and 4.2% of Caucasian women in their childbearing years (15-49 years of age) exhibit 25(OH)D <15 ng/ml, indicative of frank vitamin D deficiency in adults.[14,15] The higher incidence of vitamin D deficiency in African-American women is thought to play a role in the increased risk of rickets for African-American infants. Evaluation of the infant's vitamin D status at birth may shed light on the infant's risk of developing of rickets.

Season and latitude are also related to the risk of vitamin D deficiency. Vitamin D levels vary according to season and latitude due to variation in cutaneous photosynthesis of previtamin D.[16,17] Humans receive vitamin D in two ways-through the diet with vitamin D supplements and vitamin D-fortified foods such as milk, or through sun exposure. Ultraviolet B (UVB) light exposure leads to creation of previtamin D from 7-dehydrocholesterol which begins the path to active vitamin D formation.[16,17,18] In 1988, Webb and colleagues[17] demonstrated that the range of UVB light that allows vitamin D formation is not achieved in the northern latitudes of the United States or in Canada during the winter months. With no ability for cutaneous production of previtamin D in the winter at these latitudes, oral intake of vitamin D is essential. However, in the same study, exposure to noontime sunlight for 1 h on a cloudless day in January in Los Angeles (latitude 34°N) and in Puerto Rico (18°N) did promote conversion into previtamin D, although limited when compared to summer quantities.

In examination of the risk factors for vitamin D-deficiency rickets, understanding the effect of race, season and latitude on vitamin D status at birth is critical. The objective of this study was to measure vitamin D status at birth in a cohort of neonates born in the southeastern part of the United States (latitude 32°72') as a function of race and season.


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