Intrauterine vitamin D nutrition and postnatal growth in Asian infants.

Brooke, O G; F, Butters; Wood, Catherine

doi:10.1136/bmj.283.6298.1024

Cited by 123 publications

(78 citation statements)

References 5 publications

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“…With restricted vitamin D intake and sunlight exposure, maternal deficiency may occur, as has been documented in a number of studies. [107][108][109][110][111][112][113] Recent work has demonstrated that in men and nonpregnant women, oral vitamin D intake over a 4-to 5-month period will increase circulating 25-OH- [108][109][110][111][112][113][114][115] The significance of these findings for those who care for the pediatric population is that when a woman who has vitamin D deficiency gives birth, her neonate also will be deficient.…”

Section: Pregnancy Vitamin D and The Fetusmentioning

confidence: 99%

“…Another study of the intrauterine effect of maternal vitamin D status revealed a significant association between umbilical cord 25-OH-D concentrations and head circumference at 3 and 6 months' postnatal age that persisted after adjustment for confounding factors. 109,111 A study performed in the United Kingdom during the 1990s demonstrated that higher maternal vitamin D status during pregnancy was associated with improved bonemineral content and bone mass in children at 9 years of age. 123 Given the growing evidence that adequate maternal vitamin D status is essential during pregnancy, not only for maternal well-being but also for fetal development, 71,122,124,125 health care professionals who provide obstetric care should consider assessing maternal vitamin D status by measuring the 25-OH-D concentrations of pregnant women.…”

Section: Pregnancy Vitamin D and The Fetusmentioning

confidence: 99%

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Prevention of Rickets and Vitamin D Deficiency in Infants, Children, and Adolescents

Wagner

Greer²

2008

Pediatrics

1,370

926

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Rickets in infants attributable to inadequate vitamin D intake and decreased exposure to sunlight continues to be reported in the United States. There are also concerns for vitamin D deficiency in older children and adolescents. Because there are limited natural dietary sources of vitamin D and adequate sunshine exposure for the cutaneous synthesis of vitamin D is not easily determined for a given individual and may increase the risk of skin cancer, the recommendations to ensure adequate vitamin D status have been revised to include all infants, including those who are exclusively breastfed and older children and adolescents. It is now recommended that all infants and children, including adolescents, have a minimum daily intake of 400 IU of vitamin D beginning soon after birth. The current recommendation replaces the previous recommendation of a minimum daily intake of 200 IU/day of vitamin D supplementation beginning in the first 2 months after birth and continuing through adolescence. These revised guidelines for vitamin D intake for healthy infants, children, and adolescents are based on evidence from new clinical trials and the historical precedence of safely giving 400 IU of vitamin D per day in the pediatric and adolescent population. New evidence supports a potential role for vitamin D in maintaining innate immunity and preventing diseases such as diabetes and cancer. The new data may eventually refine what constitutes vitamin D sufficiency or deficiency.

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Section: Pregnancy Vitamin D and The Fetusmentioning

confidence: 99%

Section: Pregnancy Vitamin D and The Fetusmentioning

confidence: 99%

Prevention of Rickets and Vitamin D Deficiency in Infants, Children, and Adolescents

Wagner

Greer²

2008

Pediatrics

1,370

926

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“…In pregnant women at risk of low vitamin D status, vitamin D supplementation in mid-late gestation with doses ranging from 10 to 30 mg/d (400 to 1200 IU/d) has demonstrated greater cord and plasma Ca concentrations, lower plasma ALP concentrations, smaller fontanelle size and lower incidence of growth retardation and neonatal hypocalcaemia in the newborns (244,254 -260) and effects on subsequent infant growth (255) . Other studies have reported no effects on birth weight (260) or infant forearm bone mineral (261) .…”

Section: Influence On the Childmentioning

confidence: 99%

Calcium economy in human pregnancy and lactation

et al. 2012

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Pregnancy and lactation are times of additional demand for Ca. Ca is transferred across the placenta for fetal skeletal mineralisation, and supplied to the mammary gland for secretion into breast milk. In theory, these additional maternal requirements could be met through mobilisation of Ca from the skeleton, increased intestinal Ca absorption efficiency, enhanced renal Ca retention or greater dietary Ca intake. The extent to which any or all of these apply, the underpinning biological mechanisms and the possible consequences for maternal and infant bone health in the short and long term are the focus of the present review. The complexities in the methodological aspects of interpreting the literature in this area are highlighted and the inter-individual variation in the response to pregnancy and lactation is reviewed. In summary, human pregnancy and lactation are associated with changes in Ca and bone metabolism that support the transfer of Ca between mother and child. The changes generally appear to be independent of maternal Ca supply in populations where Ca intakes are close to current recommendations. Evidence suggests that the processes are physiological in humans and that they provide sufficient Ca for fetal growth and breast-milk production, without relying on an increase in dietary Ca intake or compromising long-term maternal bone health. Further research is needed to determine the limitations of the maternal response to the Ca demands of pregnancy and lactation, especially among mothers with marginal and low dietary Ca intake, and to define vitamin D adequacy for reproductive women.

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“…Sixty minutes later, 45 Ca and 51 Cr-EDTA were administered to the mother by intracardiac injection, and the fetuses were removed 30 min after that. PTHrP and PTHrP [67][68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86] increased the accumulation of 45 Ca/ 51 Cr-EDTA to a value not different from WT littermates, whereas PTH 1-84 and PTHrP had no significant effect (340). Importantly, injections of mid-molecular PTHrP had no effect in WT fetuses, which suggests that the WT fetus may already have maximally stimulated PTHrP responses on the placenta, such that pharmacological treatment had no additional effect.…”

Section: B Regulation Of Placental Mineral Transportmentioning

confidence: 99%

“…Peptides that contained a mid-region portion of PTHrP (PTHrP , PTHrP , and PTHrP [67][68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86] ) increased the rate of change in the concentration of 45 Ca/ 51 Cr-EDTA in the umbilical vein, whereas PTHrP 1-34 and PTH 1-34 had no effect (6,96,556). When PTHrP 38 -94 was later determined to be the structure of mid-regional PTHrP (490,517), these investigators repeated the experiments and confirmed that PTHrP 38 -94 also significantly increased the rate of placental calcium transport in perfused placentas from previously thyroparathyroidectomized fetal lambs (745).…”

Section: B Regulation Of Placental Mineral Transportmentioning

confidence: 99%

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

211

188

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Mineral and bone metabolism are regulated differently in utero compared with the adult. The fetal kidneys, intestines, and skeleton are not dominant sources of mineral supply for the fetus. Instead, the placenta meets the fetal need for mineral by actively transporting calcium, phosphorus, and magnesium from the maternal circulation. These minerals are maintained in the fetal circulation at higher concentrations than in the mother and normal adult, and such high levels appear necessary for the developing skeleton to accrete a normal amount of mineral by term. Parathyroid hormone (PTH) and calcitriol circulate at low concentrations in the fetal circulation. Fetal bone development and the regulation of serum minerals are critically dependent on PTH and PTH-related protein, but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids. After birth, the serum calcium falls and phosphorus rises before gradually reaching adult values over the subsequent 24 -48 h. The intestines are the main source of mineral for the neonate, while the kidneys reabsorb mineral, and bone turnover contributes mineral to the circulation. This switch in the regulation of mineral homeostasis is triggered by loss of the placenta and a postnatal fall in serum calcium, and is followed in sequence by a rise in PTH and then an increase in calcitriol. Intestinal calcium absorption is initially a passive process facilitated by lactose, but later becomes active and calcitriol-dependent. However, calcitriol's role can be bypassed by increasing the calcium content of the diet, or by parenteral administration of calcium.

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Intrauterine vitamin D nutrition and postnatal growth in Asian infants.

Abstract: range of movement. Follow-up for six weeks showed no bowel abnormality and minor residual swelling of the knee.

Cited by 123 publications

References 5 publications

Prevention of Rickets and Vitamin D Deficiency in Infants, Children, and Adolescents

Prevention of Rickets and Vitamin D Deficiency in Infants, Children, and Adolescents

Calcium economy in human pregnancy and lactation

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

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