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Kamis, 30 Januari 2014

Kerawanan Pangan

Kerawanan Pangan Mempengaruhi Kinerja Akademik Anak Sekolah, Berat Badan, dan Keterampilan Sosial (SHALLY MARLI MAULANA)

Food Insecurity Affects School Children’s Academic Performance, Weight Gain, and Social Skills1–3
 
Diana F. Jyoti, Edward A. Frongillo,4 and Sonya J. Jones*

Introduction
     Despite federal food assistance and private charitable programs, food insecurity is a persistent national problem (1), affecting 11% of all households (2) and 16% of households with children (3). Food insecurity refers to limited or uncertain availability of or inability to acquire nutritionally adequate, safe, and acceptable foods due to financial resource constraint (1). More specifically, food insufficiency refers toan inadequate amount of food intake due to resource constraint
(4).
     Food insecurity and insufficiency are associated with adverse health and developmental outcomes in U.S. children (5–12). Among 6- to 12-y-old children, food insufficiency was associated with poorer mathematics scores, grade repetition, absenteeism, tardiness, visits to a psychologist, anxiety, aggression, psychosocial dysfunction, and difficulty getting along with other children (13–15). Among 15- to 16-y-old adolescents, food insufficiency was associated with depressive disorders and suicide symptoms after controlling for income and other factors (16). Recently, food insecurity was associated with poor social functioning, but not with academic performance or attained BMI, in kindergarten children (17).

SUBJECTS AND METHODS
     Nonrestricted, public-use data were obtained from the ECLS-K (23), which utilized a multistage probability, cluster sample design to select a nationally representative sample of 21,260 kindergarten children
attending 1592 elementary schools in 1998–1999. Data were collected nonexperimentally by means of survey and direct assessment over 4 consecutive years. We utilized parent, teacher, and child data from spring of kindergarten (1999) and spring of 3rd grade (2002). Data from children with full response, i.e., eligible children who completed some assessment data or had a parent who completed the family section of the parent interview, were available for 20,578 children in the spring of 1999 and for 15,305 children in the spring of 2002. Attrition was due mainly to children moving outside of the primary sampling units or moving to areas in which they could not be located. Locatable movers from a random 50% of schools were followed. A small number of children became ineligible because they moved outside of the United States or died. Our 2 analytic samples consisted of the following: 1) 13,500 children for whom full data, i.e., a scored reading or mathematics assessment and parent completion of the USDA food security module, were available at kindergarten; and 2) 11,400 children for whom these full data were available
at both kindergarten and 3rd grade.

RESULTS
     Background characteristics for the subset of children with full data are summarized in Supplemental Tables 1 and 2. Included are the characteristics for the 15.6% of kindergarteners from households affirming 1 response on the USDA food security module. Supplemental Table 3 summarizes background characteristics over time. Characteristics of the entire sample at kindergarten were reported elsewhere (17). Between kindergarten and 3rd grade, 77.9% of children’s households remained food secure, 6.0% remained food insecure, 9.7% became food secure and 6.5% became food insecure (n 11,460); 22.2% experienced food insecurity at one or both times.
     Observed changes in outcomes were in the expected ranges for child age and developmental stage (Table 1). Reading IRT score increased by 70.43 points, mathematics IRT score by 53.37 points, weight by 10.96 kg, and BMI by 1.99 kg/m2. The teacher-rated social skills score changed little ( 0.06 points). Weights at kindergarten and 3rd grade were slightly above the expected norm for the U.S. population. The observed mean weight of 22.5 kg and mean age of 6.23 y at kindergarten corresponded roughly to the 65th percentile weight-for-age for the U.S. population. Three years later, the observed mean weight of 34.26 kg corresponded roughly to the 75th percentile weight-for-age for the U.S. population (25).

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Manfaat dan Risiko Mengkonsumsi Salmon

Analisis Kuantitatif Manfaat dan Risiko Mengkonsumsi  dan berternak Salmon Liar (SHALLY MARLI MAULANA)
  
Quantitative Analysis of the Benefits and Risks of Consuming Farmed and Wild Salmon1

Jeffery A. Foran,2 David H. Good,* David O. Carpenter,† M. Coreen Hamilton,**
Barbara A. Knuth,‡ and Steven J. Schwager††

Introduction
     Assessments of contaminants in salmon (1– 4) have raised health risk concerns, which are particularly important given the considerable increasing trend in salmon consumption, especially of farmed salmon (5). Over half the salmon sold globally is now farm-raised, and the annual global production of farmed salmon (predominantly Atlantic salmon) has risen from 2.7  104 to 1.3  106 metric tons during the past 2 decades (6). Contaminant-associated health risks are important because they may detract from the health benefits (prevention of cardiac death) of consuming (n-3) PUFA that occur in tissues of salmon as well as other fatty fish (7–14).
     As we reported previously (1– 4), concentrations of dioxins, polychlorinated biphenyls (PCB),3 polybrominated diphenyl ethers, and some pesticides are significantly higher in farmraised Atlantic salmon than in wild Pacific salmon, and salmon raised on European farms have significantly higher contaminant concentrations than those raised on North and South American farms. As a result, the health risks of consuming farmed salmon are greater than the risks of consuming the less contaminated wild salmon. It is unclear, however, whether the higher concentrations of (n-3) fatty acids in farmed salmon (15) outweigh or balance contaminant-associated health risks.

MATERIALS AND METHODS
     A benefit-risk ratio was developed that compares cancer and noncancer risks associated with cumulative exposure to organic contaminants in salmon with the quantities of (n-3) fatty acids, measured as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) that result from salmon consumption. The ratios were derived from 245 composite samples (3 fillets each) collected in 2001 (1). The data included 153 observations from farmed salmon purchased from wholesalers, 48 from fillets of farmed salmon purchased from retail markets in 16 cities, and 44 from wild-caught Pacific salmon.

RESULTS
     Both farmed and wild salmon can be consumed at rates that provide at least 1 g/d EPADHA per unit noncarcinogenic risk (Fig. 1). However, there are clear differences in the benefit-risk ratio for noncarcinogens among wholesale farmed salmon, farmed salmon fillets purchased from retail markets, and wild salmon (P  0.0001). Based on the benefit-noncarcinogenic risk ratio, wild salmon can be consumed at rates that approach the higher levels of (n-3) fatty acid intake recommended by the WHO (28) and AHA (7). Salmon from farms in the Faroe Islands and Scotland provide the least amount of EPADHA per unit noncarcinogenic risk, even though these fish contain some of the highest concentrations of fatty acids (15). Similarly, farmed salmon sold in European retail markets provide the least EPADHA per unit noncarcinogenic risk, suggesting that these fish derive from farms in the European north Atlantic. Of the farmed salmon, those from Chile and Washington State, and those sold in retail markets in the United States provide the highest EPADHA intake per unit noncarcinogenic risk.

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Quercetin Mengurangi Tekanan

Quercetin Mengurangi Tekanan Darah di Subjek hipertensi (SHALLY MARLI MAULANA)

 Quercetin Reduces Blood Pressure in Hypertensive Subjects1,2

Randi L. Edwards,3 Tiffany Lyon,3 Sheldon E. Litwin,4 Alexander Rabovsky,6 J. David Symons,3,5 and Thunder Jalili3*


Division of Nutrition, 4Division of Cardiology, and 5Department of Exercise and Sports Science, University of Utah, Salt Lake City, UT 84112 and 6USANA Health Sciences, Salt Lake City, UT 84120

Introduction
     Quercetin is a flavonol that belongs to a group of polyphenolic compounds known as flavonoids (1). Widespread epidemiological evidence indicates that quercetin contained in onions, apples,berries, and red wine aids in preventing cardiovascular disease and stroke (2–8). Along with these promising data, recent laboratory studies have demonstrated that quercetin has important vasorelaxant properties on isolated arteries and lowers blood pressure in the spontaneously hypertensive rat (9,10). In addition, we have shown that quercetin administered to rats prevents the development of hypertension and cardiac hypertrophy in response to pressure overload created by abdominal aortic constriction (11). The beneficial effects of quercetin concerning vasorelaxation and blood pressure in rodents have been attributed at least in part to the ability of this flavonoid to decrease indices of oxidative stress (9,11,12). Despite existing epidemiological and animal-based research concerning quercetin and cardiovascular disease, no studies have evaluated whether quercetin supplementation lowers blood pressure in hypertensive humans. Therefore, we performed a randomized, placebo-controlled crossover trial to test the hypothesis that quercetin reduces blood pressure in prehypertensive and stage 1 hypertensive subjects. Systemic markers of oxidant load also were examined as secondary outcomes to determine whether reductions in blood pressure were associated with lower indices of oxidative stress.
 
Materials and Methods
     Participants and recruitment criteria This study was approved by the University of Utah Human Use Review Committee, University of Utah Institutional Review Board, and written informed consent was obtained from each participant. Recruitment efforts in the greater Salt Lake City area targeted males and females with prehypertension (120–139 mm Hg systolic/80–89 mm Hg diastolic) and stage 1 hypertension (140–159 mm Hg systolic/90–99 mm Hg diastolic) as defined by the 7th Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (13). Figure 1 summarizes the number of subjects screened, recruited, and enrolled in this study. Initial screening consisted of asking volunteers if they had a history of high blood pressure, followed by a single blood pressure measurement using an Omron random zero blood pressure analyzer. If blood pressure criteria were met during the initial screening, subjects were referred to the Nutrition Clinic for further evaluation of blood pressure and confirmation of eligibility criteria. Subjects who met blood pressure guidelines and eligibility criteria after the clinical evaluation were enrolled in the study. We recruited participants from October 2004 to June 2005. Forty-four patients who met study criteria consented and were enrolled, 21 prehypertensive and 23 stage 1 hypertensive. Forty-one subjects completed the entire protocol and 3 withdrew (1 male and 1 female from the prehypertensive group and 1 male from the stage 1 hypertensive group).
Results
     Patient characteristics. Nearly 1000 patients were interviewed and screened for eligibility. The majority (i.e. ;800) were not considered further for participation because they met 1 or more of the exclusion criteria or did not have blood pressure within study limits. From this initial screening, 204 individuals were evaluated in more detail at a subsequent clinic visit to determine whether all inclusion/exclusion criteria were met and if blood pressure was within the study limits (Fig. 1). Forty-four subjects were initially enrolled and 41 completed the entire 12-wk study. The age of prehypertensive (n ¼ 19, n ¼ 13 males) and stage 1 hypertensive (n ¼ 22, n ¼ 13 males) subjects was 47.8 6 3.5 and 49.2 6 2.9 y old, respectively. No adverse effects of quercetin or placebo treatment were reported during the course of the study.Weight and BMI did not change between treatments in either group (Table 2). Heart rate was unchanged throughout
the study (data not shown).
     Plasma quercetin was 695 6 103 nmol/L after placebo treatment and increased to 1419 6 189 nmol/L after quercetin treatment. Our preliminary experiments indicated that a 1-wk washout period was sufficient to bring plasma quercetin concentrations to 562 6 27 nmol/L. These values are similar to those obtained from subjects who consumed placebo but had not yet been exposed to quercetin. There was also no effect of treatment order on the observed changes in blood pressure (r ¼ 0.194; P ¼ 0.388), indicating that the antihypertensive effect of quercetin did not persist in those who received quercetin supplements before
placebo.

     Our study is, to our knowledge, the first to show that quercetin reduces blood pressure in stage I hypertensive individuals. Though we used a powerful experimental design (double blinded, placebo-controlled, crossover) and found quercetin supplementation to be efficacious in reducing blood pressure, extrapolation of our results to the general population should be done with caution given the homogeneous cohort (middle-aged, Caucasian men and women) and modest sample size. Nevertheless, our data indicate that potential exists for this polyphenolic compound to be used as adjunct therapy in diet/ lifestyle interventions to help control blood pressure in hypertensive individuals.

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Imunitas dan Kapasitas Antioksidan Pada Manusia

Imunitas dan Kapasitas Antioksidan Pada Manusia  Ditingkatkan dengan Konsumsi , terenkapsulasi Buah dan Jus Sayur (SHALLY MARLI MAULANA)

Immunity and Antioxidant Capacity in Humans Is Enhanced by Consumption of a Dried, Encapsulated Fruit and Vegetable uice Concentrate1
 
Meri P. Nantz,2 Cheryl A. Rowe,2 Carmelo Nieves, Jr., and Susan S. Percival*
 
Food Science and Human Nutrition Department University of Florida Gainesville, Florida 32611

Introduction
     Components of fruits and vegetables, such as vitamins, minerals, and other phytochemicals are effective in maintaining health and immune function (1–3). The objective of this research was to evaluate the consumption of fruits and vegetables in the form of an encapsulated powder concentrate from a fruit and vegetable juice blend and to correlate ingestion of this capsule with serum antioxidant levels, immune biomarkers, and illness. An encapsulated fruit and vegetable juice concentrate (FVJC)3 has been shown to increase proliferation of peripheral blood mononuclear cells (PBMC), improve natural killer (NK) cell cytotoxicity in elderly nonsmokers, and increase IL-2 production in both smokers and nonsmokers (4). We hypothesized that consumption of this FVJC might also impact markers of immune function in a younger population, particularly related to the gd-T–cell population. gd-T cells, having characteristics of innate and acquired immunity, play a role in protecting epithelial linings, immunosurveillance against virally infected and tumor cells, and a role in wound healing (5–7). A previous study also found that FVJC consumption for 84 d reduced the amount of DNA damage in PBMC, as measured by the comet assay (4). Moreover, studies using this preparation showed that plasma carotenoids (4,8–12) and plasma vitamin C levels increase (9–11), whereas indicators of oxidative damage, such as serum lipid peroxide levels (12) and plasma malondialdehyde levels, decrease (11).
Materials and Methods
     Study design. Healthy men (n ¼ 23) and women (n ¼ 36), ranging in age from 21 to 53 y (mean 25 y), were recruited from the University of Florida’s Levin College of Law in Gainesville, Florida, during August, 2004. Exclusion criteria included the use of tobacco products, chronic or excessive alcohol consumption, use of illegal pharmaceuticals, pregnant or lactating females, and recent surgery or illness. The study was conducted over an 11-wk period. The study was approved by the University of Florida’s Institutional Review Board. Written informed consent was obtained from each subject. On d 1, subjects were randomly assigned, in a double-blind fashion, to either the placebo group, who received capsules containing microcrystalline cellulose, or the FVJC group, who received capsules containing primarily fruit and vegetable juice powder concentrate derived from acerola cherry, apple, beet, broccoli, cabbage, carrot, cranberry, kale, orange, peach, papaya, parsley, pineapple, spinach, and tomato (Juice Plus1 NSA). The FVJC capsules provided ;7.5 mg b-carotene, 234 mg vitamin C, 45 IU vitamin E, 420 mg folate, 60 mg calcium, and about 42 kJ (9–11). Subjects were instructed to consume 4 capsules/d (2 in the morning and 2 in the evening) with meals and to otherwise not alter their habitual diet.

Results
     Study attrition consisted of 1 subject due to an unrelated illness and another due to withdrawal from law school, both of which occurred within the first study week. Compliance was 87.3% 6 10.9 pills consumed in the FVJP group and 90.2% 6 9.5 in the placebo group. The 2 groups did not differ in age, body mass index, or gradepoint average at the end of the semester (Table 1). Of the individuals taking the FVJC capsule, 51.6% guessed correctly as to which capsule they took, whereas 39.3% of the placebo group guessed correctly (P ¼ 0.493, Table 1). Seventeen individuals in the FVJC group and 17 in the placebo group reported 1 or 2 illnesses. No one reported having 3 or more illnesses. The number of self-reported illnesses between the 2 groups did not differ, but there was a trend (P ¼ 0.076) for the FVJC group to have fewer total symptoms than the placebo group (Table 1). High variability in the placebo group (CV ¼ 85.2%) may be responsible for of the inability to detect a significant difference with this number of individuals.
     The percentage of circulating gd-CD31 T cells in the FVJC group increased 30% after 77 d, whereas treatment did not affect the percentage of ab-CD31 T cells in the peripheral blood (Table 2). The percentage of gd-CD31 T cells in the FVJC group after 77d of treatment was 30% greater than at baseline (P ¼ 0.091) and 30% greater than in the placebo (P ¼ 0.049). The level of INF-g produced by PMA-stimulated PBMC (after culture with IL-2) was significantly decreased in the FVJC group (1.49 6 0.19 ng/L on d 1 vs. 0.47 6 0.19 ng/L on d 77). INF-g levels in the placebo group did not significantly differ between d 1 and d 77 (1.14 6 0.20 ng/L on d 1 vs. 0.67 6 0.2 ng/L on d 77). Statistically, there was a time effect within the FVJC group (P ¼ 0.002) but no time effect in the placebo (P ¼ 0.114). There were no differences between time and/or treatment in the levels of IL-4, TGF-b, or IL-6 produced by PMAstimulated PBMC from FVJC consumers or the placebo (datanot shown).

Acknowledgments
     We thank Neal Benson and Bhavna Bhardwaj of the UF Flow Cytometry Core for assistance and guidance, Carrie NeSmith for technical assistance, and Dr. Joon-Hee Lee and Dr. Steve Talcott, for assistance with the ORAC assay. Special thanks to Gail Sassnett and Nomar Castro at the University of Florida’sLevin College of Law.
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Rabu, 29 Januari 2014

Defisiensi Besi pada Anak Muda

Defisiensi Besi pada Anak Muda di Negara Berpenghasilan Rendah dan Pendekatan Baru untuk Ini adalah Pencegahan (SHALLY MARLI MAULANA)

Iron Deficiency in Young Children in Low-Income Countries and New Approaches for Its Prevention 1,2 

Chessa K. Lutter*

Pan American Health Organization, Washington, DC 20037

Introduction
     Anemia resulting from severe iron deficiency (ID)3 is the most prevalent and widespread nutrition problem in infants and young children in the developing world (1) and has proven very resistant to prevention through public health interventions. Accumulated evidence from animal and human studies suggests that such deficiencies are associated with adverse effects on child cognitive and motor development (2–4). Therefore, effective interventions to improve iron status will likely have important health benefits.

     Action to reduce young child ID would benefit from overarching policy and programmatic guidance that informs decision makers about appropriate intervention(s) or what to do, when to do it, and also addresses appropriate delivery models or howto do it.Most policies do not consider the role of maternal iron status or birth practices in the etiology of ID; supplementation for pregnant women is recommended for maternal health and not as a broader strategy to also improve newborn iron status. Interventions that could protect iron status at birth and during the first 6 mo of life, such as delayed umbilical cord clamping (5) and promotion of exclusive breast-feeding are rarely considered. In some settings, deworming is also a useful intervention to consider (6). The opportunities for different and mutually reinforcing interventions to prevent ID in young children need to be harnessed.
     In this introductory article, I discuss how ID and iron deficiency anemia (IDA) are defined and present anemia prevalence and trend data. I also summarize how new approaches to prevent ID in young children reflect a number of factors, including the recognition of the multiple opportunities where intervention is possible and the development of new vehicles to deliver iron. I close with a description of why attention to delivery systems and monitoring and evaluation is so important and a success story to illustrate how the prevalence of young child anemia can be greatly reduced.

Diagnosis, prevalence, and trends
     WHO estimates that half of all anemias are caused by ID and that the prevalence of ID in developing countries is ;2.5 times that of anemia (7). Anemia is defined as insufficient hemoglobin (Hb) or red blood cells. Additional causes include other nutritional deficiencies (vitamins B-12, B-6, and A, riboflavin, and folic acid), chronic disease and inflammation, conditions that cause blood loss or hemolysis (e.g., parasitic infections such as hookworm or malaria or hemorrhage) and hemoglobinopathies. Anemia caused by ID is referred to as IDA. Although there is disagreement about the appropriate cutoff values for the diagnosis of ID and IDA in infants (8,9), the commonly used indicators and values for diagnosis recommended by WHO are Hb ,110 g/L and serum ferritin ,10–12 mg/L for infants 6–12 mo of age (10). Alternative cutoff levels for insufficient Hb have been proposed as ,105 g/L for infants 4 and 6 mo and ,100 g/L for infants 9 mo of age (8). Other laboratory criteria for IDA include lowHbtogether with other indications of ID; these include low erythrocyte mean cell volume, low serum ferritin, high zinc protoporphyrin, and/or high soluble transferrin receptors. However, the cutoff values for these indicators are even less well developed than those for Hb and serum ferritin.

     The prevalence of anemia is higher during infancy and early childhood than at any other time in the life cycle, including pregnancy (11). Among children ,5 y of age, the prevalence of anemia (defined as Hb ,110 g/L) ranges from ;35 to 90% in those countries where a Demographic and Health Survey conducted between 1996 and 2006 included Hb measurements (Table 1). Among infants, the prevalence ranges from 25 to nearly 100%, with the majority of countries in excess of 70%. Recent estimates put the global prevalence of anemia in young children at 41.8% (12). Iron reserves of term, normal-birthweight infants, born to iron-replete mothers and who received delayed cord clamping at birth should be adequate to meet iron needs until 6 mo of age (13). However, the very high prevalence of anemia by this age indicates that infants are becoming anemic earlier than expected and that even more are likely to be ID but not yet anemic. Even if prevalence estimates were revised to use the more conservative cutoff levels suggested above, anemia would still be the most prevalent nutritional problem (Fig. 1).

FIGURE 1 Prevalence of anemia by different cutoff values in children 6–9 mo of age in selected Latin American countries with recent nationally representative data; constructed from primary analysis of Demographic and Health Survey data for each country and year represented.


New approaches to prevention of ID Current guidelines for iron supplementation in young children
are based on the assumption that iron present at birth and in breast milk is sufficient to meet requirements for the first 6 mo of life. However, this assumption depends on a number of factors
not often present in low-income countries: adequate maternal iron status, adequate birth practices that promote the transfer of a portion of the birth iron via placental blood (5,14), and exclusive breast-feeding that avoids pathological iron loss via damage to the integrity of the intestinal wall. Breast milk contains little iron, but it is in a form that is highly bioavailable (13). Introducing other liquid or solid foods during the first 6 moof life can interfere with the absorption of the iron present in breast milk (15). Therefore, interventions to prevent ID in young children need to start early in their mother’s pregnancy (by supplementing her) and continue at birth (by delayed umbilical
cord clamping and promoting early initiation of breast-feeding).
     After 6 mo, iron of adequate amount and bioavailability is necessary to prevent ID (16). Meeting iron requirements through food alone is nearly impossible, particularly between 6 and 12
mo of age, when requirements remain very high and infants consume relatively small amounts of food (17). It is during this period that universal supplementation is recommended, except in malaria-endemic areas (18). Until recently, many Ministries of Health in Latin America recommended daily supplementation with ferrous sulfate, which is highly efficacious in preventing
and treating ID. Unlike vitamin A deficiency, however, which can be prevented through twice-yearly high-dose supplements and distributed via immunization campaigns, prevention and treatment of ID require routine supplementation (usually daily or weekly). Therefore, it has traditionally been delivered through routine, often weak, health services.
Strategies to prevent early childhood ID need to include interventions beyond the typical one of starting medicinal iron supplements at 6 mo (2 mo for low-birthweight infants), taking advantage of the full range of interventions and contact with mother-infant pairs. Its prevention requires policy and programmatic guidance that informs decision makers about what to do, when to do it, and also addresses appropriate delivery models or how to do it. It also requires addressing the multiple opportunities available for prevention; pregnancy, at birth, the immediate postnatal period, and during the first 24 mo of life, as illustrated in Table 2.



FIGURE 2 Trends in anemia (Hb ,110 g/L) in children 6–59 mo of age in selected countries with nationally representative trend data available; constructed from data presented in Table 1, except for Bolivia 2003, which was calculated from primary analysis of the Demographic and Health Survey for children ,36 mo to be consistent with the age range reported in 1998.

In conclusion, ID is themost prevalent and widespread nutrition problem in infants and young children in low-income countries, is associated with large adverse effects on cognitive development, and has been difficult to prevent through traditional public health approaches. Its prevention requires overarching policy and programmatic guidance that inform decision makers about what to do and when to do it and also address appropriate delivery models or how to do it. This also requires addressing the multiple opportunities
available for prevention: pregnancy, at birth, the immediate postnatal period, and during the first 24 mo of life. New vehicles to deliver iron as well as other micronutrients and in some cases macronutrients are efficacious in reducing anemia and appear to be more acceptable to mothers and children. However, to reduce national prevalances of anemia, the many challenges of delivery through the public health systems must be overcome.

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