Maternal Vitamin D3 Supplementation Research Articles

Maternal Vitamin D3 Supplementation in an Oxidized-Oil Diet Protects Fetus from Developmental Impairment and Ameliorates Oxidative Stress in Mouse Placenta and Fetus

BackgroundFried food has increased in popularity worldwide. However, deep frying can increase the production of peroxidative toxins in food, which might be harmful to fetal development. The antioxidative effect of vitamin D3 (VD3) has been reported previously. ObjectivesThis study aimed to explore how maternal VD3 supplementation in an oxidized-oil diet during gestation affects fetal antioxidative ability and development. MethodsPregnant mice were randomly assigned into 3 groups: Control group (diet with fresh soybean oil), OSO group [diet with oxidized soybean oil (OSO)], and OSOV group (diet with OSO and 10,000 IU/Kg VD3). Mice were fed with the corresponding diet during gestation. On day 16.5 of gestation, the placenta and fetus were harvested to analyze antioxidative status. ResultsMaternal oxidized-oil diet during gestation significantly reduced placental vessel abundance, labyrinth zone area, and fetal body weight. However, dietary VD3 supplementation prevented these negative effects of oxidized-oil diet. Maternal intake of oxidized-oil diet increased serum concentrations of malondialdehyde, total-nitric oxide synthase, and inducible nitric oxide synthase, whereas VD3 supplementation showed a protection effect on it. Additionally, maternal VD3 supplementation increased the levels of antioxidative enzymes and the nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2), thereby protecting placenta and fetus from apoptosis and oxidative stress caused by an oxidized-oil diet. The gene expression and protein levels of a fatty acid transporter solute carrier family 27 member 1 in the fetal liver were increased by maternal VD3 supplementation under oxidized-oil diet. Notably, NRF2 could be co-immunoprecipitated with the VD receptor in the placenta. ConclusionsMaternal VD3 supplementation could protect fetus from oxidized-oil diet induced developmental impairment by alleviating oxidative stress in the placenta and fetus through the VD receptor/NRF2 pathway, at least partially. Thus, ensuring adequate levels of VD3 through supplementation is often critical during pregnancy.

Association of Maternal Gestational Vitamin D Supplementation with Respiratory Health of Young Children.

This study aimed to evaluate the association between maternal gestational Vitamin D3 supplementation and early respiratory health in offspring. This was a population-based record-linkage study which used data from the French National Health Database System. Maternal Vitamin D3 supplementation consisted of a single high oral dose of cholecalciferol, (100,000 IU) from the seventh month of pregnancy, according to national guidelines. In total, 125,756 term-born singleton children were included, of which 37% had respiratory illness defined as hospital admission due to respiratory causes or inhalation treatment up to 24 months of age. Infants prenatally exposed to maternal Vitamin D3 supplementation (n = 54,596) were more likely to have a longer gestational age (GA) at birth (GA 36-38 weeks, 22% vs. 20%, p < 0.001 in exposed vs. non-exposed infants, respectively). After adjusting for the main risk factors (maternal age, socioeconomic level, mode of delivery, obstetrical and neonatal pathology, birth weight appropriateness, sex, and birth season), the risk of RD was found to be 3% lower than their counterparts (aOR [IC 95%], 0.97 [0.95-0.99], p = 0.01). In conclusion, this study provides evidence for the association between maternal gestational Vitamin D3 supplementation and improved early respiratory outcomes in young children.

EFFECTS OF MATERNAL VITAMIN D3 LEVELS DURING PREGNANCY ON PORK QUALITY CHARACTERISTICS OF OFFSPRING PIGS

Introduction. Maternal vitamin D3 levels have long lasting consequences on meat quality and growth performance. The present study was conducted to investigate maternal vitamin D3 status in sows during pregnancy on meat quality attributes, chemical composition, and low field nuclear magnetic resonance (LF-NMR) T2 relaxation times of longissimus dorsi muscle in offspring pigs.&#x0D; Materials and methods. A total of 27 sows (41st day of pregnancy) were randomly allotted to low (LD), normal (ND), and high (HD) dietary vitamin D3 groups (containing 200, 800 and 3200 IU of vitamin D3/kg experimental diet, respectively). In each group were 3 replicates with 3 sows per replicate. From parturition to weaning, all lactating sows fed the ND diet. At 150 days of age, six offspring pigs in each group (2 offspring pigs with similar body weight per replicate, gender balanced) were selected and slaughtered to evaluate pork quality characteristics.&#x0D; Results and discussion. The results showed that maternal vitamin D3 supplementation decreased L*, b* value, shear force, cooking loss, T21 and T22 relaxation times, while increased a* value, pH value, water holding capacity (WHC), crude protein (CP), crude fat (CF), calcium (Ca), and phosphorus (P) content in longissimus dorsi muscle of offspring pigs. These results demonstrated that high-dose maternal vitamin D3 level could improve meat quality characteristics of offspring pigs, and it will provide a scienfific basis for the early nutritional regulation of offspring prok quality.&#x0D; Conclusions. The findings indicated that maternal vitamin D3 supplementation has positive effects on quality characteristics of longissimus dorsi muscle, and improved eating quality of meat in offspring pigs.

Effect of Maternal Prenatal and Postpartum Vitamin D Supplementation on Offspring Bone Mass in Early Childhood: Follow-Up of a Randomized Controlled Trial

ObjectivesMaternal vitamin D status has gained substantial attention as a modifiable contributor to offspring musculoskeletal health, yet there is a paucity of trial-derived data to corroborate effects of prenatal or postpartum vitamin D supplementation on offspring bone mass accrual. Among maternal-infant pairs in Bangladesh, we aimed to examine the hypothesized causal association of early life vitamin D exposure with musculoskeletal health in childhood. MethodsIn a double-blind dose-ranging trial of maternal vitamin D3 supplementation (Maternal Vitamin D for Infant Growth Trial), healthy pregnant women (n = 1300) were recruited at 17–24 weeks’ gestation and randomly assigned to receive a prenatal; postpartum regimen of 0;0,4200;0,16,800;0,28,000;0 or 28,000;28,000 IU vitamin D3/week until 26 weeks postpartum. In a follow-up study of offspring at 4 years of age (n = 642), bone mineral content (BMC) and bone mineral density (BMD) were measured by dual-energy X-ray absorptiometry. Between-group differences were assessed by independent t-tests (28,000 IU/week prenatally vs placebo) and linear regression (each vitamin D treatment group vs placebo) with bootstrapping (1000 replications). ResultsWhole-body (WB), total-body-less-head (TBLH) and head-only BMC were similar in the combined high-dose prenatal and placebo groups (mean difference [95% CI] = 6.81g [–8.70, 22.32], 0.61g [–10.90, 12.13] and 1.71g [–3.54, 6.96], respectively). None of the mean values for WB or TBLH BMC or BMD in each vitamin D group were different from placebo (P > 0.05 for all comparisons). Although head BMD was slightly greater in offspring of women assigned to the 28,000;28,000 IU regimen compared to placebo (mean difference [95% CI] = 0.024g/cm2 [0.0009, 0.047], P = 0.042), the effect was attenuated and no longer significant upon adjustment for child height, weight, and sex (P = 0.11). ConclusionsIn a population with high prevalence of vitamin D deficiency, our findings do not support the use of maternal prenatal vitamin D supplementation, with or without postpartum supplementation, for improvement of child BMC or BMD at 4 years of age. Funding SourcesCanadian Institutes for Health Research and the Bill and Melinda Gates Foundation.

Supplementation with high-dose cholecalciferol throughout pregnancy induces fetal growth restriction through inhibiting placental proliferation and trophoblast epithelial-mesenchymal transition

Vitamin D deficiency has been associated with adverse pregnant outcomes. Several studies investigated the effects of maternal vitamin D3 supplementation on fetal development with inconsistent results. The aim of this study was to investigate the effects of maternal supplementation with different doses of vitamin D3 on fetal development. Pregnant mice were administered with different doses of cholecalciferol (0, 2,000, 10,000, 40,000 IU/kg/day) by gavage throughout pregnancy. Fetal weight and crown-rump length were measured. Placental proliferation and mesenchymal characteristics were detected. HTR-8/SVneo cells were incubated in the absence or presence of calcitriol (500 nmol/L) to evaluate the effects of active vitamin D3 on migration and invasion of human trophoblast cells. Although a low dose of cholecalciferol was safe, fetal weight and crown-rump length were decreased in dams treated with high-dose cholecalciferol throughout pregnancy. Placental weight and labyrinth thickness were reduced in mice administered with high-dose cholecalciferol. An obvious calcification was observed in placentae of mice administered with high-dose cholecalciferol. Ki67-positive cells, a marker of placental proliferation, were reduced in mice administered with high-dose cholecalciferol. N-cadherin and vimentin, two mesenchymal markers, were decreased in cholecalciferol-treated mouse placentae and calcitriol-treated human trophoblast cells. MMP-2 and MMP-9, two matrix metalloproteinases, were downregulated in cholecalciferol-treated mouse placentae and calcitriol-treated human trophoblast cells. In addition, trophoblast migration and invasion were suppressed by calcitriol. Supplementation with high-dose cholecalciferol induces fetal growth restriction partially through inhibiting placental proliferation and trophoblast epithelial-mesenchymal transition.

Effects of Maternal Vitamin D3 Supplementation on Offspring Epigenetic Clock of Gestational Age at Birth: A Post-hoc Analysis of a Randomized Controlled Trial

ABSTRACT Vitamin D could be beneficial for healthy ageing in humans. We previously found that vitamin D supplementation may slow down epigenetic ageing in young African American adults. We tested new epigenetic clocks developed for neonates among a multiethnic population, and tested the hypothesis that maternal vitamin D supplementation would slow down the epigenetic gestational age acceleration (GAA) in newborn babies. Ninety-two pregnant women (aged 29.6 ± 4.8 y; 21% African Americans, 28% Hispanics) were randomized to receive 4000 IU/day vitamin D3 or placebo, plus prenatal vitamins containing 400 IU vitamin D3 during pregnancy in a randomized controlled trial (RCT). Cord blood genome-wide methylation analysis was performed on the Illumina Infinium MethylationEPIC Beadchip. DNA methylation gestational age was calculated based on two calculations developed by Knight and Bohlin. DNA methylation gestational ages calculated by Knight’s clock and Bohlin’ clock were highly correlated with the gestational age in the placebo group (correlation coefficients = 0.88, p s< 0.001, respectively). GAA was associated with higher birth weight (p = 0.039). In the entire cohort, vitamin D3 supplementation was not associated with GAA (p > 0.05). However, vitamin D3 supplementation decreased GAA by both Knight’s clock (β = −0.89, p = 0.047) and Bohlin’s clock (β = −0.71, p = 0.005) in the African American participants. Maternal vitamin D3 supplementation may slow down the epigenetic gestational ageing process in African American neonates. Long-term follow-up studies are warranted to determine the role of epigenetic age acceleration in the growth and development of offspring.

Effects of Maternal Vitamin D3 Supplementation on Offspring Epigenetic Gestational Age Acceleration at Birth: A Randomized Controlled Trial (P11-036-19)

ObjectivesWe have previously found that vitamin D supplementation may slow down epigenetic aging in young adults. Recently, new epigenetic clocks have been developed to estimate gestational age in newborn babies. We tested the hypothesis that vitamin D supplementation would slow down the epigenetic gestational aging. MethodsA total of 92 participants (51% whites, 21% blacks, 28% Hispanics) were randomly selected from 450 pregnant women who were enrolled in a randomized controlled trial. Each mother was randomized to receive either 4000 IU/day vitamin D3 or placebo plus the standard prenatal vitamins containing 400 IU vitamin D3. Cord blood genome-wide methylation analyses were performed on the Illumina Infinium MethylationEPIC Beadchip. DNA methylation gestational age (DNAmGA) was calculated based on two methods developed by Knight and Bohlin. The effects of vitamin D3 supplementation on DNA methylation-based gestational age acceleration (∆DNAmGA) were estimated in linear regressions adjusted for maternal age, race, smoking status and sex of the babies. ResultsGestational age was highly correlated with DNAmGAKnight and DNAmGABohlin having the same correlation coefficients of 0.88 (ps < 0.001). Both DNAmGAKnight and DNAmGABohlin clocks also performed well in black and Hispanic populations with correlation coefficients ranging from 0.80 to 0.98 (ps < 0.001). Vitamin D3 supplementation decreased ∆DNAmGA by both Knight’s clock (β = –0.89, P = 0.047) and Bohlin’s clock (β = –0.71, P = 0.005) only in the black participants. ConclusionsBoth Knight’s and Bohlin’s epigenetic gestational clocks were highly correlated with gestational age in this multiethnic cohort. Vitamin D3 supplementation decreased epigenetic gestational age acceleration at birth, but only in black babies. A follow-up study is warranted to evaluate the role of accelerated gestational aging in offspring growth and development. Funding SourcesW. K. Kellogg Foundation and the South Carolina Clinical & Translational Research (SCTR) Institute, at the Medical University of South Carolina, NIH/NCAT Grant UL1TR000062. YD and HZ are also supported by AHA 14GRANT20480211.

Comparison of the effect of daily versus bolus dose maternal vitamin D3 supplementation on the 24,25-dihydroxyvitamin D3 to 25-hydroxyvitamin D3 ratio.

Supplementing lactating mothers with high doses of vitamin D3 can adequately meet vitamin D requirements of the breastfed infant. We compared the effect of bolus versus daily vitamin D3 dosing in lactating mothers on vitamin D3 catabolism. We hypothesized that catabolism of 25(OH)D3 to 24,25(OH)2D3 would be greater in the bolus than in the daily dose group. Randomized controlled trial (clinicaltrials.govNCT01240265) in 40 lactating women. Subjects were randomized to receive vitamin D3 orally, either a single dose of 150,000IU or 5000IU daily for 28days. Vitamin D metabolites were measured in serum and breast milk at baseline, 1, 3, 7, 14 and 28days. Temporal changes in the serum 24,25(OH)2D3/25(OH)D3 ratio. The concentration of serum 24,25(OH)2D3 was directly related to that of 25(OH)D in both groups (r2=0.63; p<0.001). The mean (±SD) 24,25(OH)2D3/25(OH)D3 ratio remained lower at all time points than baseline values in the daily dose group (0.093±0.024, 0.084±0.025, 0.083±0.024, 0.080±0.020, 0.081±0.023, 0.083±0.018 at baseline, 1, 3, 7, 14, and 28days, respectively). In the single dose group, the increase in 24,25(OH)2D3 lagged behind that of 25(OH)D, but the 24,25(OH)2D3/25(OH)D3 values (0.098±0.032, 0.067±0.019, 0.081±0.017, 0.092±0.024, 0.103±0.020, 0.106±0.024, respectively) exceeded baseline values at 14 and 28days and were greater than the daily dose group at 14 and 28days (p=0.003). The 24,25(OH)2D3/25(OH)D3 ratio remained in the normal range with both dosing regimens. Greater breast milk vitamin D3 values in the single dose group were inversely associated with the 24,25(OH)2D3/25(OH)D3 ratio (r2=0.14, p<0.001), but not with daily dosing. After a 14-day lag, a single high dose of vitamin D led to greater production of 24,25(OH)2D3, presumably via induction of the 24-hydroxylase enzyme (CYP24A1), relative to the 25(OH)D3 value than did daily vitamin D supplementation, and this effect persisted for at least 28days after vitamin D administration. A daily dose of vitamin D may have more lasting effectiveness in increasing 25(OH)D3 with lesser diversion of 25(OH)D3 to 24,25(OH)2D3 than does larger bolus dosing.

Effect of maternal vitamin D3 supplementation on maternal health, birth outcomes, and infant growth among HIV-infected Tanzanian pregnant women: study protocol for a randomized controlled trial

BackgroundVitamin D has significant immunomodulatory effects on both adaptive and innate immune responses. Observational studies indicate that adults infected with HIV with low vitamin D status may be at increased risk of mortality, pulmonary tuberculosis, and HIV disease progression. Growing observational evidence also suggests that low vitamin D status in pregnancy may increase the risk of adverse birth and infant health outcomes. As a result, antiretroviral therapy (ART) adjunct vitamin D3 supplementation may improve the health of HIV-infected pregnant women and their children.Methods/designThe Trial of Vitamins-5 (ToV5) is an individually randomized, double-blind, placebo-controlled trial of maternal vitamin D3 (cholecalciferol) supplementation conducted among 2300 HIV-infected pregnant women receiving triple-drug ART under Option B+ in Dar es Salaam, Tanzania. HIV-infected pregnant women of 12–27 weeks gestation are randomized to either: 1) 3000 IU vitamin D3 taken daily from randomization in pregnancy until trial discharge at 12 months postpartum; or 2) a matching placebo regimen. Maternal participants are followed-up at monthly clinic visits during pregnancy, at delivery, and then with their children at monthly postpartum clinic visits. The primary efficacy outcomes of the trial are: 1) maternal HIV disease progression or death; 2) risk of small-for-gestational age (SGA) births; and 3) risk of infant stunting at 1 year of age. The primary safety outcome of the trial is incident maternal hypercalcemia. Secondary outcomes include a range of clinical and biological maternal and child health outcomes.DiscussionThe ToV5 will provide causal evidence on the effect of vitamin D3 supplementation on HIV progression and death, SGA births, and infant stunting at 1 year of age. The results of the trial are likely generalizable to HIV-infected pregnant women and their children in similar resource-limited settings utilizing the Option B+ approach.Trial registrationClinicalTrials.gov identifier: NCT02305927. Registered on 29 October 2014.

Maternal vitamin D sufficiency and reduced placental gene expression in angiogenic biomarkers related to comorbidities of pregnancy

IntroductionMaternal circulating 25-hydroxyvitamin D [25(OH)D] has been shown to optimize production of 1,25-dihydroxyvitamin D [1,25(OH)2D] during pregnancy at approximately 100nmoles/L, which has pronounced effects on fetal health outcomes. Additionally, associations are noted between low maternal 25(OH)D concentrations and vascular pregnancy complications, such as preeclampsia. To further elucidate the effects of vitamin D activity in pregnancy, we investigated the role of maternal 25(OH)D, the nutritional indicator of vitamin D status, in relation to placental maintenance and, specifically, expression of placental gene targets related to angiogenesis and vitamin D metabolism. MethodsA focused analysis of placental mRNA expression related to angiogenesis, pregnancy maintenance, and vitamin D metabolism was conducted in placentas from 43 subjects enrolled in a randomized controlled trial supplementing 400IU or 4400IU of vitamin D3 per day during pregnancy. Placental mRNA was isolated from biopsies within one hour of delivery, followed by quantitative PCR. We classified pregnant women with circulating concentrations of <100nmoles/L as deficient and those with ≥100nmoles/L as sufficient. The value of each gene’s change in the PCR cycle threshold (ΔCT), which is a relative measure of target concentration, was compared with maternal 25(OH)D concentrations <100nmoles/L and ≥100nmoles/L based on a two-sample Wilcoxon test. ResultsSoluble FMS-like tyrosine kinase 1 (sFlt-1) and vascular endothelial growth factor (VEGF) gene expression was significantly downregulated in the maternal subgroup with circulating 25(OH)D ≥100ng/mL compared to the subgroup <100ng/mL. DiscussionHere, we report a significant association between maternal vitamin D status and the expression of sFlt-1 and VEGF at the mRNA level. Achieving maternal circulating 25(OH)D ≥100nmoles/L suggests the impact of maternal vitamin D3 supplementation on gene transcription in the placenta, thereby potentially decreasing antiangiogenic factors that may contribute to vascular pregnancy complications.

Maternal vitamin D3 supplementation at 50 μg/d protects against low serum 25-hydroxyvitamin D in infants at 8 wk of age: a randomized controlled trial of 3 doses of vitamin D beginning in gestation and continued in lactation

Vitamin D supplementation is recommended for breastfed infants. Maternal supplementation beginning in gestation is a potential alternative, but its efficacy in maintaining infant 25-hydroxyvitamin D [25(OH)D] concentration after birth is unknown. We determined the effect of 3 doses of maternal vitamin D supplementation beginning in gestation and continued in lactation on infant serum 25(OH)D and compared the prevalence of infant serum 25(OH)D cutoffs (>30, >40, >50, and >75 nmol/L) by dose at 8 wk of age. Pregnant women (n = 226) were randomly allocated to receive 10, 25, or 50 μg vitamin D₃/d from 13 to 24 wk of gestation until 8 wk postpartum, with no infant supplementation. Mother and infant blood was collected at 8 wk postpartum. At 8 wk postpartum, mean [nmol/L (95% CI)] infant 25(OH)D at 8 wk was higher in the 50-μg/d [75 (67, 83)] than in the 25-μg/d [52 (45, 58)] or 10-μg/d [45 (38, 52)] vitamin D groups (P < 0.05). Fewer infants born to mothers in the 50-μg/d group had a 25(OH)D concentration <30 nmol/L (indicative of deficiency) than infants in the 25- and 10-μg/d groups, respectively (2% compared with 16% and 43%; P < 0.05). Fewer than 15% of infants in the 10- or 25-μg/d groups achieved a 25(OH)D concentration >75 nmol/L compared with 44% in the 50-μg/d group (P < 0.05). Almost all infants (∼98%, n = 44) born to mothers in the 50-μg/d group achieved a 25(OH)D concentration >30 nmol/L. At 8 wk postpartum, mean maternal 25(OH)D concentration was higher in the 50-μg/d [88 (84, 91)] than in the 25-μg/d [78 (74, 81)] or 10-μg/d [69 (66, 73)] groups (P < 0.05). Maternal supplementation beginning in gestation with 50 μg vitamin D₃/d protects 98% of unsupplemented breastfed infants against 25(OH)D deficiency (<30 nmol/L) to at least 8 wk, whereas 10 or 25 μg vitamin D/d protects only 57% and 84% of infants, respectively.

Evaluating the Effects of Maternal Vitamin D Supplementation on the Subsequent Growth Performance and Carcass Characteristics of a Subsample Population of Growing Pigs

A subsample of 448 growing pigs (PIC 327 × 1050), or approximately 50% of pigs weaned from sows fed varying dietary vitamin D regimens, were used in a split-plot design to determine the influence of maternal and nursery vitamin D regimens on growth performance. Sows were previously administered diets containing vitamin D as either: 1) low vitamin D3 (363 IU/lb); 2) medium vitamin D3 (907 IU/lb); 3) high vitamin D3 (4,354 IU/lb); or 4) 23 μg 25(OH)D3/lb (Hy-D, DSM Nutritional Products Inc, Parsippany, NJ) as described by Flohr et al. (20153) throughout gestation and lactation. A total of 52 total litters from 2 consecutive weaning groups were represented in the subsample population for growth performance. Once weaned, pigs were allotted to pens in the nursery based on previously administered maternal vitamin D regimens, then pens were randomly assigned to 1 of 2 nursery vitamin D regimens (907 IU of vitamin D3/lb, or 23 μg 25(OH)D3/lb). Pigs remained on nursery vitamin D regimens for 35 d, then they were provided common growing and finishing diets until market. One pig per pen was bled at weaning and on d 17, 35, and 70 post-weaning to determine growing pig serum vitamin metabolites. At weaning, pig BW was increased (quadratic, P = 0.001) with increased maternal vitamin D3 supplementation. This was because pigs from sows fed the medium concentration of vitamin D3 were heavier at weaning compared to pigs from sows fed the low or high concentration of vitamin D3. Overall from d 0 to 35 in the nursery, pigs from sows fed increasing vitamin D3 had increased (quadratic, P < 0.003) ADG and ADFI, but F/G was similar regardless of maternal Vitamin D regimen. Pigs from sows fed the low concentration of vitamin D3 had poorer (P < 0.002) ADG and final nursery BW compared to those from sows fed 25(OH)D3. Throughout finishing (d 35 post-weaning until market), ADG was increased (quadratic, P = 0.005) and ADFI tended to increase (quadratic, P = 0.055) with increasing maternal vitamin D3 supplementation because pigs from sows fed the medium concentration of vitamin D3 had greater ADG and numerically greater ADFI compared to pigs from sows fed the low or high concentration of vitamin D3. Average daily gain of pigs from sows fed the low concentration of vitamin D3 was lower (P < 0.004) compared to those from sows fed 25(OH)D3. Carcass data were also collected from 734 pigs (approximately 65% of pigs weaned from sows administered vitamin D regimens) from 3 out of the 4 weaning groups used for the experiment. At marketing, live BW and HCW were heavier (P < 0.030) for pigs from sows fed 25(OH)D3 compared to pigs from sows fed the high concentration of vitamin D3. Also, percentage carcass yield increased (quadratic, P = 0.003) with increasing maternal vitamin D3 supplementation. Loin depth (linear P = 0.047) and BF (quadratic, P = 0.031) were both decreased with increasing vitamin D3 supplementation. Overall, it appears that vitamin D3 and 25(OH)D3, whether through maternal supplementation or through the diet, are useful sources of vitamin D to increase serum 25(OH)D3 concentrations in growing pigs. Additionally, 25(OH)D3 (in the nursery diet) can increase serum 25(OH)D3 of nursery pigs more than feeding the same international unit equivalency of vitamin D3. Pigs from sows fed the medium concentration of vitamin D3 performed better after weaning compared to pigs from sows fed the low or high concentrations of vitamin D3; however, this difference may have been confounded with the variance in weaning weight associated with the subsample population used for the growth portion of the study. Also, it is perceived that pigs from sows fed 25(OH)D3 had increased live weight and HCW compared to pigs from sows fed the high concentration of vitamin D3. This research report is available in Kansas Agricultural Experiment Station Research Reports: http://newprairiepress.org/kaesrr/ vol1/iss7/24

An evaluation of the effects of added vitamin D3 in maternal diets on sow and pig performance1,2

A total of 84 sows (PIC 1050) and their litters were used to determine the effects of supplementing maternal diet with vitamin D3 on sow and pig performance, serum 25-hydroxyvitamin D3 (25(OH)D3), milk vitamin D3, neonatal bone mineralization, and neonatal tissue vitamin D3. After breeding, sows were randomly assigned to 1 of 3 dietary vitamin D3 treatments (1,500, 3,000, or 6,000 IU/kg of complete diets). Sows were bled on d 0 and 100 of gestation and at farrowing and weaning (d 21). Pig BW was recorded at birth and weaning, and serum was collected from 2 pigs/litter at birth, on d 10 and at weaning. A total of 54 pigs (18/treatment) were euthanized at birth and necropsied to sample bones and tissues. Sow and suckling pig performance and neonatal bone ash and bone density did not differ among maternal vitamin D3 treatments; however, sow 25(OH)D3 and milk vitamin D3 increased (linear, P < 0.01) with increasing maternal vitamin D3 supplementation. Piglet serum 25(OH)D3 increased (quadratic, P < 0.03) with increased maternal vitamin D3. Neonatal kidney vitamin D3 tended (quadratic, P = 0.08) to decrease with increasing maternal vitamin D3, but liver vitamin D3 tended (linear, P = 0.09) to increase with increasing maternal vitamin D3. At weaning, a subsample of 180 pigs (PIC 327 × 1050) were used in a 3 × 2 split plot design for 35 d to determine the effects of maternal vitamin D3 and 2 levels of dietary vitamin D3 (1,800 or 18,000 IU/kg) from d 0 to 10 postweaning on nursery growth and serum 25(OH)D3. Overall (d 0 to 35), nursery ADG and G:F were not affected by either concentration of vitamin D3, but ADFI tended (quadratic, P < 0.06) to decrease with increasing maternal vitamin D3 as pigs from sows fed 3,000 IU had lower ADFI compared with pigs from sows fed 1,500 or 6,000 IU/kg. Nursery pig serum 25(OH)D3 increased with increasing maternal vitamin D3 (weaning) on d 0 (linear, P < 0.01), and maternal × diet interactions (P < 0.01) were observed on d 10 and 21 because pigs from sows fed 1,500 IU had greater increases in serum 25(OH)D3 when fed 18,000 IU compared with pigs from sows fed 3,000 IU. In conclusion, sow and pig serum 25(OH)D3, milk vitamin D3, and neonatal tissue vitamin D3 can be increased by increasing maternal vitamin D3, and nursery pig 25(OH)D3 can be increased by increasing dietary vitamin D3; however, sow and pig performance and neonatal bone mineralization was not influenced by increasing vitamin D3 dietary levels.

Maternal Vitamin D3 Supplementation during the Third Trimester of Pregnancy: Effects on Infant Growth in a Longitudinal Follow-Up Study in Bangladesh

To estimate the effects of prenatal vitamin D supplementation on infant growth in Dhaka, Bangladesh. Longitudinal follow-up of infants born at term or late preterm (≥34 weeks) to participants in a randomized double-blind trial of maternal third-trimester vitamin D3 (35 000 IU/wk; vitamin D ) vs placebo. Anthropometry was performed at birth, 1, 2, 4, 6, 9, and 12 months of age. The primary analysis (n = 145 overall; n = 134 at 1year) was a comparison of mean length-for-age z-score (LAZ) based on World Health Organization standards. LAZ was similar between groups at birth, but 0.44 (95% CI, 0.06-0.82) higher in vitamin D vs placebo at 1 year, corresponding to a sex-adjusted increase of 1.1 cm (95% CI, 0.06-2.0). Mean change in LAZ from birth to 1month was significantly greater in vitamin D (0.53 per month) vs placebo (0.19 per month; P = .004); but there was no significant divergence thereafter. In longitudinal (repeated-measures) analysis, average LAZ during infancy was 0.41 higher in vitamin D vs placebo (95% CI, 0.11-0.71, P = .01). Stunting was less common in vitamin D (17% of infants were ever stunted) vs placebo (31%; P = .049). Other anthropometric indices were similar between groups. Maternal vitamin D3 supplementation (35 000 IU/wk) during the third trimester of pregnancy enhanced early postnatal linear growth in a cohort of infants in Bangladesh.

Cord Blood Vitamin D Deficiency Is Associated With Respiratory Syncytial Virus Bronchiolitis

Respiratory syncytial virus (RSV) is the most important pathogen causing severe lower respiratory tract infection (LRTI) in infants. Epidemiologic and basic studies suggest that vitamin D may protect against RSV LRTI. To determine the association between plasma vitamin D concentrations at birth and the subsequent risk of RSV LRTI. A prospective birth cohort study was performed in healthy term neonates. Concentrations of 25-hydroxyvitamin D (25-OHD) in cord blood plasma were related to RSV LRTI in the first year of life, defined as parent-reported LRTI symptoms in a daily log and simultaneous presence of RSV RNA in a nose-throat specimen. The study population included 156 neonates. Eighteen (12%) developed RSV LRTI. The mean plasma 25-OHD concentration was 82 nmol/L. Overall, 27% of neonates had 25-OHD concentrations < 50 nmol/L, 27% had 50-74 nmol/L and only 46% had 25-OHD 75 nmol/L. Cord blood 25-OHD concentrations were strongly associated with maternal vitamin D3 supplementation during pregnancy. Concentrations of 25-OHD were lower in neonates who subsequently developed RSV LRTI compared with those who did not (65 nmol/L versus 84 nmol/L, P = .009). Neonates born with 25-OHD concentrations <50 nmol/L had a sixfold (95% confidence interval: 1.6-24.9; P = .01) increased risk of RSV LRTI in the first year of life compared with those with 25-OHD concentrations ≥ 75 nmol/L. Vitamin D deficiency in healthy neonates is associated with increased risk of RSV LRTI in the first year of life. Intensified routine vitamin D supplementation during pregnancy may be a useful strategy to prevent RSV LRTI during infancy.