Impact Of Maternal Vitamin Research Articles

Low vitamin D during pregnancy is associated with infantile eczema by up-regulation of PI3K/AKT/mTOR signaling pathway and affecting FOXP3 expression: A bidirectional cohort study

Vitamin D has received increasing attention because of its association with atopic disease development. Limited studies that have been done on the impact of maternal vitamin D levels during pregnancy on infantile eczema are still debatable. We wanted to discover the effect of maternal vitamin D on infantile eczema and explore whether regulatory T cells (Treg) play a role in this process. 219 pairs of mothers and children were enrolled. Maternal fasting venous blood was collected in pregnancy's second and third trimesters to determine vitamin D levels. Cord blood and placenta samples were collected during childbirth for detecting levels of genes, proteins and cytokines. Pediatricians followed up the prevalence of eczema in infants within 1 year. The reported rate of vitamin D deficiency and insufficiency was 35.6% and 28.3%. Lower maternal 25(OH)D3 levels were related to a higher risk of infantile eczema. Foxp3 gene expression is lower in cord blood of infants with eczema compared to infants without eczema. There was a positive correlation between maternal 25(OH)D3 levels and the expression of FOXP3 gene in cord blood. Compared to vitamin D sufficiency women, vitamin D deficiency women's placental FOXP3 protein expression was decreased and PI3K/AKT/mTOR protein was up-regulated. Our study demonstrates that low prenatal maternal vitamin D levels increased the risk of infantile eczema aged 0–1 year, which might be related to the downregulating of the FOXP3 gene expression in cord blood and decreased placental FOXP3 protein expression. Low placental FOXP3 protein was related with activating PI3K/AKT/mTOR signaling pathway.

Impact of Maternal Vitamin D Supplementation during Breastfeeding on Infant Serum Vitamin D Levels: A Narrative Review of the Recent Evidence.

Vitamin D supplementation for breastfed infants is recommended due to low levels of vitamin D in human milk and the high prevalence of vitamin D deficiency. The relationship between maternal vitamin D supplementation while breastfeeding and infant serum vitamin D levels is beginning to be described. A literature review was conducted that investigated the impact of maternal supplementation, with at least 4000 IU of vitamin D, on infant serum vitamin D levels. Inclusion criteria were publication between 2016-2022, primary research, exclusively breastfed infants, and mothers taking vitamin D supplements while breastfeeding. Exclusion criteria were publication prior to 2016, review articles, results that did not include infant serum vitamin D levels, and research using participants already included in this review. Over 90% of infants whose mothers took vitamin D supplements while breastfeeding had adequate serum vitamin D levels. The final mean serum vitamin D of all infant participants whose mothers consumed vitamin D supplementation was 66.7 nmol/L, while mean serum vitamin D in those whose mothers did not consume supplements was 33.5 nmol/L. Consumption of vitamin D supplements by lactating women exclusively breastfeeding their infants can lead to adequate serum vitamin D levels in their infants.

The Impact of Maternal Vitamin D Levels on Infant Health: A Review Article

Pregnancy is a unique and demanding time in terms of calcium and phosphate metabolism. Studies have shown that prevalence of vitamin D deficiency among pregnant women varies, as being 33% in US, 24% in Canada and 20-77% in Europe. Low maternal levels of vitamin D during pregnancy are associated with many neonatal outcomes, including small for gestational age (SGA), preterm birth, detrimental effect on offspring teeth and bone development in addition to the susceptibility to infectious diseases. Background: Pregnancy is a unique and demanding time in terms of calcium and phosphate metabolism. Vitamin D is one important for the developmental process and plays a crucial role for mineral balance, with rapidly growing bone susceptible to mineralization defects such as rickets [1]. Vitamin D deficiency has become a global public health issue, especially for pregnant women [2]. Several studies conducted on a large population have evaluated the effect of vitamin D deficiency during pregnancy and relate it to many adverse outcomes for both the mother and the child [3].

Maternal vitamin D deficiency affects the morphology and function of glycolytic muscle in adult offspring rats.

BackgroundFetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D (Vit. D) deficiency (VDD) on offspring lean mass development in the adult life of male and female animals.MethodsFemale rats (Wistar Hannover) were fed either a control (1000 IU Vit. D3/kg) or a VDD diet (0 IU Vit. D3/kg) for 6 weeks and during gestation and lactation. At weaning, male and female offspring were randomly separated and received a standard diet up to 180 days old.ResultsVitamin D deficiency induced muscle atrophy in the male (M‐VDD) offspring at the end of weaning, an effect that was reverted along the time. Following 180 days, fast‐twitch skeletal muscles [extensor digitorum longus (EDL)] from the M‐VDD showed a decrease (20%; P < 0.05) in the number of total fibres but an increase in the cross‐sectional area of IIB (17%; P < 0.05), IIA (19%; P < 0.05) and IIAX (21%; P < 0.05) fibres. The fibre hypertrophy was associated with the higher protein levels of MyoD (73%; P < 0.05) and myogenin (55% %; P < 0.05) and in the number of satellite cells (128.8 ± 14 vs. 91 ± 7.6 nuclei Pax7 + in the M‐CTRL; P < 0.05). M‐VDD increased time to fatigue during ex vivo contractions of EDL muscles and showed an increase in the phosphorylation levels of IGF‐1/insulin receptor and their downstream targets related to anabolic processes and myogenic activation, including Ser 473Akt and Ser 21/9GSK‐3β. In such muscles, maternal VDD induced a compensatory increase in the content of calcitriol (two‐fold; P < 0.05) and CYP27B1 (58%; P < 0.05), a metabolizing enzyme that converts calcidiol to calcitriol. Interestingly, most morphological and biochemical changes found in EDL were not observed in slow‐twitch skeletal muscles (soleus) from the M‐VDD group as well as in both EDL and soleus muscles from the female offspring.ConclusionsThese data show that maternal VDD selectively affects the development of type‐II muscle fibres in male offspring rats but not in female offspring rats and suggest that the enhancement of their size and fatigue resistance in fast‐twitch skeletal muscle (EDL) is probably due to a compensatory increase in the muscle content of Vit. D in the adult age.

Maternal serum retinol, 25(OH)D and 1,25(OH)2D concentrations during pregnancy and peak bone mass and trabecular bone score in adult offspring at 26-year follow-up.

BackgroundVitamin A and D deficiency is prevalent in pregnant women worldwide. Both vitamins are involved in fetal skeletal development. A positive association between maternal vitamin D levels and offspring bone mineral density (BMD) at adulthood has been observed. The impact of maternal vitamin A status in pregnancy on offspring peak bone mass remains unclear.Method and findingsForty-one mother-child pairs were recruited from a population-based prospective cohort study in Trondheim, Norway, where pregnant women were followed from gestational week 17. Their term-born infants were followed from birth (1986–88). Regression analyses were performed for vitamin A (retinol), 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)2D] in maternal serum (gestational weeks 17, 33, 37) and cord blood. Offspring BMD and spine trabecular bone score (TBS), a measure of bone quality, were analyzed by dual x-ray absorptiometry at 26 years. Average levels during pregnancy of retinol, 25(OH)D and 1,25(OH)2D were 1.66 (0.32) μmol/L, 59.0 (20.6) nmol/L, and 251.3 (62.4) pmol/L, respectively. 1,25(OH)2D levels were similar in those with 25(OH)D levels <30 and >75 nmol/L. After adjustment for maternal age, BMI, smoking, and education, and offspring birth weight, maternal serum retinol was positively associated with offspring spine BMD [mean change 30.8 (CI 7.6, 54.0) mg/cm2 per 0.2 μmol/L retinol], and with offspring TBS, although non-significant (p = 0.08). No associations were found between maternal 25(OH)D and 1,25(OH)2D levels and offspring bone parameters. Vitamin levels in cord blood were not associated with offspring BMD or TBS.ConclusionsThis is the first study to show an association between maternal vitamin A status and offspring peak bone mass. Our findings may imply increase future risk for osteoporotic fracture in offspring of mothers with suboptimal vitamin A level. No associations were observed between 25(OH)D and 1,25(OH)2D and offspring BMD.

Impact of maternal vitamin D deficiency on neonatal health and development

In recent years, domestic and foreign studies have found that vitamin D deficiency is widespread in adults and children.Neonates and pregnant women are at high risk of vitamin D deficiency.Vitamin D deficiency during pregnancy is associated with adverse pregnancy outcomes, such as premature birth, limited fetal growth and also has an adverse impact on the development of neonatal nervous system and respiratory disease susceptibility.This paper reviews the effects of vitamin D deficiency on neonates during pregnancy. Key words: Neonates; Pregnant women; Vitamin D deficiency

Early newborn ritual foods correlate with delayed breastfeeding initiation in rural Bangladesh.

BackgroundEarly and exclusive breastfeeding may improve neonatal survival in low resource settings, but suboptimal breastfeeding still exists in areas with high infant mortality. Prelacteal feeding, the practice of giving a non-breastmilk food as a neonate’s first food, has been associated with suboptimal breastfeeding practices. We examined the association of feeding a non-breastmilk food in the first three days of life (early neonatal food, or ENF) with time from birth to initiation of breastfeeding among 25,286 Bangladeshi mother-neonate pairs, in a secondary analysis of a randomized controlled trial in northwestern rural Bangladesh conducted from 2001–2007.MethodsTrained interviewers assessed the demographic characteristics during pregnancy. At three months postpartum, the interviewers visited participants again and retrospectively assessed demographic and breastfeeding characteristics surrounding the birth. We assessed the relationship between ENF and time to initiation of breastfeeding in hours in both unadjusted and adjusted linear regression analyses. We also calculated reverse cumulative distribution curves for time to initiation of breastfeeding and analyses were stratified by an infant’s ability to breastfeed normally at birth.ResultsThe mean ± SD time from birth to initiation of breastfeeding was 30.6 ± 27.9 hours. Only 2,535 (10.0%) of women reported initiating breastfeeding in the first hour after birth and 10,207 (40.4%) reported initiating breastfeeding in the first 12 hours after birth. In adjusted linear regression analyses, feeding ENF was associated with a significant increase in time, in hours, to breastfeeding initiation both among children not able to breastfeed at birth (37.4; 95% CI 33.3, 41.5) and among children able to breastfeed at birth (13.3; 95% CI 12.7, 14.0).ConclusionsFeeding ENF was strongly associated with delayed initiation of breastfeeding, even after adjusting for other related factors and stratifying on the neonate’s ability to suckle normally after birth. More research is needed to understand the impact of these findings on optimal breastfeeding in this setting. It is possible that ENF feeding and the ability to breastfeed immediately after birth are interrelated in their respective associations to suboptimal breastfeeding initiation. This study in a large population representative of other populations in rural South Asia, demonstrates significantly longer times to breastfeeding initiation than previously appreciated, with a possible important role of ENF feeding.Trial registrationThe randomized controlled trial on which this analysis is based, “Impact of Maternal Vitamin A or Beta-Carotene Supplementation on Maternal and Infant Mortality in Bangladesh”, was registered with ClinicalTrials.gov as trial number ID GHS-A-00-03-00019-00 and identifier NCT00198822. The identifier was first received September 12, 2005 (retrospectively registered). The first participant was enrolled in August 2001.Electronic supplementary materialThe online version of this article (doi:10.1186/s13006-016-0090-9) contains supplementary material, which is available to authorized users.

Maternal Vitamin A Supplementation Expands Adipose Progenitor Population through Promoting Vascular Development

Retinoic acid regulates various types of progenitor differentiation and tissue development including adipose development. However, the impact of maternal vitamin A supplementation on fetal adipose development and its long‐term consequence in adulthood remain unclear. To address, we supplemented maternal mice with 0, 15 or 30 IU/mL retinyl palmitate in water during gestation and lactation. Adipose tissue and serum of weanling offspring, and E7.5, 12.5 and 18.5 fetuses were collected. We found that retinoic acid is the main retinoid in fetuses that was elevated by maternal vitamin A supplementation. The populations of platelet‐derived growth factor receptor alpha positive (PDGFRα+) adipocyte progenitors in both fetuses and weaned offspring were increased due to vitamin A supplementation, which were correlated with heightened vascular density in adipose tissue at weaning. We further found that retinoic acid upregulated vascular endothelial growth factor α (VEGFα) which might explain the enhanced vasculogenesis in adipose tissue of fetuses supplemented with vitamin A. Using florescence tracing, we found that, under cold or retinoic acid stimulation, PDGFRα+ progenitor cells were located in neovascular system. In summary, our results reveal that maternal vitamin A supplementation increases offspring adipose progenitor populations by promoting vascular system development during the fetal stage, which is mediated by retinoic acid receptor signaling.Support or Funding InformationSupported by NIH R01HD067449 and USDA‐NIFA 2015‐67015‐23219

Maternal Vitamin D Status and Development of Asthma and Allergy in Early Childhood.

Vitamin D has an indisputable immunodulatory role in both lung and immune system development, which is initiated during fetal life and is mainly accomplished in the first years of extrauterine life. Several published studies have shown that low levels of vitamin D may increase the risk of developing asthma and allergic diseases. Moreover, vitamin D deficiency epidemic reported over the last decades coincides with an increase in the prevalence of asthma and allergies in westernized societies. Since placental transfer of 25(OH)D is the major source of vitamin D in the developing fetus, important questions concerning the impact of maternal vitamin D status on the outcome of pregnancy have arisen. The aim of this review is to present the current evidence regarding the determinants of vitamin D status in pregnancy as well as its role in the development of asthma and allergies in early childhood.

Impact of Maternal Vitamin D Insufficiency on Neonatal Bone and Fat Mass

Impact of Maternal Vitamin D Insufficiency on Neonatal Bone and Fat Mass

Vitamin D supplementation in pregnancy.

Vitamin D supplementation in pregnancy.

Maternal vitamin D deficiency causes smaller muscle fibers and altered transcript levels of genes involved in protein degradation, myogenesis, and cytoskeleton organization in the newborn rat

Epidemiologic data reveal associations between low serum concentrations of 25-hydroxyvitamin D (25(OH)D) and higher risk of falls and muscle weakness. Fetal stage is critical for the development of skeletal muscle, but little information is available on the impact of maternal vitamin D deficiency on muscles of offspring. To investigate the morphology and transcriptome of gastrocnemius muscle in newborns in response to maternal vitamin D deficiency, 14 female rats were fed either a vitamin D₃ deficient (0 IU/kg) or a vitamin D₃ adequate diet (1000 IU/kg) 8 weeks prior to conception, during pregnancy, and lactation. Analysis of cholecalciferol, 25(OH)D₃ and 1,25-dihydroxyvitamin D₃ show that dams fed the vitamin D deficient diet and their newborns suffered from a relevant vitamin D deficiency. Muscle cells of vitamin D deficient newborns were smaller than those of vitamin D adequate newborns (p < 0.05). Muscle transcriptome of the newborns revealed 426 probe sets as differentially expressed (259 upregulated, 167 downregulated) in response to vitamin D deficiency (fold change ≥1.5, p < 0.05). The effected genes are involved in protein catabolism, cell differentiation and proliferation, muscle cell development, and cytoskeleton organization. Maternal vitamin D deficiency has a major impact on morphology and gene expression profile of skeletal muscle in newborns.

Impact of Maternal Vitamin D Status During Pregnancy on the Prevalence of Neonatal Vitamin D Deficiency

Maternal vitamin D deficiency is not uncommon. The lack of vitamin D during pregnancy may result in poor fetal growth and altered neonatal development that may persist into later life. Recognition of risk factors and early detection of vitamin D deficiency during pregnancy is important in order to prevent neonatal vitamin D deficiency and related complications. The aim of the current study is to assess the effect of maternal vitamin D status on the neonatal vitamin D stores. A total of 92 pregnant women at the end of the 3rd trimester and their newborns were recruited from Al Khafji Joint Operation Hospital, Saudi Arabia, during the year 2011. Maternal and cord blood samples were taken for determination of serum levels of circulating 25-hydroxyvitamin D3 [25(OH)D3] concentration, serum calcium (Ca++), phosphorus (PO4) and alkaline phosphatase (ALP). Compared with pregnant women with adequate vitamin D levels, women deficient in vitamin D had infants with vitamin D deficiency (X±SD 33.44±18.33 nmol/L vs 55.39±17.37 nmol/L, P=0.01). Maternal and neonatal serum 25(OH)D3 levels showed a positive correlation with serum Ca++ and negative correlation with serum PO4 and ALP. Neonatal 25(OH)D was related to maternal 3rd trimester levels (r=0.89, P=0.01). The newborn serum 25(OH)D3 concentrations rely on maternal vitamin D status. Poor maternal vitamin D status may adversely affect neonatal vitamin D status and, consequently, calcium homeostasis.

The impact of vitamin D in pregnancy on extraskeletal health in children: a systematic review

The impact of maternal vitamin D status in pregnancy on the extraskeletal health of the offspring has become a "hot topic" with a potential for cost-beneficial prevention. The objective of this study was to systematically review the level I and II evidence. PubMed, Embase and Cochrane databases were searched using the MeSH terms "vitamin D" AND "pregnancy" until 1 January 2012. The search was limited to randomized controlled trials (evidence level I) and observational studies (evidence level II) in humans and in the English language. Papers reporting on vitamin D supplementation in combination with other supplements, or not reporting on 25OHD or outcomes of the offspring were excluded. Six randomized controlled trials and 24 observational studies were finally included. In randomized controlled studies, vitamin D supplementation resulted in increased birthweight in one study, but showed no effect in five other studies. In cohort and case-control studies, higher vitamin D intake, or higher 25OHD, was associated with increased birthweight in large studies only, and modified by vitamin D receptor polymorphisms and by race (U-shaped in Caucasians in one unconfirmed study). The risks of HIV mother-to-child transmission, rhinitis symptoms and eczema were lower. Data were conflicting on the effect on respiratory infections and wheezing, whereas U-shaped associations to inhalant allergen-specific IgE at five years and to schizophrenia were reported in unconfirmed studies. The risk of type 1 diabetes at 15 years was lower or unchanged. It is concluded that observational studies suggest an effect of vitamin D on several outcomes. U-Shaped associations warrant caution.

Role of vitamin D in modulating gestational diabetes

Low maternal levels of major circulating form of vitamin D could be a perplexing factor that leads to expression of gestational diabetes mellitus (GDM). Insufficient or deficient levels of vitamin D may allow diabetic insult during pregnancy leading to gestational diabetes and inducing changes in a variety of key functional molecules and gene expression. Autocrine metabolism of vitamin D promotes anti-inflammatory response to maternal decidua and fetal trophoblasts. Immunomodulatory actions of vitamin D are likely to be compromised under conditions of low vitamin D levels with potential detrimental physiological consequences. Recent data are now available to implicate autocrine/paracrine impact of maternal vitamin D status can result in both increased insulin resistance and reduced insulin secretion, linking inflammation to metabolic disorder in the mother. Insulin and cytokines are the main contributors to the cascade of events and potential regulators of placental function in GDM. This article aims at exploring the possible mechanisms underlying GDM that could be regulated by pleotropic effects of vitamin D.