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Vitamin D supplementation in pregnancy, lactation and infancy: why is it fundamental?

02 May 2020
12 min read
Volume 28 · Issue 5

Abstract

Vitamin D is mainly made in the skin following exposure to sunlight but can also be taken in via specific natural or fortified food sources. It is essential for intestinal calcium absorption and thereby bone mineralisation. Deficiency in vitamin D, or low dietary calcium intake, therefore results in defective bone mineralisation causing osteomalacia in children and adults and rickets in growing children. The leading causes of rickets and osteomalacia worldwide are solar vitamin D deficiency and/or nutritional calcium deficiency. Long-standing severe vitamin D deficiency can lead to craniotabes, large fontanelle, leg bowing, stunted growth and obstructed labour. The deficient state in the infant is almost always acquired from the mother. Therefore, robust antenatal and infant vitamin D supplementation programmes are obligatory to prevent complications. Conversely, lack of programme monitoring and conflicting recommendations can lead to confusion among healthcare professionals and poor uptake in the population. Factors shown to improve adherence to supplementation include universal supplementation of breast- and bottle-fed infants, monitoring supplementation at antenatal/postnatal healthcare visits, providing information to families at discharge from the neonatal unit and financial family support.

Vitamin D, known as the ‘sunshine vitamin’, is made in the skin in response to ultraviolet B (UVB) radiation, and once activated in the body to the hormone calcitriol (1,25 dihydroxy-vitamin D), it regulates a wide variety of processes; the most important of which being intestinal calcium and phosphate absorption (Wacker and Holick, 2013). Calcium – phosphate crystals (hydroxyapatite) – are the main building blocks for bone mineralisation and are therefore essential to maintain adequate bone hardness and strength. Hence, lack of vitamin D can lead to inadequate mineralisation resulting in osteomalacia in adults and children, and rickets in growing children (Uday and Högler, 2018a).

Vitamin D status is measured by serum concentration of 25-hydroxyvitamin D (25OHD) which is the most stable form (Nair and Maseeh, 2012). 25OHD concentration below 30 nmol/L (12ng/L) is classed as deficiency (Rosen et al, 2012; Munns et al, 2016). Prolonged severe rickets/osteomalacia in girls during growth can later result in obstructed labour which worsens with subsequent pregnancies (Konje and Ladipo, 2000). Vitamin D deficiency has also been implicated in gestational diabetes mellitus, pre-eclampsia and preterm labour (Mulligan et al, 2010). The deficiency state in the mother is naturally passed on to the fetus and the newborn whose 25OHD levels are about 50%–78% of the mother's (VioStreym et al, 2013; O'Callaghan et al, 2018). Vitamin D supplementation during pregnancy is associated with higher 25OHD concentrations, greater birth weight and birth length in the neonate (Pérez-López et al, 2015).

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