Selenium Status Of Infants Research Articles

Infant Iodine and Selenium Status in Relation to Maternal Status and Diet During Pregnancy and Lactation.

Iodine and selenium are essential trace elements. Recent studies indicate that pregnant and lactating women often have insufficient intake of iodine and selenium, but the impact on fetal and infant status is unclear. Here, we assessed iodine and selenium status of infants in relation to maternal intake and status of these trace elements in the birth cohort NICE, conducted in northern Sweden (n = 604). Iodine was measured in urine (UIC) in gestational week 29, and in breast milk and infant urine 4 months postpartum, while selenium was measured in maternal plasma and erythrocytes in gestational week 29, and in breast milk and infant erythrocytes 4 months postpartum, in both cases using ICP-MS. Maternal intake was assessed with semi-quantitative food frequency questionnaires in gestational week 34 and at 4 months postpartum. The median intake of iodine and selenium during pregnancy (98 and 40 μg/d, respectively) and lactation (108 and 39 μg/d, respectively) was below recommended intakes, reflected in insufficient status (median UIC of 113 μg/L, median plasma selenium of 65 μg/L). Also, breast milk concentrations (median iodine 77 μg/L, median selenium 9 μg/L) were unlikely to meet infant requirements. Median UIC of the infants was 114 μg/L and median erythrocyte selenium 96 μg/kg, both similar to the maternal concentrations. Infant UIC correlated strongly with breast milk levels (rho = 0.64, p < 0.001). Their erythrocyte selenium correlated with maternal erythrocyte selenium in pregnancy (rho = 0.38, p < 0.001), but not with breast milk selenium, suggesting formation of prenatal reserves. Our results indicate that the transport of iodine and selenium to the fetus and infant is prioritized. Still, it is uncertain whether most infants had sufficient intakes. Further, the results might indicate an involvement of iodine in asthma development during the first year of life, which is essential to follow up. The low maternal and infant dietary intake of both iodine and selenium, especially when the mothers did not use supplements or iodized table salt, suggest a need for a general screening of women and young children.

Factors Affecting Selenium Status in Infants on Parenteral Nutrition Therapy.

Selenium is an essential micronutrient that must be supplemented in infants and young children on exclusive parenteral nutrition (PN). We examined selenium status and clinical factors associated with a deficiency in infants on PN. This was a retrospective cohort study of pediatric patients receiving PN with routine monitoring of selenium status. Deficiency was diagnosed using age-based norms of plasma selenium status. Associations between selenium deficiency and the following clinical factors were examined: birthweight status: extremely low birthweight (ELBW) versus very low birthweight (VLBW) versus low birthweight (LBW) versus normal birthweight (NBW), serum albumin status, presence of cholestasis, and co-administration of enteral feeds. A total of 42 infants were included with gestational age [median (interquartile range)] 28 weeks (25,34). The prevalence of selenium deficiency was 80% and the prevalence of albumin deficiency was 87.5%. The odds of selenium deficiency were higher in ELBW infants (odds ratio = 17.84, 95% confidence interval [4.04-78.72], P < 0.001) and VLBW infants (odds ratio = 16.26, 95% confidence interval [1.96-135.04], P < 0.001) compared to NBW infants. The odds of selenium deficiency were 5-fold higher in patients with low serum albumin (odds ratio = 5.33, 95% confidence interval [1.39-20.42], P = 0.015). There were no associations seen between selenium status and presence of cholestasis or co-administration of enteral feeds. In this cohort of infants on PN therapy, the main clinical factors associated with selenium deficiency were presence of hypoalbuminemia and history of ELBW or VLBW. These findings support dual measurement of serum albumin and serum selenium to improve interpretation of selenium status.

Feeding Selenium Supplemented Formula Improves Selenium Status in Infants With Bronchopulmonary Dysplasia

LEARNING OUTCOME: To determine if a selenium supplemented formula could improve selenium status in infants with BPD.The objective of this study was to determine if a selenium supplemented formula designed for bronchopulmonary dysplasia (BPD) could improve the depressed selenium and respiratory status associated with infants who have BPD. Thirty-two infants with BPD were randomly assigned to receive a selenate supplemented formula (BPD30; 35 μg Se/L) or a traditional premature infant formula (PF24) not supplemented with selenium (7.8 nq Se/L) for four weeks beginning on the first day the infants were capable of receiving > 120 kcal/kg of formula per day. Plasma and erythrocyte selenium concentrations and glutathione peroxidase (GPx) activities were analyzed at day 1 and day 28 of the study. At study day 28, plasma selenium (μg/L) and plasma GPx activities (units/ml) were significantly greater (P <.05) for infants fed BPD30 than for infants fed PF24. There were no significant differences in outcome variables during the four week study. The results of this study indicate that it is possible to improve the plasma selenium and GPx activity of infants with BPD through selenium supplementation with selenate.

Selenium status in infants and children with phenylketonuria and in maternal phenylketonuria.

The selenium status was investigated in 87 patients of the German Collaborative Study of Phenylketonuria (PKU) (mean age 9.7 years). The selenium values and glutathione peroxidase activity in plasma and erythrocytes were negatively correlated to the quality of dietary management (mean plasma phenylalanine value). Despite a low selenium state, the children showed no clinical sign of deficiency and almost all biochemical parameters checked were normal. In the low selenium state thyroxine values are increased and decline during selenium supplementation, whereas tri-iodothyronine and thyroid stimulating hormone levels remain unchanged. The reduction in glutathione peroxidase activity in plasma was more pronounced than in the erythrocytes pointing to a different availability of both enzymes for selenium. In addition we estimated the selenium status in 29 women with PKU during pregnancy. In 32 healthy pregnant women we observed a decrease in plasma selenium values and the glutathione peroxidase activity in the third trimester, whereas the erythrocyte glutathione peroxidase activity remained stable. In contrast to the healthy women we found in the PKU group a steady decrease of all selenium parameters tested during the whole pregnancy. During the long-term low-dose selenium supplementation in PKU children the glutathione peroxidase activity of plasma and erythrocytes increased. They reached a similar plateau after the application of inorganic or organic selenium compounds. In contrast the selenium values of plasma and whole blood showed only a plateau after the application of sodium selenite. The supplementation with low doses of selenium in the form of selenomethionine increased the plasma and whole blood selenium values constantly within the first 9 months. Therefore selenomethionine supplementation cannot be recommended.

Selenium status of infants is influenced by supplementation of formula or maternal diets

Plasma selenium of infants fed proprietary formula was significantly less than that in infants fed human milk. Addition of selenite to the formula (0.253 mumol Se/L) increased plasma selenium and activities of glutathione peroxidase (GPx) and total peroxidase (Px). However, erythrocyte selenium decreased significantly during the 12-wk study in infants receiving human milk or formula with or without supplemental selenite. Infants fed human milk from women receiving 0 or 200 micrograms supplemental selenium as selenomethionine or selenium-enriched yeast had plasma selenium that paralleled changes in their selenium intake. Plasma GPx and Px activities were unrelated to human milk selenium intake. Milk from women given either selenium supplement prevented the decline in infant erythrocyte selenium. Results of these studies suggest that the method of feeding modifies the infant's apparent selenium status and that the molecular form of selenium provided and/or its interaction with other milk constituents are determinants of infant selenium status.

The vitamin E and selenium status of infants and the sudden infant death syndrome

The selenium levels in plasma and whole blood samples from confirmed sudden infant death (SID) victims, normal infants, adults, and full term mothers, as well as plasma vitamin E levels in SID victims and normal adults, have been determined. The SID plasma vitamin E levels are low but still comparable to published values for normal and premature infants. The selenium levels of SID whole blood and plasma are also significantly lower than normal adult values, but nearly identical to those of infant controls. Although these results do not confirm the hypothesis that vitamin E and/or selenium deficiency has a primary role in the etiology of SID, their low levels in infants merits further attention as a possible secondary factor in the etiology of SID and as a general problem in infant nutrition and health.