Onset and evolution of stunting in infants and children. Examples from the Human Nutrition Collaborative Research Support Program. Kenya and Egypt studies
Division of Population and Family Health, UCLA School of Public Health and School of Medicine (Pediatrics) 90024. European Journal of Clinical Nutrition
(Impact Factor: 2.71).
03/1994; 48 Suppl 1(Suppl 1):S90-102.
The etiology of the early onset of stunting is diverse among populations of varying biological, environmental and cultural circumstances. This is exemplified within the Nutrition CRSP project, which took place in three different populations and ecological conditions. Within each study area a different mix and varying proportions of causative factors were identified. At least in Kenya, and probably in Mexico, the problem has its antecedents in prepregnancy and pregnancy. Powerful determinants of the infants' size at birth and during the first 6 months of life are maternal size upon entry into pregnancy, and weight and fat gain during pregnancy and lactation. In all three countries a low pregnancy weight gain was observed. Notably in Kenya, where the energy intake of the mother decreases progressively throughout pregnancy, not only do mothers gain only half as much as European or North American women, but they even lose weight and fat in the last month of pregnancy, and some mothers gain no weight or lose weight during the whole of pregnancy. Mothers in Kenya start lactation with relatively poor fat stores. Although their energy intake increases somewhat during lactation, preliminary estimates suggest that these increases may be insufficient to maintain their bodily integrity, to carry out their normal tasks of daily living, and to produce a sufficient amount of milk for optimal infant growth. In addition to an energy deficit, diet quality is a problem, particularly in Kenya and Mexico and less so in Egypt. Intakes of animal products and animal protein are very low. Zinc and iron intakes are not only low, but the bioavailability of these nutrients is poor because of the high phytate, fiber and tea content of the diet. Also vitamin B12 intake is extremely low, and at least mild-to-moderate iodine deficiency (IDD) is present in Kenya. The above micronutrients have been demonstrated to affect the linear growth of the Kenyan children, even after confounding factors have been controlled. The early use of supplemental feeding in Kenya is a double-edged sword. On the one hand, there is a slight increase in febrile illness and possible displacement of breast milk intake in the supplemented infants, although mothers do not decrease breast feeding frequency and duration. On the other hand, even the modest amounts of available zinc and B12 in supplemental foods appear to have a positive effect on linear growth.(ABSTRACT TRUNCATED AT 400 WORDS)
Available from: Emilie Erin Vomhof-DeKrey
- "In humans  and in animal models     , maternal low protein (LP) diets reduce offspring birth weight. Low birth weight (LBW) promotes rapid adipose tissue growth during adolescence, further adult-onset weight gain  and increased risk for insulin resistance . "
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ABSTRACT: Brown adipose tissue (BAT) plays an important role in regulating body weight (BW) by modifying thermogenesis. Maternal low protein (LP) diets reduce offspring birth weight. Increased BAT thermogenesis in utero may be one mechanism for the lower BW. However, whether maternal LP nutrition alters BAT thermogenesis and BW of offspring in utero is not yet known. We fed obese-prone Sprague-Dawley dams 8% LP or 20% normal protein (NP) diets for 3weeks prior to breeding and through pregnancy. BW and gene expression of interscapular BAT (iBAT) thermogenic markers were measured in male fetal (gestation day 18) and neonatal (day 0 or 1) offspring. BW of neonatal LP males was lower than NP males but no difference was observed in females. Gene and protein expression of UCP-1 and transcription factors PRDM16 and PPARα in iBAT were 2- to 6-fold greater in LP than in NP male neonatal offspring. FNDC5, a precursor of irisin and activator of thermogenesis, was expressed 2-fold greater in neonatal LP iBAT than NP males. However, fetal iBAT UCP-1, PRDM16, PPARα and irisin mRNA did not differ between LP and NP groups. Maternal LP diet had no effects on placental irisin and UCP-2 expression. These results suggest that prenatal protein restriction increases the risk for low BW through mechanisms affecting full-term offspring iBAT thermogenesis but not greatly altering fetal iBAT or placental thermogenesis.
Copyright © 2015. Published by Elsevier Inc.
Available from: Martin H Schoeni
- "Having discussed the importance of Zn2+ as well as their individual intracellular transporters it comes without any surprise that an adequate Zn2+ concentration in the child's plasma is of high importance for normal growth and development [1, 3, 28, 47–49]. "
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ABSTRACT: Suboptimal dietary zinc (Zn(2+)) intake is increasingly appreciated as an important public health issue. Zn(2+) is an essential mineral, and infants are particularly vulnerable to Zn(2+) deficiency, as they require large amounts of Zn(2+) for their normal growth and development. Although term infants are born with an important hepatic Zn(2+) storage, adequate Zn(2+) nutrition of infants mostly depends on breast milk or formula feeding, which contains an adequate amount of Zn(2+) to meet the infants' requirements. An exclusively breast-fed 6 months old infant suffering from Zn(2+) deficiency caused by an autosomal dominant negative G87R mutation in the Slc30a2 gene (encoding for the zinc transporter 2 (ZnT-2)) in the mother is reported. More than 20 zinc transporters characterized up to date, classified into two families (Slc30a/ZnT and Slc39a/Zip), reflect the complexity and importance of maintaining cellular Zn(2+) homeostasis and dynamics. The role of ZnTs is to reduce intracellular Zn(2+) by transporting it from the cytoplasm into various intracellular organelles and by moving Zn(2+) into extracellular space. Zips increase intracellular Zn(2+) by transporting it in the opposite direction. Thus the coordinated action of both is essential for the maintenance of Zn(2+) homeostasis in the cytoplasm, and accumulating evidence suggests that this is also true for the secretory pathway of growth hormone.
Available from: ncbi.nlm.nih.gov
- "This could be explained by the fact that intakes of animal products and animal protein are very low due to low socio-economic status of the population. In addition, Zn intake is not only low, but its bioavailability is poor because of the high phytate, fiber and tea content of the diet among Egyptian population . Zn deficiency during the period of growth results in growth failure and lack of gonadal development, especially in males. "
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ABSTRACT: The relationship between zinc (Zn) and growth hormone-insulin growth factor (GH-IGF) system and how Zn therapy stimulates growth in children has not been clearly defined in humans. Thus, we aimed to assess GH-IGF axis in short children with Zn deficiency and to investigate the effect of Zn supplementation on these parameters.
Fifty pre-pubertal Egyptian children with short stature and Zn deficiency were compared to 50 age-, sex-, and pubertal stage- matched controls. All subjects were subjected to history, auxological assessment and measurement of serum Zn, IGF-1, insulin growth factor binding protein-3 (IGFBP-3); and basal and stimulated GH before and 3 months after Zn supplementation (50 mg/day).
After 3 months of Zn supplementation in Zn-deficient patients, there were significant increases in height standard deviation score (SDS, P = 0.033), serum Zn (P < 0.001), IGF-1 (P < 0.01), IGF-1 standard deviation score (SDS,P < 0.01) and IGFBP-3 (P = 0.042). Zn rose in all patients but reached normal ranges in 64 %, IGF-1 levels rose in 60 % but reached normal ranges in 40 % and IGFBP-3 levels rose in 40 % but reached reference ranges in 22 %. Growth velocity (GV) SDS did not differ between cases and controls (p = 0.15) but was higher in GH-deficient patients than non-deficient ones, both having Zn deficiency (p = 0.03).
Serum IGF-1 and IGFBP-3 levels were low in short children with Zn deficiency, and increased after Zn supplementation for 3 months but their levels were still lower than the normal reference ranges in most children; therefore, Zn supplementation may be necessary for longer periods.
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