Epilepsy is a nervous system abnormality that may be caused by unknown exposures during fetal development. Studies have shown neuroprotective effects of early exposure to vitamin D in other neurological disorders, and seasonal variation in birth of children with epilepsy. We aimed to investigate if neonatal 25(OH)D₃ was associated with risk of childhood epilepsy.

This case-cohort study compared neonatal 25(OH)D₃ levels from children with epilepsy (n = 403) and a random selected cohort of controls (n = 1163), assessing the hazard of first epilepsy diagnosis between 1 and 4 years of age from a weighted Cox proportional hazard model. Analyses were adjusted for parental education, maternal age, maternal epilepsy, maternal ethnicity, and gestational age, and additionally for season of birth and smoking during pregnancy.

The mean (standard deviation [SD]) of neonatal 25(OH)D₃ levels were 30.8(19.6) nmol/L among cases and 28.5(19.4) nmol/L among the cohort. The hazard ratio (HR) of epilepsy was in a dose-response pattern higher among children from the highest neonatal 25(OH)D₃ quintiles (P-trend = .004). Results were unchanged after including season of birth in the analysis, where a significantly higher HR of epilepsy was observed among children in the two highest quintiles compared to children in the lowest quintile (Q4: HR_adj  1.62, 95% CI 1.07-2.47 and Q5: HR_adj  1.86, 95% CI 1.21-2.86).

In this study, the risk of childhood epilepsy increased with neonatal 25(OH)D₃ categories in a dose-response pattern, suggesting an association between a high neonatal 25(OH)D₃ and the risk of childhood epilepsy. Considering that adjusting for season of birth strengthened the results, we conclude that maternal intake of vitamin D, and not vitamin D from sun exposure, was the vitamin D source associated with epilepsy. Although we cannot, in the present study, control for compounds in the diet like pollutants or heavy metals, which may correlate with dietary vitamin D, future studies investigating fetal origin of epilepsy should focus on compounds correlating with vitamin D.

Intelligence has a strong influence on life capability, and thus, identifying early modifiable risk factors related to cognitive ability is of major public health interest. During pregnancy, vitamin D is transported from the mother to the fetus through the placenta in the form of 25-hydroxyvitamin D (25(OH)D). Levels of 25(OH)D have in some studies been associated with childhood neurodevelopment; however, results from all studies are not in agreement. We investigated if neonatal 25(OH)D₃ concentrations were associated with Børge Priens IQ test score (BPP) in young adulthood.

In this nested cohort study, 25(OH)D₃ concentrations were measured in dried blood spots from 818 newborns. We followed the children for their IQ BPP test scores in the Danish Conscription Register, which holds information on test results from the BPP test on individuals who have been recruited for Danish mandatory military draft board examination. Using general linear models, we investigated the crude and adjusted relationship between quintiles of 25(OH)D₃ concentrations and BPP IQ test results.

The study population consisted of 95.8% men, with a mean age of 19.4 years. The median and range of the neonatal 25(OH)D₃ levels were 26.2 nmol/L (0-104.7 nmol/L). The overall Wald test did not show an association between neonatal 25(OH)D₃ levels and BPP IQ scores (p = 0.23); however, individuals within the 3rd (BPP IQ = 101.0, 98.0-103.9) and 4th (BPP IQ = 101.2, 99.1-104.3) quintiles had slightly higher BPP IQ scores than individuals from the first quintile (BPP IQ = 97.6, 94.6-100.6).

Our results support the hypothesis that individuals with the lowest levels of neonatal vitamin D might have slightly lower BPP. However, more studies are needed with larger study populations to confirm our results.

The aim of this work was to assess whether neonatal levels of 25-hydroxyvitamin D (25(OH)D) are associated with risk of developing type 1 diabetes before the age of 18 years.

Two large-scale studies with different designs-a case-cohort and a case-control-were conducted using Danish national register data and biobank material. Weighted Cox regression and conditional logistic regression were used to calculate HRs and ORs, respectively. The concentration of 25(OH)D was assessed from neonatal dried blood spots using highly sensitive liquid chromatography-tandem mass spectrometry. Quintiles of 25(OH)D3 were used in the main analyses.

The case-cohort study included 912 type 1 diabetes cases and 2866 individuals without type 1 diabetes born in Denmark between 1981 and 2002 and followed up until the end of 2012. The case-control study included 527 matched case-control pairs born between 1981 and 1999 and followed up until May 2004. Both studies found no association between 25(OH)D3 levels and later risk of developing type 1 diabetes. The neonatal total 25(OH)D levels in the studies were low: 46% (case-cohort study) and 51% (case-control study) of individuals had 25(OH)D levels <25 nmol/l.

Our two large-scale national studies showed that 25(OH)D3 levels around the time of birth were not associated with later type 1 diabetes risk. Whether higher levels of 25(OH)D3 during pregnancy, acquired by higher doses of supplementation than are recommended today in most countries, could protect the offspring against type 1 diabetes cannot be ruled out by the present studies.

Insufficient supply of vitamin D during early development may negatively affect offspring growth.

We examined the association between umbilical cord (UC) serum 25-hydroxyvitamin D (25(OH)D) concentrations and infant size in a study of two Faroese birth cohorts of 1038 singleton infants. In the third trimester, the pregnant women completed questionnaires, and clinical examination included birthweight, head circumference, and infant length at age 14 days.

Fifty-three percent of the newborn population had UC 25(OH)D < 25 nmol/L as determined by LC-MS/MS. Using multiple linear regression models with adjustment for pre-pregnancy BMI, sex, parity, gestational age, or infant age at examination, season of birth, smoking, gestational diabetes, examiner, and cohort identity, we found no relationship between birthweight or head circumference and UC 25(OH)D. However, infants with vitamin D status <12 nmol/L had a 0.49 (95% confidence interval 0.05, 0.93) cm lower length than infants with vitamin D status >50 nmol/L in models further adjusted for birthweight.

Our data suggest that umbilical cord serum 25(OH)D concentrations are positively associated with infant length but not with birthweight and head circumference. Although the paediatric relevance of the observed association is unclear, the possible long-term consequences of late-pregnancy hypovitaminosis D deserve attention.

Neonatal osteopenia is an important area of interest for neonatologists due to continuing increased survival of preterm infants. It can occur in high-risk infants such as preterm infants, infants on long-term diuretics or corticosteroids, and those with neuromuscular disorders. Complications such as rickets, pathological fractures, impaired respiratory function and poor growth in childhood can develop and may be the first clinical evidence of the condition. It is important for neonatologists managing such high-risk patients to regularly monitor biochemical markers for evidence of abnormal bone turnover and inadequate mineral intake in order to detect the early phases of impaired bone mineralization. Dual-energy X-ray absorptiometry has become an increasingly used research tool for assessing bone mineral density in children and neonates, but more studies are still needed before it can be used as a useful clinical tool. Prevention and early detection of osteopenia are key to the successful management of this condition and oral phosphate supplements should be started as soon as is feasible.

Fetal and postnatal bone development is by tradition viewed as a process of bone mineral accretion or an increase in bone mass. Accordingly, previous approaches to bone development in neonatology and early childhood have emphasized the determinants of peak bone mass and their relationship to osteopenia, osteoporosis and fractures in later life. This suggests that the neonatal period and early childhood is an important period for bone mineral accrual, and that peak bone mass may be correlated with subsequent skeletal health. Nevertheless, describing fetal and postnatal bone development just in terms of changes in mass or density means looking at bones as if they were amorphous heaps of calcium and phosphorus. In reality, of course, bones are complex three-dimensional structures. It is therefore important to create conditions that stimulate bones to become more stable. We suggest that functional bone physiology can be used to explain fetal and postnatal bone development and to devise strategies for improved bone development in both premature infants and neonates.

Vitamins A and E are two potent antioxidant nutrients that play a significant role in immune function. In contrast to the numerous studies of vitamin A and E status in children, adolescents, and adults, information on term infants, particularly breast-fed infants, is scarce. The goals of the present investigation were to examine the vitamins A and E nutritional status of term breast-fed infants at birth and to assess retinol and tocopherol plasma levels during a 3-month supplementation trial.

The study was a prospective, blinded comparison of a supplementation protocol with a placebo in a group of consecutively recruited term newborns. The supplemented group received 3000 IU vitamin A and 5 IU vitamin E orally. The placebo group received a solution of similar viscosity and organoleptic characteristics. Vitamin A and E were separated by reverse-phase high-performance liquid chromatography on a C18 Spectrasyl column and quantified by ultraviolet spectrophotometry.

Vitamin A and E levels steadily increased with age in both groups of infants. However, levels at 3 months were higher in the supplemented than in the control group.

The data show that supplementation with 3000 IU vitamin A and 5 IU vitamin E for 3 months increases circulating vitamin levels in newborn term babies compared with those in nonsupplemented infants.

During pregnancy, maternal serum concentrations of 25-hydroxyvitamin D, the circulating form of vitamin D, correlate with dietary vitamin D intake. Maternal serum concentrations of 1,25-dihydroxyvitamin D, the hormonal circulating and active form of vitamin D, are elevated during pregnancy; 1,25-dihydroxyvitamin D is synthesized mainly by the decidual cells of the placenta and allows for increased calcium absorption. The fetus is entirely dependent on the mother for its supply of 25-hydroxyvitamin D, which is believed to cross the placenta. Hypocalcemia and increased parathyroid hormone secretion induce synthesis of 1,25-dihydroxyvitamin D after birth in both full-term and preterm neonates. Nevertheless, serum concentrations of 25-hydroxyvitamin D are a rate-limiting factor in the synthesis of 1,25-dihydroxyvitamin D. In vitamin D-replete infants, circulating 1,25-dihydroxyvitamin D concentrations are higher than those observed in older infants. In countries where dairy products are not routinely supplemented with vitamin D, maternal vitamin D supplementation during pregnancy is necessary. However, there is no indication for the use of pharmacologic doses of vitamin D or its metabolites in the perinatal period.