Vitamin D is an essential nutrient for bone health and may influence the risks of respiratory illness, adverse pregnancy outcomes, and chronic diseases of adulthood. Because many countries have a relatively low supply of foods rich in vitamin D and inadequate exposure to natural ultraviolet B (UVB) radiation from sunlight, an important proportion of the global population is at risk of vitamin D deficiency. There is general agreement that the minimum serum/plasma 25‐hydroxyvitamin D concentration (25(OH)D) that protects against vitamin D deficiency–related bone disease is approximately 30 nmol/L; therefore, this threshold is suitable to define vitamin D deficiency in population surveys. However, efforts to assess the vitamin D status of populations in low‐ and middle‐income countries have been hampered by limited availability of population‐representative 25(OH)D data, particularly among population subgroups most vulnerable to the skeletal and potential extraskeletal consequences of low vitamin D status, namely exclusively breastfed infants, children, adolescents, pregnant and lactating women, and the elderly. In the absence of 25(OH)D data, identification of communities that would benefit from public health interventions to improve vitamin D status may require proxy indicators of the population risk of vitamin D deficiency, such as the prevalence of rickets or metrics of usual UVB exposure. If a high prevalence of vitamin D deficiency is identified (>20% prevalence of 25(OH)D < 30 nmol/L) or the risk for vitamin D deficiency is determined to be high based on proxy indicators (e.g., prevalence of rickets >1%), food fortification and/or targeted vitamin D supplementation policies can be implemented to reduce the burden of vitamin D deficiency–related conditions in vulnerable populations.

Dietary calcium deficiency is considered to be widespread globally, with published estimates suggesting that approximately half of the world's population has inadequate access to dietary calcium. Calcium is essential for bone health, but inadequate intakes have also been linked to other health outcomes, including pregnancy complications, cancers, and cardiovascular disease. Populations in low‐ and middle‐income countries (LMICs) are at greatest risk of low calcium intakes, although many individuals in high‐income countries (HICs) also do not meet recommendations. Paradoxically, many LMICs with lower calcium intakes show lower rates of osteoporotic fracture as compared with HICs, though data are sparse. Calcium intake recommendations vary across agencies and may need to be customized based on other dietary factors, health‐related behaviors, or the risk of calcium‐related health outcomes. The lack of standard methods to assess the calcium status of an individual or population has challenged efforts to estimate the prevalence of calcium deficiency and the global burden of related adverse health consequences. This paper aims to consolidate available evidence related to the global prevalence of inadequate calcium intakes and associated health outcomes, with the goal of providing a foundation for developing policies and population‐level interventions to safely improve calcium intake and status where necessary.

Objectives To estimate the effects of vitamin D supplementation during pregnancy on 11 maternal and 27 neonatal/infant outcomes; to determine frequencies at which trial outcome data were missing, unreported, or inconsistently reported; and to project the potential contributions of registered ongoing or planned trials. Design Systematic review and meta-analysis of randomised controlled trials; systematic review of registered but unpublished trials. Data sources Medline, Embase, PubMed, Cochrane Database of Systematic Reviews, and Cochrane Central Register of Controlled Trials from inception to September 2017; manual searches of reference lists of systematic reviews identified in the electronic search; and online trial registries for unpublished, ongoing, or planned trials. Eligibility criteria for study selection Trials of prenatal vitamin D supplementation with randomised allocation and control groups administered placebo, no vitamin D, or vitamin D ≤600 IU/day (or its equivalent), and published in a peer reviewed journal. Results 43 trials (8406 participants) were eligible for meta-analyses. Median sample size was 133 participants. Vitamin D increased maternal/cord serum concentration of 25-hydroxyvitamin D, but the dose-response effect was weak. Maternal clinical outcomes were rarely ascertained or reported, but available data did not provide evidence of benefits. Overall, vitamin D increased mean birth weight of 58.33 g (95% confidence interval 18.88 g to 97.78 g; 37 comparisons) and reduced the risk of small for gestational age births (risk ratio 0.60, 95% confidence interval 0.40 to 0.90; seven comparisons), but findings were not robust in sensitivity and subgroup analyses. There was no effect on preterm birth (1.0, 0.77 to 1.30; 15 comparisons). There was strong evidence that prenatal vitamin D reduced the risk of offspring wheeze by age 3 years (0.81, 0.67 to 0.98; two comparisons). For most outcomes, meta-analyses included data from a minority of trials. Only eight of 43 trials (19%) had an overall low risk of bias. Thirty five planned/ongoing randomised controlled trials could contribute 12 530 additional participants to future reviews. Conclusions Most trials on prenatal vitamin D published by September 2017 were small and of low quality. The evidence to date seems insufficient to guide clinical or policy recommendations. Future trials should be designed and powered to examine clinical endpoints, including maternal conditions related to pregnancy (such as pre-eclampsia), infant growth, and respiratory outcomes. Systematic review registration PROSPERO CRD42016051292

It is unclear whether maternal vitamin D supplementation during pregnancy and lactation improves fetal and infant growth in regions where vitamin D deficiency is common. We conducted a randomized, double-blind, placebo-controlled trial in Bangladesh to assess the effects of weekly prenatal vitamin D supplementation (from 17 to 24 weeks of gestation until birth) and postpartum vitamin D supplementation on the primary outcome of infants’ length-for-age z scores at 1 year according to World Health Organization (WHO) child growth standards. One group received neither prenatal nor postpartum vitamin D (placebo group). Three groups received prenatal supplementation only, in doses of 4200 IU (prenatal 4200 group), 16,800 IU (prenatal 16,800 group), and 28,000 IU (prenatal 28,000 group). The fifth group received prenatal supplementation as well as 26 weeks of postpartum supplementation in the amount of 28,000 IU (prenatal and postpartum 28,000 group). Among 1164 infants assessed at 1 year of age (89.5% of 1300 pregnancies), there were no significant differences across groups in the mean (±SD) length-for-age z scores. Scores were as follows: placebo, −0.93±1.05; prenatal 4200, −1.11±1.12; prenatal 16,800, −0.97±0.97; prenatal 28,000, −1.06±1.07; and prenatal and postpartum 28,000, −0.94±1.00 (P=0.23 for a global test of differences across groups). Other anthropometric measures, birth outcomes, and morbidity did not differ significantly across groups. Vitamin D supplementation had expected effects on maternal and infant serum 25-hydroxyvitamin D and calcium concentrations, maternal urinary calcium excretion, and maternal parathyroid hormone concentrations. There were no significant differences in the frequencies of adverse events across groups, with the exception of a higher rate of possible hypercalciuria among the women receiving the highest dose. In a population with widespread prenatal vitamin D deficiency and fetal and infant growth restriction, maternal vitamin D supplementation from midpregnancy until birth or until 6 months post partum did not improve fetal or infant growth. (Funded by the Bill and Melinda Gates Foundation; ClinicalTrials.gov number, NCT01924013.)

The term “stunting” has become pervasive in international nutrition and child health research, program, and policy circles. Although originally intended as a population-level statistical indicator of children's social and economic deprivation, the conventional anthropometric definition of stunting (height-for-age z scores <−2 SD) is now widely used to define chronic malnutrition. Epidemiologists often portray it as a disease, making inferences about the causes of growth faltering based on comparisons between stunted (i.e., undernourished) and nonstunted children. Stunting is commonly used to monitor public health and nutrition program effectiveness alongside calls for the “elimination of stunting.” However, there is no biological basis for the –2 SD cutoff to define stunting, making it a poor individual-level classifier of malnutrition or disease. In fact, in many low- and middle-income countries, children above and below the threshold are similarly affected by growth-limiting exposures. We argue that the common use of stunting as an indicator of child linear growth has contributed to unsubstantiated assumptions about the biological mechanisms underlying linear growth impairment in low- and middle-income countries and has led to a systematic underestimation of the burden of linear growth deficits among children in low-resource settings. Moreover, because nutrition-specific short-term public health interventions may result in relatively minor changes in child height, the use of stunting prevalence to monitor health or nutrition program effectiveness may be inappropriate. A more nuanced approach to the application and interpretation of stunting as an indicator in child growth research and public health programming is warranted.

The causes of early childhood linear growth faltering (known as stunting) in low-income and middle-income countries remain inadequately understood. We aimed to determine if the progressive postnatal decline in mean height-for-age Z score (HAZ) in low-income and middle-income countries is driven by relatively slow growth of certain high-risk children versus faltering of the entire population. Distributions of HAZ (based on WHO growth standards) were analysed in 3-month age intervals from 0 to 36 months of age in 179 Demographic and Health Surveys from 64 low-income and middle-income countries (1993-2015). Mean, standard deviation (SD), fifth percentiles, and 95th percentiles of the HAZ distribution were estimated for each age interval in each survey. Associations between mean HAZ and SD, fifth percentile, and 95th percentile were estimated using multilevel linear models. Stratified analyses were performed in consideration of potential modifiers (world region, national income, sample size, year, or mean HAZ in the 0-3 month age band). We also used Monte Carlo simulations to model the effects of subgroup versus whole-population faltering on the HAZ distribution. Declines in mean HAZ from birth to 3 years of age were accompanied by declines in both the fifth and 95th percentiles, leading to nearly symmetrical narrowing of the HAZ distributions. Thus, children with relatively low HAZ were not more likely to have faltered than taller same-age peers. Inferences were unchanged in surveys regardless of world region, national income, sample size, year, or mean HAZ in the 0-3 month age band. Simulations showed that the narrowing of the HAZ distribution as mean HAZ declined could not be explained by faltering limited to a growth-restricted subgroup of children. In low-income and middle-income countries, declines in mean HAZ with age are due to a downward shift in the entire HAZ distribution, revealing that children across the HAZ spectrum experience slower growth compared to the international standard. Efforts to mitigate postnatal linear growth faltering in low-income and middle-income countries should prioritise action on community-level determinants of childhood HAZ trajectories. Bill & Melinda Gates Foundation.