The role of folic acid and Vitamin B12 in genomic stability of human cells

Folic acid plays a critical role in the prevention of chromosome breakage and hypomethylation of DNA. This activity is compromised when Vitamin B12 (B12) concentration is low because methionine synthase activity is reduced, lowering the concentration of S-adenosyl methionine (SAM) which in turn may diminish DNA methylation and cause folate to become unavailable for the conversion of dUMP to dTMP. The most plausible explanation for the chromosome-breaking effect of low folate is excessive uracil misincorporation into DNA, a mutagenic lesion that leads to strand breaks in DNA during repair. Both in vitro and in vivo studies with human cells clearly show that folate deficiency causes expression of chromosomal fragile sites, chromosome breaks, excessive uracil in DNA, micronucleus formation and DNA hypomethylation. In vivo studies show that Vitamin B12 deficiency and elevated plasma homocysteine are significantly correlated with increased micronucleus formation. In vitro experiments indicate that genomic instability in human cells is minimised when folic acid concentration in culture medium is >227nmol/l. Intervention studies in humans show: (a) that DNA hypomethylation, chromosome breaks, uracil misincorporation and micronucleus formation are minimised when red cell folate concentration is >700nmol/l folate; and (b) micronucleus formation is minimised when plasma concentration of Vitamin B12 is >300pmol/l and plasma homocysteine is <7.5micromol/l. These concentrations are achievable at intake levels in excess of current RDIs i.e. more than 200-400microgram folic acid per day and more than 2microgram Vitamin B12 per day. A placebo-controlled study with a dose-response suggests that based on the micronucleus index in lymphocytes, an RDI level of 700microgram/day for folic acid and 7microgram/day for Vitamin B12 would be appropriate for genomic stability in young adults. Dietary intakes above the current RDI may be particularly important in those with extreme defects in the absorption and metabolism of these Vitamins, for which ageing is a contributing factor.     

Folate (vitamin B9) and vitamin B12 and their function in the maintenance of nuclear and mitochondrial genome integrity

Folate plays a critical role in the prevention of uracil incorporation into DNA and hypomethylation of DNA. This activity is compromised when vitamin B12 concentration is low because methionine synthase activity is reduced, lowering the concentration of S-adenosyl methionine (SAM) which in turn may diminish DNA methylation and cause folate to become unavailable for the conversion of dUMP to dTMP. The most plausible explanation for the chromosome-breaking effect of low folate is excessive uracil misincorporation into DNA, a mutagenic lesion that leads to strand breaks in DNA during repair. Both in vitro and in vivo studies with human cells clearly show that folate deficiency causes expression of chromosomal fragile sites, chromosome breaks, excessive uracil in DNA, micronucleus formation, DNA hypomethylation and mitochondrial DNA deletions. In vivo studies show that folate and/or vitamin B12 deficiency and elevated plasma homocysteine (a metabolic indicator of folate deficiency) are significantly correlated with increased micronucleus formation and reduced telomere length respectively. In vitro experiments indicate that genomic instability in human cells is minimised when folic acid concentration in culture medium is greater than 100nmol/L. Intervention studies in humans show (a) that DNA hypomethylation, chromosome breaks, uracil incorporation and micronucleus formation are minimised when red cell folate concentration is greater than 700nmol/L and (b) micronucleus formation is minimised when plasma concentration of vitamin B12 is greater than 300pmol/L and plasma homocysteine is less than 7.5μmol/L. These concentrations are achievable at intake levels at or above current recommended dietary intakes of folate (i.e. >400μg/day) and vitamin B12 (i.e. >2μg/day) depending on an individual's capacity to absorb and metabolise these vitamins which may vary due to genetic and epigenetic differences.     

Uracil misincorporation into DNA of leukocytes of young women with positive folate balance depends on plasma vitamin B12 concentrations and methylenetetrahydrofolate reductase polymorphisms. A pilot study

Changes in the folate and vitamin B12 status in the body influence the extent of uracil misincorporation (UrMis) into DNA, which is one of the biomarkers of genomic stability and, thus, portends a risk of cancer. In our study, the level of UrMis into DNA was evaluated by the comet assay (using the specific DNA repair enzyme, uracil DNA glycosylase) in leukocytes from blood donated by healthy young women with positive folate balance achieved by 4 weeks of folic acid supplementation (400 microg/day). The nutritional status was evaluated on the basis of nine food diaries recorded by the subjects during two winter months. The data were computerized, and the intake of nutrients and micronutrients was estimated using the DIETA 2 program (Food and Nutrition Institute, Warsaw, Poland) linked to recently updated Polish food tables. The plasma folate and vitamin B12 concentration, as well as methylenetetrahydrofolate reductase (MTHFR) polymorphisms, were evaluated to determine their influence on the level of UrMis into DNA. The mean value of B12 intake for all subjects reached 100% of the Polish recommended dietary allowances (RDA), whereas the mean value of folate intake, before folate supplementation, was 50%, suggesting moderate deficiency. Folic acid supplementation brought the folate intake way above the RDA, and plasma folate concentration in each individual was above the deficient range (mean value 14.67 ng/ml). The UrMis did not correlate with the plasma folate concentration, but the level of UrMis was significantly lower in subjects with plasma vitamin B12 concentration above 400 pg/ml (P=.02) only after folic acid supplementation. The concentration of folate in plasma correlated (P相似文献   

Imbalanced base excision repair in response to folate deficiency is accelerated by polymerase beta haploinsufficiency

The mechanism by which folate deficiency influences carcinogenesis is not well established, but a phenotype of DNA strand breaks, mutations, and chromosomal instability suggests an inability to repair DNA damage. To elucidate the mechanism by which folate deficiency influences carcinogenicity, we have analyzed the effect of folate deficiency on base excision repair (BER), the pathway responsible for repairing uracil in DNA. We observe an up-regulation in initiation of BER in liver of the folate-deficient mice, as evidenced by an increase in uracil DNA glycosylase protein (30%, p < 0.01) and activity (31%, p < 0.05). However, no up-regulation in either BER or its rate-determining enzyme, DNA polymerase beta (beta-pol) is observed in response to folate deficiency. Accordingly, an accumulation of repair intermediates in the form of DNA single strand breaks (37% increase, p < 0.03) is observed. These data indicate that folate deficiency alters the balance and coordination of BER by stimulating initiation without subsequently stimulating the completion of repair, resulting in a functional BER deficiency. In directly establishing that the inability to induce beta-pol and mount a BER response when folate is deficient is causative in the accumulation of toxic repair intermediates, beta-pol-haploinsufficient mice subjected to folate deficiency displayed additional increases in DNA single strand breaks (52% increase, p < 0.05) as well as accumulation in aldehydic DNA lesions (38% increase, p < 0.01). Since young beta-polhaploinsufficient mice do not spontaneously exhibit increased levels of these repair intermediates, these data demonstrate that folate deficiency and beta-pol haploinsufficiency interact to increase the accumulation of DNA damage. In addition to establishing a direct role for beta-pol in the phenotype expressed by folate deficiency, these data are also consistent with the concept that repair of uracil and abasic sites is more efficient than repair of oxidized bases.     

Micronutrient Levels and Supplement Intake in Pregnancy after Bariatric Surgery: A Prospective Cohort Study

Background

Studies report frequent micronutrient deficiencies after bariatric surgery, but less is known about micronutrient levels of pregnant women after bariatric surgery.

Objective

To prospectively evaluate micronutrient levels and supplement intake in pregnancy following bariatric surgery.

Design

A multicenter prospective cohort study including women with restrictive or malabsorptive types of bariatric surgery. Nutritional deficiencies, together with supplement intake, were screened during pregnancy.

Results

The total population included 18 women in the restrictive and 31 in the malabsorptive group. Most micronutrients were depleted and declined significantly during pregnancy. The proportion of women with low vitamin A and B-1 levels increased to respectively 58 and 17% at delivery (P = 0.005 and 0.002). The proportion of women with vitamin D deficiency decreased from 14% at trimester 1 to 6% at delivery (P = 0.030). Mild anemia was found in respectively 22 and 40% of the women at trimester 1 and delivery. In the first trimester, most women took a multivitamin (57.1%). In the second and third trimester, the majority took additional supplements (69.4 and 73.5%). No associations were found between supplement intake and micronutrient deficiencies.

Conclusion

Pregnant women with bariatric surgery show frequent low micronutrient levels. Supplementation partially normalizes low levels of micronutrients.     

A role for supplements in optimizing health: the metabolic tune-up

An optimum intake of micronutrients and metabolites, which varies with age and genetic constitution, would tune up metabolism and give a marked increase in health, particularly for the poor, young, obese, and elderly, at little cost. (1) DNA damage. Deficiency of vitamins B-12, folic acid, B-6, C or E, or iron or zinc appears to mimic radiation in damaging DNA by causing single- and double-strand breaks, oxidative lesions or both. Half of the population may be deficient in at least one of these micronutrients. (2) The Km concept. Approximately 50 different human genetic diseases that are due to a poorer binding affinity (Km) of the mutant enzyme for its coenzyme can be remedied by feeding high-dose B vitamins, which raise levels of the corresponding coenzyme. Many polymorphisms also result in a lowered affinity of enzyme for coenzyme. (3) Mitochondrial oxidative decay. This decay, which is a major contributor to aging, can be ameliorated by feeding old rats the normal mitochondrial metabolites acetyl carnitine and lipoic acid at high levels. Many common micronutrient deficiencies, such as iron or biotin, cause mitochondrial decay with oxidant leakage leading to accelerated aging and neural decay.     

Dietary choline deficiency causes DNA strand breaks and alters epigenetic marks on DNA and histones

Dietary choline is an important modulator of gene expression (via epigenetic marks) and of DNA integrity. Choline was discovered to be an essential nutrient for some humans approximately one decade ago. This requirement is diminished in young women because estrogen drives endogenous synthesis of phosphatidylcholine, from which choline can be derived. Almost half of women have a single nucleotide polymorphism that abrogates estrogen-induction of endogenous synthesis, and these women require dietary choline just as do men. In the US, dietary intake of choline is marginal. Choline deficiency in people is associated with liver and muscle dysfunction and damage, with apoptosis, and with increased DNA strand breaks. Several mechanisms explain these modifications to DNA. Choline deficiency increases leakage of reactive oxygen species from mitochondria consequent to altered mitochondrial membrane composition and enhanced fatty acid oxidation. Choline deficiency impairs folate metabolism, resulting in decreased thymidylate synthesis and increased uracil misincorporation into DNA, with strand breaks resulting during error-prone repair attempts. Choline deficiency alters DNA methylation, which alters gene expression for critical genes involved in DNA mismatch repair, resulting in increased mutation rates. Any dietary deficiency which increases mutation rates should be associated with increased risk of cancers, and this is the case for choline deficiency. In rodent models, diets low in choline and methyl-groups result in spontaneous hepatocarcinomas. In human epidemiological studies, there are interesting data that suggest that this also may be the case for humans, especially those with SNPs that increase the dietary requirement for choline.     

A screen for suppressors of gross chromosomal rearrangements identifies a conserved role for PLP in preventing DNA lesions

Genome instability is a hallmark of cancer cells. One class of genome aberrations prevalent in tumor cells is termed gross chromosomal rearrangements (GCRs). GCRs comprise chromosome translocations, amplifications, inversions, deletion of whole chromosome arms, and interstitial deletions. Here, we report the results of a genome-wide screen in Saccharomyces cerevisiae aimed at identifying novel suppressors of GCR formation. The most potent novel GCR suppressor identified is BUD16, the gene coding for yeast pyridoxal kinase (Pdxk), a key enzyme in the metabolism of pyridoxal 5' phosphate (PLP), the biologically active form of vitamin B6. We show that Pdxk potently suppresses GCR events by curtailing the appearance of DNA lesions during the cell cycle. We also show that pharmacological inhibition of Pdxk in human cells leads to the production of DSBs and activation of the DNA damage checkpoint. Finally, our evidence suggests that PLP deficiency threatens genome integrity, most likely via its role in dTMP biosynthesis, as Pdxk-deficient cells accumulate uracil in their nuclear DNA and are sensitive to inhibition of ribonucleotide reductase. Since Pdxk links diet to genome stability, our work supports the hypothesis that dietary micronutrients reduce cancer risk by curtailing the accumulation of DNA damage and suggests that micronutrient depletion could be part of a defense mechanism against hyperproliferation.     

The Global Hidden Hunger Indices and Maps: An Advocacy Tool for Action

The unified global efforts to mitigate the high burden of vitamin and mineral deficiency, known as hidden hunger, in populations around the world are crucial to the achievement of most of the Millennium Development Goals (MDGs). We developed indices and maps of global hidden hunger to help prioritize program assistance, and to serve as an evidence-based global advocacy tool. Two types of hidden hunger indices and maps were created based on i) national prevalence data on stunting, anemia due to iron deficiency, and low serum retinol levels among preschool-aged children in 149 countries; and ii) estimates of Disability Adjusted Life Years (DALYs) attributed to micronutrient deficiencies in 136 countries. A number of countries in sub-Saharan Africa, as well as India and Afghanistan, had an alarmingly high level of hidden hunger, with stunting, iron deficiency anemia, and vitamin A deficiency all being highly prevalent. The total DALY rates per 100,000 population, attributed to micronutrient deficiencies, were generally the highest in sub-Saharan African countries. In 36 countries, home to 90% of the world’s stunted children, deficiencies of micronutrients were responsible for 1.5-12% of the total DALYs. The pattern and magnitude of iodine deficiency did not conform to that of other micronutrients. The greatest proportions of children with iodine deficiency were in the Eastern Mediterranean (46.6%), European (44.2%), and African (40.4%) regions. The current indices and maps provide crucial data to optimize the prioritization of program assistance addressing global multiple micronutrient deficiencies. Moreover, the indices and maps serve as a useful advocacy tool in the call for increased commitments to scale up effective nutrition interventions.     

An assay for uracil in human DNA at baseline: effect of marginal vitamin B6 deficiency

Improvements are made to our gas-chromatography-mass-spectrometry-based assay for quantifying low levels of DNA-uracil. Folate deficiency leads to increased deoxyuridine monophosphate/thymidylate (dUMP/dTMP) ratios and uracil misincorporation into DNA, which may increase cancer risk. Vitamin B6 (B6) deficiency might also result in increased DNA-uracil because B6 is a cofactor for serine hydroxymethyltransferase, which catalyzes the methylation of tetrahydrofolate (THF) to methylene-THF, the folate form that is required to convert dUMP to dTMP. However, the low baseline levels of DNA-uracil in healthy human lymphocytes are difficult to measure accurately. This version of the assay (Uracil assay V3) has an approximately 10-fold increase in signal strength over the previous method and a 10-fold lower detection limit (0.2 pg uracil). Five micrograms of DNA, the amount in about 1 ml of human blood, is a suitable amount for this assay. Using this improved assay, DNA-uracil was measured in lymphocytes from 12 healthy smoking or nonsmoking young men and women who consumed a B6-restricted diet (0.7 mg B6/day, or approximately half the recommended dietary allowance) for 28 days. DNA-uracil concentration was not significantly related to B6 status or smoking. More severe and/or prolonged B6 deficiency may be necessary to detect significant changes in DNA-uracil in humans. The average concentration of DNA-uracil in these subjects was found to be approximately 3,000 uracils per diploid lymphocyte, which is comparable to steady state levels of one of the oxidative adducts of DNA, 8-oxoguanine.     

Folate deficiency inhibits the proliferation of primary human CD8+ T lymphocytes in vitro

Folate is required for one-carbon transfer reactions and the formation of purines and pyrimidines for DNA and RNA synthesis. Deficiency of folate can lead to many clinical abnormalities, including macrocytic anemia, cardiovascular diseases, birth defects, and carcinogenesis. The nucleotide imbalance due to folate deficiency causes cell cycle arrest in the S phase and uracil misincorporation into DNA, which may result in DNA double-strand breaks during repair. The role of folate in the immune system has not been fully characterized. We cultured PHA-activated human T lymphocytes in varying concentrations of folate, and measured proliferation, cell cycle, apoptosis, uracil misincorporation, and proportions of Th cells (CD4(+)) and cytotoxic T (CD8(+)) cells. Folate deficiency reduced proliferation of T lymphocytes, induced cell cycle arrest in the S phase, induced apoptosis, and increased the level of uracil in DNA. Folate deficiency also increased the CD4(+) to CD8(+) ratio due to a marked reduction of CD8(+) cell proliferation. Folate or nucleoside repletion of folate-deficient cells rapidly restored T lymphocyte proliferation and normal cell cycle, reduced the DNA uracil content, and lowered the CD4(+) to CD8(+) ratio. These data suggest that folate status may affect the immune system by reducing the capacity of CD8(+) cells to proliferate in response to activation.     

The interactive effect of methyl-group diet and polymorphism of methylenetetrahydrofolate reductase on the risk of colorectal cancer

Higher intakes of vegetables have been reported to be associated with a reduced risk of colorectal cancer. Folate, a water-soluble B vitamin, and one of the major micronutrients in vegetables, may be partly responsible for this beneficial effect. Conversely, a high alcohol intake has been related to an increased risk of colorectal cancer. The combination of high folate and low alcohol intake, "methyl group diets", was reported to have a strong protective effect. These findings support a role of methyl group availability as an underlying mechanism for an effect of folate on colorectal carcinogenesis. The protective effect of the homozygous variant TT form of the MTHFR genotype (C677T) on the risk of colorectal cancer seems to be modified by the level of methyl diets, that is, by folate, which has a protective effect, or conversely by alcohol. Recommendation of higher intake of folate and lower intake of alcohol to the target population, especially those with TT genotype of MTHFR, may be an effective preventive approach against colorectal cancer.     

Global malnutrition overlaps with pollinator-dependent micronutrient production

Pollinators contribute around 10% of the economic value of crop production globally, but the contribution of these pollinators to human nutrition is potentially much higher. Crops vary in the degree to which they benefit from pollinators, and many of the most pollinator-dependent crops are also among the richest in micronutrients essential to human health. This study examines regional differences in the pollinator dependence of crop micronutrient content and reveals overlaps between this dependency and the severity of micronutrient deficiency in people around the world. As much as 50% of the production of plant-derived sources of vitamin A requires pollination throughout much of Southeast Asia, whereas other essential micronutrients such as iron and folate have lower dependencies, scattered throughout Africa, Asia and Central America. Micronutrient deficiencies are three times as likely to occur in areas of highest pollination dependence for vitamin A and iron, suggesting that disruptions in pollination could have serious implications for the accessibility of micronutrients for public health. These regions of high nutritional vulnerability are understudied in the pollination literature, and should be priority areas for research related to ecosystem services and human well-being.     

Uracil in DNA, determined by an improved assay, is increased when deoxynucleosides are added to folate-deficient cultured human lymphocytes

Folate deficiency leads to increased dUMP/dTMP ratios and uracil misincorporation into DNA, which may increase cancer risk. We improved a previously described gas chromatography-mass spectrometry (GC-MS) assay for uracil in DNA and validated the assay by analyzing the DNA-uracil content of normal, primary human lymphocytes that were cultured in 0-3000 nM folic acid. In addition, the effects of nucleoside mixtures T or TdCA (T, thymidine; A, adenosine; dC, deoxycytidine) were investigated. Over 4 consecutive days, the inter- and intraassay coefficients of variation (CVs) were 2.3-3.9 and 0.6-2.2%. Mean recovery was 99.4%. Oligonucleotides containing 100 pg of uracil yielded a mean uracil measurement of 110.1 pg (CV=2.7%). Cells grown in different concentrations of folate showed a bimodal response, with maximum DNA-uracil at 12 nM, and minima at 0 and 3000 nM folate. Extremely folate-deficient cells may incorporate less uracil because DNA synthesis is reduced. A wide response to folate deficiency was seen in cells from different donors, suggesting that genetic background plays a critical role in individual susceptibility to DNA damage and cancer risk. Unexpectedly, TdCA supplementation caused increased DNA-uracil (vs 3000 nM folate for 10 days, P > 0.05), probably due to the conversion of deoxycytidine to deoxyuridine by cytidine deaminase, leading to elevated dUMP/dTMP ratios. This improved uracil assay could serve as a useful tool in the study of the mechanism of uracil misincorporation into DNA. The assay requires 3 microg of DNA per folate-deficient sample, but more may be required for baseline DNA-uracil detection in healthy humans.     

Micronutrient Deficiencies and Related Factors in School-Aged Children in Ethiopia: A Cross-Sectional Study in Libo Kemkem and Fogera Districts,Amhara Regional State

Introduction

The present study describes the distribution of selected micronutrients and anaemia among school-aged children living in Libo Kemkem and Fogera (Amhara State, Ethiopia), assessing differences by socio-demographic characteristics, health status and dietary habits.

Methods

A cross-sectional survey was carried out during May–December 2009. Socio-demographic characteristics, health status and dietary habits were collected. Biomarkers were determined for 764 children. Bivariate and multivariable statistical methods were employed to assess micronutrient deficiencies (MD), anaemia, and their association with different factors.

Results

More than two thirds of the school-aged children (79.5%) had at least one MD and 40.5% had two or more coexisting micronutrient deficiencies. The most prevalent deficiencies were of zinc (12.5%), folate (13.9%), vit A (29.3%) and vit D (49%). Anaemia occurred in 30.9% of the children. Children living in rural areas were more likely to have vit D insufficiency [OR: 5.9 (3.7–9.5)] but less likely to have folate deficiency [OR: 0.2 (0.1–0.4)] and anaemia [OR: 0.58 (0.35–0.97)]. Splenomegaly was positively associated with folate deficiency and anaemia [OR: 2.77 (1.19–6.48) and 4.91 (2.47–9.75)]. Meat and fish consumption were inversely correlated with zinc and ferritin deficiencies [OR: 0.2 (0.1–0.8) and 0.2 (0.1–0.9)], while oil consumption showed a negative association with anaemia and deficiencies of folate and vitamin A [0.58 (0.3–0.9), OR: 0.5 (0.3–0.9) and 0.6 (0.4–0.9)]. Serum ferritin levels were inversely correlated to the presence of anaemia (p<0.005).

Conclusion

There is a high prevalence of vitamin A deficiency and vitamin D insufficiency and a moderate prevalence of zinc and folate deficiencies in school-aged children in this area. The inverse association of anaemia and serum ferritin levels may be due to the presence of infectious diseases in the area. To effectively tackle malnutrition, strategies should target not only isolated micronutrient supplementation but also diet diversification.     

Nitrate assimilation in rice seedlings as affected by mineral nutrition

Deficiencies of each macronutrient (N, P, K, Ca, Mg and Fe)in the culture solution depressed the specific activities ofnitrate reductase (NR) and nitrite reductase (NiR) from riceseedlings. Nitrate and potassium deficiencies especially loweredNR induction, whereas phosphorus deficiency caused the leastdecrease in enzyme induction. On the other hand the activityof NiR was decreased most by deficiencies of nitrate and phosphorus.Potassium deficiency was not as effective in suppressing theinduction of NiR. Sulfur deficiency slightly promoted the inductionof both NR and NiR. Generally, micronutrient deficiencies didnot affect either enzyme. NR induction was slightly decreasedby B, Zn, Cu and Mo deficiencies, and increased by Mn deficiency;whereas NiR activity was slightly increased by B and Cu deficiencies,and was not affected by other micronutrients. Nitrate contentwas decreased by deficiencies of N, P, K, Ca, and micronutrients,and unaffected by Mg, Fe and S deficiencies. Glutamic acid dehydrogenase(GDH) activity was increased by N, Fe and P deficiencies, anddecreased by Mo and Zn deficiencies, and unaffected by othernutrient treatments. (Received August 25, 1976; )     

Vitamins/minerals and genomic stability in humans

Recommended dietary allowances (RDAs) of micronutrients have been traditionally derived as those levels necessary to prevent symptoms of deficiency diseases. There is increasing evidence that higher levels of many such micronutrients may be necessary for various DNA maintenance reactions, and that the current RDAs for some micronutrients may be inadequate to protect against genomic instability. Supplementation of a normal diet, with either vitamins and/or minerals or with isolated plant polyphenols, is becoming increasingly common in most Western populations. However, there is no clear agreement as to how much supplementation should occur, if at all, and genotypic differences are not accounted for. The 14 mini-reviews in this special issue summarise the role of specific micronutrients in various aspects of DNA maintenance: DNA synthesis, DNA repair, DNA methylation, gene mutation, chromosome breakage, chromosome segregation, gene expression, oxidative stress, necrosis and apoptosis. Evidence has been collated from mammalian and human experiments, both using in vitro cultures and in vivo approaches. Authors were asked to critically assess the strength of evidence as to whether the micronutrient can affect genomic stability in humans at realistic intake levels, and to estimate optimal dietary ranges where possible. Information on further research necessary is also documented. These reviews are an essential step towards a definition of RDAs designed to maintain genomic stability.     

Intra-Individual Double Burden of Overweight and Micronutrient Deficiencies among Vietnamese Women

Background

Vietnamese Living Standard Surveys showed that the rate of overweight and obese in Vietnamese adults doubled between 1992 and 2002, from 2% to 5.5%, respectively with no significant difference in the proportions of overweight/obesity between men and women.

Objectives

Considering the increasing public health concern over the double burden of malnutrition in Vietnam, we investigated micronutrient deficiencies among women of reproductive age according to their Body Mass Index.

Methods

A transversal study was conducted in 2010 among 1530 women of reproductive age from 19 provinces. Participating women were asked to give a non-fasting blood sample for plasma iron, vitamin A, folate, vitamin B₁₂ and zinc assessment.

Results

Although % body fat was associated with haemoglobin, ferritin, retinol and zinc concentrations, BMI category was only associated with marginal vitamin A status (19% among underweight vs 7% among overweight/obese; p<0.0001) and not with iron deficiency anemia, zinc deficiency, vitamin B₁₂ deficiency or folate status. The prevalence of iron, and vitamin B₁₂ deficiencies was respectively 11.4% and 15% among the 20% overweight/obese women; prevalence of zinc deficiency and marginal/deficient folate status was much higher, affecting respectively 61.1% and 25.8%. Intra-individual double burden of malnutrition (overweight/obesity (OW) and micronutrient deficiency) was observed among 2.0% for OW-anemia, 2.3% OW-iron deficient, 3.0% for OW-Vitamin B₁₂ deficiency, 12.2% for OW-Zinc deficiency and 5.2% for OW-marginal/deficient folate status.

Conclusions

This large, cross-sectional survey demonstrated that micronutrient deficiencies are an issue across the weight spectrum among women in Vietnam, with only vitamin A status being better among overweight than underweight women. It is therefore essential for Vietnam to actively prevent women of reproductive age from overweight/obesity and at same time to control micronutrient deficiencies in this population to limit their economic and health consequences.     

Malnutrition,anemia, micronutrient deficiency and parasitic infections among schoolchildren in rural Tanzania

BackgroundMalnutrition, anemia, micronutrient deficiency and parasitic infections continue to impact the nutritional status and health of children in lower-income countries. However, not enough data concerning this issue is available. The aim of this study was to assess the distribution of nutritional indicators, anemia and micronutrient deficiency and their underlying risk factors among schoolchildren in south-eastern Tanzania.Methodology/Principal findingsThis cross-sectional study enrolled primary schoolchildren aged 6–12 years from Kikwawila and Kiberege wards, Tanzania. In total, 471 schoolchildren underwent a physical examination and provided blood, stool and urine samples for an assessment of the levels of different micronutrients, nutritional and anemia status, and parasitic infection status. We employed bivariate and multivariate logistic regression to determine the association between nutritional statuses, anemia, micronutrient deficiency and parasitic infections. We found that 23.90%, 12.60% and 16.20% of schoolchildren were stunted, underweight and wasted, respectively. About 14.0% of schoolchildren were found to be anemic. Children diagnosed with Plasmodium falciparum infection were more likely to have low levels of ferritin (aOR: 10.40, 95% CI: 2.88-40.53) and elevated levels of serum soluble transferrin receptor (aOR: 3.59, 95% CI: 1.27-11.23), respectively. Vitamin A (34.71%) and vitamin B12 (8.79%) were the most prevalent micronutrients found to be deficient in diagnosed children. Finally, we found that schoolchildren attending the most rural schools were five times more likely to be diagnosed with at least one micronutrient deficiency (aOR: 5.04, 95% CI: 2.38–11.44).Conclusions/SignificanceMalnutrition, anemia and micronutrient deficiency still pose a significant health burden among schoolchildren living in rural Tanzania. To effectively tackle this burden, health interventions such as deworming, micronutrient supplementation, vector control, health education and access to clean water and improved sanitation should be strengthened and made sustainable.