Zinc is required for multiple metabolic processes as a structural, regulatory, or catalytic ion. Cellular, tissue, and whole-body zinc homeostasis is tightly controlled to sustain metabolic functions ...over a wide range of zinc intakes, making it difficult to assess zinc insufficiency or excess. The BOND (Biomarkers of Nutrition for Development) Zinc Expert Panel recommends 3 measurements for estimating zinc status: dietary zinc intake, plasma zinc concentration (PZC), and height-for-age of growing infants and children. The amount of dietary zinc potentially available for absorption, which requires an estimate of dietary zinc and phytate, can be used to identify individuals and populations at risk of zinc deficiency. PZCs respond to severe dietary zinc restriction and to zinc supplementation; they also change with shifts in whole-body zinc balance and clinical signs of zinc deficiency. PZC cutoffs are available to identify individuals and populations at risk of zinc deficiency. However, there are limitations in using the PZC to assess zinc status. PZCs respond less to additional zinc provided in food than to a supplement administered between meals, there is considerable interindividual variability in PZCs with changes in dietary zinc, and PZCs are influenced by recent meal consumption, the time of day, inflammation, and certain drugs and hormones. Insufficient data are available on hair, urinary, nail, and blood cell zinc responses to changes in dietary zinc to recommend these biomarkers for assessing zinc status. Of the potential functional indicators of zinc, growth is the only one that is recommended. Because pharmacologic zinc doses are unlikely to enhance growth, a growth response to supplemental zinc is interpreted as indicating pre-existing zinc deficiency. Other functional indicators reviewed but not recommended for assessing zinc nutrition in clinical or field settings because of insufficient information are the activity or amounts of zinc-dependent enzymes and proteins and biomarkers of oxidative stress, inflammation, or DNA damage.
BACKGROUND:Poor lifestyle behaviors are leading causes of preventable diseases globally. Added sugars contribute to a diet that is energy dense but nutrient poor and increase risk of developing ...obesity, cardiovascular disease, hypertension, obesity-related cancers, and dental caries.
METHODS AND RESULTS:For this American Heart Association scientific statement, the writing group reviewed and graded the current scientific evidence for studies examining the cardiovascular health effects of added sugars on children. The available literature was subdivided into 5 broad subareaseffects on blood pressure, lipids, insulin resistance and diabetes mellitus, nonalcoholic fatty liver disease, and obesity.
CONCLUSIONS:Associations between added sugars and increased cardiovascular disease risk factors among US children are present at levels far below current consumption levels. Strong evidence supports the association of added sugars with increased cardiovascular disease risk in children through increased energy intake, increased adiposity, and dyslipidemia. The committee found that it is reasonable to recommend that children consume ≤25 g (100 cal or ≈6 teaspoons) of added sugars per day and to avoid added sugars for children <2 years of age. Although added sugars most likely can be safely consumed in low amounts as part of a healthy diet, few children achieve such levels, making this an important public health target.
The rapid pace of fetal development by far exceeds any other stage of the life span, and thus, environmental influences can profoundly alter the developmental course. Stress during the prenatal ...period, including malnutrition and inflammation, impact maternal and fetal neurodevelopment with long-term consequences for physical and mental health of both the mother and her child. One primary consequence of maternal malnutrition, inflammation, and other sources of prenatal stress is a poor birth outcome, such as prematurity or growth restriction. These phenotypes are often used as indications of prenatal adversity. In fact, the original evidence supporting the fetal programming hypothesis came from studies documenting an association between birth phenotype and the development of subsequent physical and mental health problems. Fetal growth restriction in both term and preterm infants is associated with neonatal morbidities and a wide variety of behavioral and psychological diagnoses in childhood and adolescence, including attention-deficit/hyperactivity disorder, anxiety, depression, internalizing and thought problems, poor social skills, and autism spectrum disorder. Improving maternal-child health requires interventions that begin before pregnancy and continue throughout gestation and into the postpartum period. Such interventions might include supporting pregnancy intention, maternal nutrition, health/medical care, mental health, and providing social support. This article discusses the impact of maternal nutrition and inflammation during preconception and pregnancy among women living in low-resource settings, with an emphasis on key knowledge gaps that need to be addressed to guide program and policy decisions at local, regional and global levels.
The critical importance of adequate zinc status to human health, including normal growth and development, is indisputable. The high prevalence of zinc deficiency on a global basis and its importance ...to public health have been well documented through large-scale randomized controlled zinc supplementation trials. Similar evidence in the clinical setting, however, is much less widely available due to the nonspecific features of zinc deficiency and to the lack of sensitive biomarkers to detect zinc deficiency, especially that of a mild degree of severity. The current understanding of zinc homeostasis indicates that the primary determinants of zinc absorption are the amount of zinc ingested and dietary phytate, the latter having a major effect on zinc bioavailability. In normal as well as in many pathologic conditions, the gastrointestinal tract is the major site of zinc losses resulting from secretion of endogenous zinc into the lumen and subsequent excretion in the feces. The amount excreted is dependent on host status, the amount reabsorbed, and sometimes the presence of pathophysiologic conditions, including diarrhea and steatorrhea. Assessment in the clinical setting dictates that the clinician obtain a careful medical and diet history, recognize clinical presentations in which zinc adequacy may be compromised, and link this risk with nonspecific but plausible manifestations of deficiency. Examples discussed in this article include primary zinc deficiency due to dietary inadequacy (older breastfed infants or toddlers without zinc-rich complementary foods); genetically based deficiency (acrodermatitis enteropathica, acquired zinc deficiency of lactogenic origin), and acquired secondary deficiency in low birth weight and prematurity, gastrointestinal and hepatic disease, and cystic fibrosis. Evidence for efficacy of zinc therapy with pharmacologic doses for two conditions, Wilson’s disease and viral upper respiratory infections, is also discussed.
Iron deficiency is the most common micronutrient deficiency in the world and disproportionately affects pregnant women and young children. Iron deficiency has negative effects on pregnancy outcomes ...in women and on immune function and neurodevelopment in children. Iron supplementation programs have been successful in reducing this health burden. However, iron supplementation of iron-sufficient individuals is likely not necessary and may carry health risks for iron-sufficient and potentially some iron-deficient populations. This review considers the physiology of iron as a nutrient and how this physiology informs decision-making about weighing the benefits and risks of iron supplementation in iron-deficient, iron-sufficient, and iron-overloaded pregnant women and children.
Preterm birth remains a common cause of neonatal mortality, with a disproportionately high burden in low-income and middle-income countries. Meta-analyses of low-dose aspirin to prevent pre-eclampsia ...suggest that the incidence of preterm birth might also be decreased, particularly if initiated before 16 weeks of gestation.
ASPIRIN was a randomised, multicountry, double-masked, placebo-controlled trial of low-dose aspirin (81 mg daily) initiated between 6 weeks and 0 days of pregnancy, and 13 weeks and 6 days of pregnancy, in nulliparous women with an ultrasound confirming gestational age and a singleton viable pregnancy. Participants were enrolled at seven community sites in six countries (two sites in India and one site each in the Democratic Republic of the Congo, Guatemala, Kenya, Pakistan, and Zambia). Participants were randomly assigned (1:1, stratified by site) to receive aspirin or placebo tablets of identical appearance, via a sequence generated centrally by the data coordinating centre at Research Triangle Institute International (Research Triangle Park, NC, USA). Treatment was masked to research staff, health providers, and patients, and continued until 36 weeks and 7 days of gestation or delivery. The primary outcome of incidence of preterm birth, defined as the number of deliveries before 37 weeks' gestational age, was analysed in randomly assigned women with pregnancy outcomes at or after 20 weeks, according to a modified intention-to-treat (mITT) protocol. Analyses of our binary primary outcome involved a Cochran-Mantel-Haenszel test stratified by site, and generalised linear models to obtain relative risk (RR) estimates and associated confidence intervals. Serious adverse events were assessed in all women who received at least one dose of drug or placebo. This study is registered with ClinicalTrials.gov, NCT02409680, and the Clinical Trial Registry-India, CTRI/2016/05/006970.
From March 23, 2016 to June 30, 2018, 14 361 women were screened for inclusion and 11 976 women aged 14–40 years were randomly assigned to receive low-dose aspirin (5990 women) or placebo (5986 women). 5780 women in the aspirin group and 5764 in the placebo group were evaluable for the primary outcome. Preterm birth before 37 weeks occurred in 668 (11·6%) of the women who took aspirin and 754 (13·1%) of those who took placebo (RR 0·89 95% CI 0·81 to 0·98, p=0·012). In women taking aspirin, we also observed significant reductions in perinatal mortality (0·86 0·73–1·00, p=0·048), fetal loss (infant death after 16 weeks' gestation and before 7 days post partum; 0·86 0·74–1·00, p=0·039), early preterm delivery (<34 weeks; 0·75 0·61–0·93, p=0·039), and the incidence of women who delivered before 34 weeks with hypertensive disorders of pregnancy (0·38 0·17–0·85, p=0·015). Other adverse maternal and neonatal events were similar between the two groups.
In populations of nulliparous women with singleton pregnancies from low-income and middle-income countries, low-dose aspirin initiated between 6 weeks and 0 days of gestation and 13 weeks and 6 days of gestation resulted in a reduced incidence of preterm delivery before 37 weeks, and reduced perinatal mortality.
Eunice Kennedy Shriver National Institute of Child Health and Human Development.
Background: High intake of cow-milk protein in formula-fed infants is associated with higher weight gain and increased adiposity, which have led to recommendations to limit protein intake in later ...infancy. The impact of protein from meats for breastfed infants during complementary feeding may be different.Objective: We examined the effect of protein from meat as complementary foods on growth and metabolic profiles of breastfed infants.Design: This was a secondary analysis from a trial in which exclusively breastfed infants (5–6 mo old from the Denver, CO, metro area) were randomly assigned to receive commercially available pureed meats (Meat group; n = 14) or infant cereal (Cereal group; n = 28) as their primary complementary feedings for ∼5 mo. Anthropometric measures and diet records were collected monthly from 5 to 9 mo of age; intakes from complementary feeding and breast milk were assessed at 9 mo of age.Results: The Meat group had significantly higher protein intake, whereas energy, carbohydrate, and fat intakes from complementary feeding did not differ by group over time. At 9 mo of age, mean (±SEM) intakes of total (complementary feeding plus breast milk) protein were 2.9 ± 0.6 and 1.4 ± 0.4 g · kg−1 · d−1, ∼17% and ∼9% of daily energy intake, for Meat and Cereal groups, respectively (P < 0.001). From 5 to 9 mo of age, the weight-for-age z score (WAZ) and length-for-age z score (LAZ) increased in the Meat group (ΔWAZ: 0.24 ± 0.19; ΔLAZ: 0.14 ± 0.12) and decreased in the Cereal group (ΔWAZ: −0.07 ± 0.17; ΔLAZ: −0.27 ± 0.24) (P-group by time < 0.05). The change in weight-for-length z score did not differ between groups. Total protein intake at 9 mo of age and baseline WAZ were important predictors of changes in the WAZ (R2 = 0.23, P = 0.01).Conclusion: In breastfed infants, higher protein intake from meats was associated with greater linear growth and weight gain but without excessive gain in adiposity, suggesting that potential risks of high protein intake may differ between breastfed and formula-fed infants and by the source of protein.
Protein intake from cow milk–based infant formula has been associated with rapid weight gain and increased adiposity, but the effect of protein from complementary foods has not been prospectively ...evaluated, and the effect of protein from sources other than formula during complementary feeding is not clear.
The aim of this study was to directly compare the effect of protein from 2 common complementary food sources, meat and dairy, on infant growth and weight trajectory.
Healthy term, formula-fed infants were recruited from the metro Denver area, matched by sex and race/ethnicity and randomly assigned to a meat or a dairy complementary food group from 5 to 12 mo of age. Total protein intake during this 7-mo intervention was ∼3 g ⋅ kg−1 ⋅ d−1 for both groups. Intakes of infant formula, cereal, fruit, and vegetables were ad libitum. Caregivers also completed 3-d diet records at 5, 10, and 12 mo of age. Anthropometric measures were obtained during monthly home visits, and blood samples were collected at 5 and 12 mo of age.
Sixty-four infants completed the intervention (meat: n = 32; dairy: n = 32). The average total protein intake (mean ± SD) increased from 2.01 ± 0.06 g ⋅ kg−1 ⋅ d−1 at 5 mo to 3.35 ±0.12 g ⋅ kg−1 ⋅ d−1 at 12 mo and did not differ between groups. Over time, weight and weight-for-age z score increased by 0.48 ± 0.07. However, there was a significant group-by-time interaction for both length-for-age z score (LAZ) and weight-for-length z score (WLZ). Post hoc analysis showed that LAZ increased in the meat group (+0.33 ± 0.09; P = 0.001 over time) and decreased in the dairy group (−0.30 ± 0.10; P = 0.0002 over time); WLZ significantly increased in the dairy group (0.76 ± 0.21; P = 0.000002 over time) compared with the meat group (0.30 ± 0.17; P = 0.55 over time). Insulin-like growth factor I and insulin-like growth factor-binding protein 3 both increased over time without group differences.
Protein source may have an important role in regulating growth. In these formula-fed older infants, meat- and dairy-based complementary foods led to distinct growth patterns, especially for length. This trial was registered at www.clinicaltrials.gov as NCT02142647.
Iron supplementation may have adverse health effects in infants, probably through manipulation of the gut microbiome. Previous research in low-resource settings have focused primarily on anemic ...infants. This was a double blind, randomized, controlled trial of home fortification comparing multiple micronutrient powder (MNP) with and without iron. Six-month-old, non- or mildly anemic, predominantly-breastfed Kenyan infants in a rural malaria-endemic area were randomized to consume: (1) MNP containing 12.5 mg iron (MNP+Fe,
= 13); (2) MNP containing no iron (MNP-Fe,
= 13); or (3) Placebo (CONTROL,
= 7), from 6-9 months of age. Fecal microbiota were profiled by high-throughput bacterial 16S rRNA gene sequencing. Markers of inflammation in serum and stool samples were also measured. At baseline, the most abundant phylum was Proteobacteria (37.6% of rRNA sequences). The proteobacterial genus
was the most abundant genus across all phyla (30.1% of sequences). At the end of the intervention, the relative abundance of
significantly decreased in MNP-Fe (-16.05 ± 6.9%,
= 0.05) and CONTROL (-19.75 ± 4.5%,
= 0.01), but not in the MNP+Fe group (-6.23 ± 9%,
= 0.41). The second most abundant genus at baseline was
(17.3%), the relative abundance of which significantly decreased in MNP+Fe (-6.38 ± 2.5%,
= 0.02) and CONTROL (-8.05 ± 1.46%,
= 0.01), but not in MNP-Fe (-4.27 ± 5%,
= 0.4445).
increased in MNP-Fe only (1.9 ± 0.5%,
= 0.02). No significant differences were observed in inflammation markers, except for IL-8, which decreased in CONTROL. MNP fortification over three months in non- or mildly anemic Kenyan infants can potentially alter the gut microbiome. Consistent with previous research, addition of iron to the MNP may adversely affect the colonization of potential beneficial microbes and attenuate the decrease of potential pathogens.
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