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Background: Overweight is increasing in transition countries, while iron deficiency remains common. In industrialized countries, greater adiposity increases risk of iron deficiency. Higher hepcidin levels in obesity may reduce dietary iron absorption. Therefore, we investigated the association between body mass index (BMI) and iron absorption, iron status and the response to iron fortification in populations from three transition countries (Thailand, Morocco and India). Methods: In Thai women (n=92), we examined the relationship between BMI and iron absorption from a reference meal containing 4 mg of isotopically labeled fortification iron. We analyzed data from baseline (n=1688) and intervention (n=727) studies in children in Morocco and India to look for associations between BMI Z-scores and baseline hemoglobin, serum ferritin and transferrin receptor, whole blood zinc protoporphyrin and body iron stores, and changes in these measures after provision of iron. Results: In the Thai women, 20% were iron deficient and 22% were overweight. Independent of iron status, a higher BMI Z-score was associated with decreased iron absorption (P=0.030). In the Indian and Moroccan children, 42% were iron deficient and 6.3% were overweight. A higher BMI Z-score predicted poorer iron status at baseline (P<0.001) and less improvement in iron status during the interventions (P<0.001). Conclusions: Adiposity in young women predicts lower iron absorption, and pediatric adiposity predicts iron deficiency and a reduced response to iron fortification. These data suggest the current surge in overweight in transition countries may impair efforts to control iron deficiency in these target groups. Interactions of the 'double burden' of malnutrition during the nutrition transition may have adverse consequences.

Objectives Since the 1990s, programs for the control of micronutrient deficiencies became a public health priority for many governments, including the countries partnering the project “Sustainable Micronutrient Interventions to Control Deficiencies and Improve Nutritional Status and General Health in Asia” (SMILING): Cambodia, Indonesia, Laos-PDR, Thailand and Vietnam. The aim of this study was to map which micronutrient deficiencies have been addressed and which interventions were in place in the SMILING countries. Methods The mapping covered the period up to 2012. Updated information from relevant surveys after 2012 is included in this paper after the completion of the SMILING project. The mapping of micronutrient status was limited to either national or at least large-scale surveys. Information on nutrition interventions obtained through a systematic mapping of national programs combined with a snowball collection from various sources. Results Among the five SMILING countries, Thailand differed historically by an early implementation of a nationwide community-based nutrition program, contributing to reductions in undernutrition and micronutrient deficiencies. For Cambodia, Indonesia, Laos PDR, and Vietnam, some national programs addressing micronutrients have been implemented following adjusted international recommendations. National surveys on micronutrient status were scattered and inconsistent across the countries in design and frequency. Conclusion for practice In conclusion, some micronutrient deficiencies were addressed in national interventions but the evidence of effects was generally lacking because of limited nationally representative data collected. Improvement of intervention programs to efficiently reduce or eliminate micronutrient deficiencies requires more systematic monitoring and evaluation of effects of interventions in order to identify best practices.

To evaluate effects of Fe supplementation and sex on the prevalence of anaemia and Fe status in infants in South-East Asia, biochemical data from four parallel, randomized, double-blind trials with Fe and/or Zn supplementation in infants (n 2452) in Indonesia, Thailand and Vietnam was pooled. At recruitment (5 months of age), Hb concentrations were slightly but significantly lower in boy infants compared with girl infants (108·7 g/l v. 111.4 g/l, P = 0·04). At 11 months of age, boy infants not receiving Fe had significantly lower Hb (106·2 g/l v. 111.0 g/l, P < 0·001) and lower serum ferritin concentrations (14·3 μg/l v. 21.1 g/l, P < 0·001) than girl infants not receiving Fe. Consequently, boy infants had a relative risk of 1·6 (95 % CI 1·3, 2·1) to be anaemic, and of 3·3 (95 % CI 2·1, 5·0) for having Fe deficiency anaemia compared with girl infants. Fe supplementation significantly increased Hb concentrations in both boys and girls. There was no sex difference in Fe status in infants receiving Fe for 6 months. This study shows that the markedly higher risk for anaemia and Fe deficiency indicates higher Fe requirements in boy than in girl infants. In South-East Asia, standard infant feeding practices do not provide sufficient Fe to meet requirements of infants, especially boys. Current daily recommended intake for Fe in infancy is the same for boy and girl infants however. Our findings suggest that in especially the second half of infancy, Fe requirements for boy infants are approximately 0·9 mg/d higher than for girl infants.

Introduction: Micronutrient deficiencies during childhood can contribute to impairments in growth, immune competence, and mental and physical development, and the coexistence of several such deficiencies can adversely affect the efficacy of single micronutrient interventions. Objective: To assess the prevalence of zinc and iodine deficiency and their interrelationships with vitamin A deficiency and anemia and associations with socio-economic status, hemoglobin type, and anthropometry in a cross-sectional study. Setting: A total of 10 primary schools in North East Thailand. Methods: Non-fasting venipuncture blood samples and casual urine samples were collected from 567 children aged 6-13 years. Anthropometric measures and serum zinc, albumin, C-reactive protein and urinary iodine, are reported here and integrated with published data on vitamin A, anemia, and socio-economic status. Results: Of the children, 57% had low serum zinc and 83% had urinary iodine levels below the 100 micrograms/l cutoff. Suboptimal serum zinc and urinary iodine concentrations may result from low intakes of zinc and iodized salt. Significant risk factors for low serum zinc were serum retinol <1.05 micromol/l and being male. Those for urinary iodine <100 micrograms/l were height-for-age score>median and being female. For serum retinol <1.05 micromol/l, risk factors were low hemoglobin, low serum zinc, and <9 years, and for low hemoglobin indicative of anemia risk factors were <9 years, AE hemoglobinopathy, and serum retinol <1.05 micromol/l. Of the children, 60% were at risk of two or more coexisting micronutrient deficiencies, most commonly suboptimal urinary iodine and low serum zinc. Conclusion: The findings emphasize the need for multimicronutrient interventions in North East Thailand.

This study evaluated the impact of a nutrition education intervention on child feeding practices and children's nutritional status. Using a randomized controlled trial, we conducted an intervention for 6 months among caregivers with children aged 6–17 months in two subdistricts of Kendari, SE Sulawesi Province, Indonesia. In all, 22 integrated health posts were randomly assigned to an educational intervention or control group with 266 participants in both groups. Participants in the intervention group attended four nutrition classes and received a monthly home visit by cadres (community volunteers), whereas participants in the control group only received standard monthly health care at the health post. The primary study outcome was children's dietary diversity scores (DDSs). Mixed model analysis was conducted to examine the intervention effects on DDS and children's growth adjusting for clustering within subvillages. The study showed the educational intervention had a significant effect on children's DDS. Children in the intervention group had a larger DDS compared with children in the control group (Beta [mean difference] = 0.34, 95% CI: 0.02 to 0.66, P = 0.038). The intervention effect on height‐for‐age z‐score (HAZ) could not be shown (Beta = 0.24, 95% CI: −0.06 to 0.56, P = 0.112). However, stunting prevalence remained stable in the intervention group but increased in the control group. These results indicated nutrition education delivered through nutrition classes combined with regular home visits by cadres as influencers provided a great potential to be adopted to complement other nutrition programmes in community health centres.

Background and objectives: Iodine deficiency during pregnancy may be associated with lower IQ in offspring. It is unknown whether iodine supplementation in mildly iodine-deficient pregnant women improves cognitive function in their children. Methods: We randomized Indian and Thai pregnant women to receive daily 200 µg oral iodine or placebo until term. Primary outcomes were child development assessed at 1 and 2 years using the Bayley Scales of Infant Development (BSID)-III and at 5-6 years using the Wechsler Preschool and Primary Scale of Intelligence (WPPSI)-III. Secondary outcomes were maternal and infant thyroid function, pregnancy outcomes and child hearing performance. The trial was double-masked and analysis was by intention- to-treat using mixed effects models. Results: Pregnant women (n=832) entered the trial at a mean±SD gestational age of 10.7±2.7 weeks; their median (IQR) urinary iodine concentration (mUIC) was 131 (81, 213) µg/L, indicating mild iodine deficiency. Compliance with supplementation was 87%; mUICs in the 2nd and 3rd trimester were higher in the iodine group (p<0.001). There were no significant group differences in the cognitive and the combined motor and language BSID-III scores at 1 or 2 years. At 5.4 years, mean differences (95% CI) between iodine and placebo for WPPSI-III scores were: -0.7 (-2.9,1.4), p=0.87 for verbal IQ; -1.6 (-4.5,1.3), p=0.60 for performance IQ; -1.7 (-4.3,0.9), p=0.39 for processing speed; and -1.3 (-3.6,1.1), p=0.63 for full scale IQ. Conclusions: Daily supplementation with 200 µg iodine in mildly iodine deficient pregnant women increased iodine intakes into the sufficient range but had no effect on child neurodevelopment.

Stunting in school-age years may result in a decrease in adult size, and thus reduced work capacity and adverse reproductive outcomes. We have compared the mean intakes of energy, protein and selected growth-limiting nutrients in fifty-eight stunted children and 172 non-stunted controls drawn from 567 children aged 6–13 years attending ten rural schools in NE Thailand. Control children were selected randomly after stratifying children by age in each school. Dietary data were calculated from 24-h recalls using nutrient values from Thai food composition data and chemical analysis. Inter-relationships between stunting and sociodemographic, anthropometric and biochemical variables were also examined. Biochemical variables investigated were serum albumin, zinc, ferritin, transferrin receptor and retinol, and iodine in casual urine samples. Significantly more males than females were stunted (males, n 38, 65·5 % v. females, n 20, 34·5 %; P = 0·025). Stunted males had lower mean intakes of energy, protein, calcium, phosphorus and zinc, and a lower mean (95 % CI) serum zinc (9·19 (8·53, 9·84) v. 9·70 (8·53, 9·29) μmol/l) than non-stunted males; no other biochemical differences were noted. Stunted males also had a lower mean arm muscle area (P = 0·015), after adjusting for age, than non-stunted males. In conclusion, the lower dietary intakes of the stunted males compared to their non-stunted counterparts may be associated with anorexia and hypogeusia induced by zinc deficiency. Hence, zinc deficiency may be a factor limiting linear growth, especially among boys in NE Thailand, but more research is needed to establish whether other factors also play a role.

Thalassemia and abnormal hemoglobins are common genetic disorders in Asia. Thalassemia is not only an important public health problem but also a socio-economic problem of many countries in the region. The approach to deal with the thalassemic problem is to prevent and control birth of new cases. This requires an accurate identification of the couple at high risk for thalassemia. However, the diagnosis of thalassemia carrier states need several tests which are not practical for screening the population at large. Recently we have used two simple laboratory tests to screen for potential thalassemia carriers and hemoglobin E individuals. There is also a new development in using the automatic HPLC to diagnose thalassemic diseases and the carriers. This system gives both qualitative and quantitative analysis of hemoglobin components in the same run with good precision and reproducibility. The system has been applied to study thalassemia and abnormal Hb in adult and cord blood. This system has enabled us to do both prenatal and postnatal diagnosis of thalassemia within the few minutes. However, none of these screening tests can accurately give specific diagnosis of the thalassemia genotype. Specific thalassemia mutation can be carried out by DNA analysis. Many DNA techniques have been used for point mutation detection and small deletion. For the last few years there is a development of DNA chip technology that has been applied for thalassemia mutation as well. Clinically, thalassemia is very heterogeneous in the manifestation. In spite of seemingly identical genotypes, severity of beta thalassemic patients can vary greatly. Heterogeneity in the clinical manifestation of beta thalassemic diseases may occur from the nature of beta globin gene mutation, alpha thalassemia gene interaction and difference in the amount of Hb F production which is partly associated with a specific beta globin haplotype. However, there is still some beta thalassemia cases that have a mild clinical symptom without those known genetic fators interaction suggesting that there are other additional factors responsible for the mildness of the disease.

Due to genetic heterogeneity of beta-thalassemia (beta-thal) patients, several efforts have been undertaken to determine the efficacy of hydroxyurea treatment. The aim of this work is to determine the responder and nonresponder for hydroxyurea treatment in beta-thal intermedia based on gamma-globin mRNA and fetal hemoglobin (HbF) induction in human erythroid progenitor cells purified from a patient's peripheral blood. Eighteen beta-thal/hemoglobin E patients [13 beta(E)/codon41/42(-TCTT), 4 beta(E)/codon17, and 1 beta(E)/IVS-654], requiring blood transfusion occasionally, with Hb levels of 5.20-8.50 g/dl were studied. The relative levels of gamma-globin mRNA was measured by real-time reverse-transcription polymerase chain reaction and HbF by high-performance liquid chromatography. The results indicated that erythroid progenitor cells treated with 30 mumol/l hydroxyurea for 96 h preferentially enhanced (G)gamma-and (A)gamma-globin mRNA. The mean values of (G)gamma-globin mRNA fold induction were higher than (A)gamma-globin mRNA (12+/-4 vs 4+/-0.30), the Pearson's correlation of (G)gamma-and (A)gamma-globin mRNA was r=0.80. Induction of (G)gamma/(A)gamma globin mRNA is up to ninefold. A 30% increase in the proportion of HbF out of the total Hb was found in cultures derived from four patients, 20-30% in cultures from nine patients, and less than 20% in cultures from five patients. In cultures from only two patients, increase in the proportion of HbF was less than 3%, and (G)gamma/(A)gamma globin mRNA is less than 0.50.

Hereditary persistence of fetal hemoglobin (HPFH) is associated with a high level of hemoglobin F (HbF) synthesis in adult heterozygotes. In this study, 2 of 6 unrelated HPFH Thai families were found to be Southeast Asian-type HPFH (SEA-HPFH) by analyses of the hematologic data and Southern blot hybridization with polymerase chain reaction-amplified DNA probes. DNA mapping with a probe for a delta-globin fragment showed a 27-kb deletion of DNA that included the beta-globin gene and the 3' deoxyribonuclease I hypersensitive site 1 (3'HS1) sequence downstream. Deletion of the insulator, 3'HS1, and the juxta-position of the HPFH-3 core enhancer downstream to the 3' breakpoint have been postulated to be the cause of high HbF production in these individuals. To test this hypothesis, we transfected K562 cells with 4 different bacterial artificial chromosome constructs containing the enhanced green fluorescent protein (EGFP) gene at the position of the Agamma-globin gene (pEBAC/148beta:EGFP). Flow cytometry was used to compare EGFP expression from the pEBAC/148beta:EGFP construct with the HPFH-3 core enhancer immediately 5' to the SEA-HPFH breakpoint (pEnH), from the pEBAC/148beta:EGFP construct with 8 kb of the breakpoint sequence and the HPFH-3 core enhancer (pSEA-HPFH), and from the construct with 3'HS1 followed by the pSEA-HPFH sequence (pSEA-HPFH_3pHS1). The results show that high HbF production in SEA-HPFH occurs from a deletion of the 3'HS1 sequence and the juxtaposition of the HPFH-3 enhancer downstream to the delta-globin gene.