ORIGINAL ARTICLE Maternal vitamin D supplementation during pregnancy prevents vitamin D deficiency in the newborn: an open-label randomized controlled trial C.P. Rodda* , † , ‡, J.E. Benson§, A.J. Vincent¶ , **, C.L. Whitehead††, A. Polykov‡‡ , §§ and B. Vollenhoven¶¶ , *** *Department of Paediatrics, University of Melbourne, Parkville, Vic., †Department of Paediatrics, Monash University, Clayton, Vic., ‡Paediatric Department, Sunshine Hospital, St Albans, Vic., §Department of Obstetrics and Gynaecology, Barwon Health, Geelong, Vic., ¶Monash Centre for Health Research and Implementation, School of Public Health and Preventative Medicine, Monash University, **Clinical Nutrition and Metabolism Unit, Monash Health, Clayton, Vic., ††Department of Obstetrics and Gynaecology, University of Melbourne, ‡‡Reproductive Biology Unit, Royal Women’s Hospital, Parkville, Vic., §§Melbourne IVF, East Melbourne, Vic., ¶¶Department of Obstetrics and Gynaecology, Monash University, and ***Gynaecology Unit, Monash Health, Clayton, Vic., Australia Summary Objective To determine whether maternal vitamin D supple- mentation, in the vitamin D deficient mother, prevents neonatal vitamin D deficiency. Design Open-label randomized controlled trial. Setting Metropolitan Melbourne, Australia, tertiary hospital routine antenatal outpatient clinic. Participants Seventy-eight women with singleton pregnancies with vitamin D deficiency/insufficiency (serum 25-OH Vit D < 75 nmol/l) at their first antenatal appointment at 12–16- week gestation were recruited. Intervention Participants were randomized to vitamin D sup- plementation (2000–4000 IU cholecalciferol) orally daily until delivery or no supplementation. Main outcome measures The primary outcome was neonatal serum 25-OH vit D concentration at delivery. The secondary out- come was maternal serum 25-OH vit D concentration at delivery. Results Baseline mean maternal serum 25-OH vit D concentra- tions were similar (P = 0Á9) between treatment (32 nmol/l, 95% confidence interval 26–39 nmol/l) and control groups (33 nmol/l, 95% CI 26–39 nmol/l). Umbilical cord serum 25-OH vit D con- centrations at delivery were higher (P < 0Á0001) in neonates of treatment group mothers (81 nmol/l, 95% CI; 70–91 nmol/l) compared with neonates of control group mothers (42 nmol/l, 95% CI; 34–50 nmol/l) with a strongly positive correlation between maternal serum 25-OH Vit D and umbilical cord serum 25-OH vit D concentrations at delivery (Spearman rank correla- tion coefficient 0Á88; P < 0Á0001). Mean maternal serum 25-OH Vit D concentrations at delivery were higher (P < 0Á0001) in the treatment group (71 nmol/l, 95% CI; 62–81 nmol/l) compared with the control group (36 nmol/l, 95% CI; 29–42 nmol/l). Conclusion Vitamin D supplementation of vitamin D deficient pregnant women prevents neonatal vitamin D deficiency. (Received 5 October 2014; returned for revision 13 February 2015; finally revised 25 February 2015; accepted 26 February 2015) Introduction Vitamin D deficiency in women in the reproductive age group is increasing due to lifestyle factors, including increased time spent indoors both in the workplace and domestically, increasingly pre- valent maternal obesity and possible overuse of broad-spectrum sunscreens. 1 These risk factors are exacerbated in highly pig- mented women and/or by clothing practices resulting in minimal direct skin sun exposure. 2 For the developing foetus, the source of vitamin D is from maternal transplacental transfer. 3 Consequently, foetal and neonatal serum 25-OH Vit D concentrations directly reflect maternal serum 25-OH Vit D concentrations. 3–7 Further- more, although breast milk is strongly recommended for all infants, it must be recognized that breast milk is a poor source of vitamin D (containing 20–70 IU/l). 7–9 Infants born vitamin D deficient secondary to maternal vitamin D deficiency, and subse- quently exclusively breastfed with negligible sun exposure, are at high risk of developing rickets in the first year of life with associ- ated skeletal deformity and hypocalcaemia. 2,10 The definition of vitamin D adequacy during pregnancy, infancy and in later child- hood and adolescence remains controversial 10 and is complicated by technical issues related to various assays used. 11 At the time of Correspondence: Christine P. Rodda, North West Academic Centre, Western Centre for Health Research and Education, Western Health, Sunshine Hospital, The University of Melbourne, Room 5.056, Level 3, PO Box 294, 176 Furlong Road, St Albans, Vic. 3021, Australia. Tel.: 613 8395 8161; E-mail: christine.rodda@unimelb.edu.au Trial registration: Australian and New Zealand Clinical Trials Registry ANZCTR12609000142235. © 2015 John Wiley & Sons Ltd 363 Clinical Endocrinology (2015) 83, 363–368 doi: 10.1111/cen.12762