Dietary vitamin a intake, coverage of vitamin a megadose supplementation, and prevalence of vitamin a deficiency among marginalized children 6–59 months in anganwadis of Chandigarh: A multistage cluster sampling survey

ABSTRACT Background Biochemical vitamin A deficiency (VAD) is believed to be a serious public health problem (low serum retinol prevalence >20%) in Indian children, justifying universal high-dose vitamin A supplementation (VAS). Objective To evaluate in Indian children younger than 5 y the risk of biochemical VAD from the Comprehensive National Nutrition Survey, as well as dietary vitamin A inadequacy and excess over the tolerable upper limit of intake (TUL) from national and subnational surveys, factoring in fortification and VAS. Methods Child serum retinol data, corrected for inflammation, were examined to evaluate national- and state-level prevalence of VAD. Simultaneously, dietary intakes from the National Sample Survey Office and the National Nutrition Monitoring Bureau were examined for risk of dietary vitamin A deficiency against its average requirement (AR) derived for Indian children. Theoretical estimates of risk reduction with oil and milk vitamin A fortification were evaluated along with the risk of exceeding the TUL, as well as when combined with intake from VAS. Results The national prevalence of biochemical VAD measured in 9563 children was 15.7% (95% CI: 15.2%, 16.3%), and only 3 states had prevalence significantly >20%. The AR of vitamin A was 198 and 191 µg/d for boys and girls; the risk of dietary inadequacy was ∼70%, which reduced to 25% with oil and milk fortification. Then, the risk of exceeding the TUL was 2% and 1% in 1- to 3-y-old and 4- to 5-y-old children, respectively, but when the VAS dose was added to this intake in a cumulative 6-mo framework, the risk of exceeding the TUL rose to 30% and 8%, respectively. Conclusion The national prevalence of VAD risk is below 20% in Indian children. Because there is risk of excess intake with food fortification and VAS, serious consideration should be given to a targeted approach in place of the universal VAS program in India.

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Improving the Dietary Vitamin A Content of Rural Communities in South Africa by Replacing Non-Biofortified White Maize and Sweet Potato with Biofortified Maize and Sweet Potato in Traditional Dishes

Nutrients ◽

10.3390/nu11061198 ◽

2019 ◽

Vol 11 (6) ◽

pp. 1198 ◽

Cited By ~ 5

Author(s):

Laurencia Govender ◽

Kirthee Pillay ◽

Muthulisi Siwela ◽

Albert Thembinkosi Modi ◽

Tafadzwanashe Mabhaudhi

Keyword(s):

South Africa ◽

Rural Communities ◽

Vitamin A ◽

Sweet Potato ◽

Vitamin A Deficiency ◽

Nutritional Composition ◽

Dietary Vitamin ◽

Micronutrient Deficiencies ◽

Isoleucine Leucine ◽

Lower Protein

Biofortification of staple crops has a potential for addressing micronutrient deficiencies, such as vitamin A deficiency (VAD), which are prevalent in South Africa. The poor acceptability of provitamin A (PVA)-biofortified foods could be improved by combining them with other food items to produce modified traditional dishes. The nutritional composition of the dishes could also be improved by the modification. The study aimed to investigate the effect of replacing white maize and cream-fleshed sweet potato (CFSP)] with PVA-biofortified maize and orange-fleshed sweet potato (OFSP) on the nutritional composition of South African traditional dishes. The protein, fibre, total mineral (ash), lysine, and iron concentrations of the PVA maize phutu (traditional porridge) composite dishes (control), were not significantly different (P > 0.05) from those of white maize phutu composite dishes. However, the PVA concentration of PVA maize phutu composite dishes was higher than that of the white phutu composite dishes (P > 0.05). The OFSP had a significantly lower protein concentration, but a significantly higher (P > 0.05) fibre, ash, lysine, isoleucine, leucine, and PVA concentration, relative to the CFSP. The findings indicate that composite dishes in which white maize is replaced with PVA-biofortified maize, and switching over from CFSP to OFSP, would contribute to combating VAD in South Africa, and in other developing counties.

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Vitamin A-Deficient Diet Accelerated Atherogenesis in Apolipoprotein E−/−Mice and Dietaryβ-Carotene Prevents This Consequence

BioMed Research International ◽

10.1155/2015/758723 ◽

2015 ◽

Vol 2015 ◽

pp. 1-9 ◽

Cited By ~ 18

Author(s):

Noa Zolberg Relevy ◽

Dror Harats ◽

Ayelet Harari ◽

Ami Ben-Amotz ◽

Rafael Bitzur ◽

...

Keyword(s):

Vitamin A ◽

Apolipoprotein E ◽

Vitamin A Deficiency ◽

Plasma Cholesterol ◽

Atherosclerotic Lesion ◽

Dietary Vitamin ◽

Control Group ◽

Chow Diet ◽

Deficient Diet ◽

Aortic Sinus

Vitamin A is involved in regulation of glucose concentrations, lipid metabolism, and inflammation, which are major risk factors for atherogenesis. However, the effect of vitamin A deficiency on atherogenesis has not been investigated. Therefore, the objective of the current study was to examine whether vitamin A deficiency accelerates atherogenesis in apolipoprotein E-deficient mice (apoE−/−). ApoE−/−mice were allocated into the following groups: control, fed vitamin A-containing chow diet; BC, fed chow diet fortified withDunaliellapowder containingβc isomers; VAD, fed vitamin A-deficient diet; and VAD-BC group, fed vitamin A-deficient diet fortified with aDunaliellapowder. Following 15 weeks of treatment, liver retinol concentration had decreased significantly in the VAD group to about 30% that of control group. Vitamin A-deficient diet significantly increased both plasma cholesterol concentrations and the atherosclerotic lesion area at the aortic sinus (+61%) compared to the control group. Dietaryβc fortification inhibited the elevation in plasma cholesterol and retarded atherogenesis in mice fed the vitamin A-deficient diet. The results imply that dietary vitamin A deficiency should be examined as a risk factor for atherosclerosis and that dietaryβc, as a sole source of retinoids, can compensate for vitamin A deficiency.

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Evaluation of a two-generation rat model for vitamin A deficiency and the interrelationship with iron metabolism

British Journal Of Nutrition ◽

10.1079/bjn19950172 ◽

1995 ◽

Vol 74 (5) ◽

pp. 689-700 ◽

Cited By ~ 3

Author(s):

Annet J. C. Roodenburg ◽

Clive E. West ◽

Robert Hovenier ◽

Anton C. Beynen

Keyword(s):

Vitamin A ◽

Rat Model ◽

Binding Capacity ◽

Vitamin A Deficiency ◽

Dietary Vitamin ◽

Vitamin A Status ◽

Normal Vitamin ◽

Before And After ◽

Pregnancy And Lactation ◽

Plasma Retinol

In order to induce a range of vitamin A-deficient states in young growing rats and to study the effect of vitamin A deficiency on Fe status, we designed the following two-generation experiment. Dams were fed on diets with one of five vitamin A levels from 2 weeks before and throughout pregnancy and lactation. The pups received the same diets as their mothers both before and after weaning. The five dietary levels of vitamin A were 1200, 450, 150, 75 and 0 retinol equivalents/kg feed. Vitamin A intake did not affect reproduction outcome, nor were body and liver weights of the pups affected when they were 3·5 weeks old. Male pups with normal vitamin A status had higher plasma retinol levels than female pups. Vitamin A status of the offspring was affected from 3·5 weeks onwards. Body and liver weights were decreased in the male pups given the lowest dietary vitamin A levels from week 6·5 onwards but not in the female pups. Fe status was marginally affected. Haemoglobin levels were increased and total Fe-binding capacity was decreased in the groups given no dietary vitamin A at week 9·5. Splenic Fe was increased only in the male pups given the lowest levels of dietary vitamin A. However, as a whole, Fe status was only mildly affected and subject to considerable variation. We conclude that the two-generation rat model described here is not suitable for studying effects of vitamin A deficiency on Fe metabolism.

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Vitamin A deficiency suppresses fish immune function with differences in different intestinal segments: the role of transcriptional factorNF-κBandp38 mitogen-activated protein kinasesignalling pathways

British Journal Of Nutrition ◽

10.1017/s0007114516003342 ◽

2017 ◽

Vol 117 (1) ◽

pp. 67-82 ◽

Cited By ~ 40

Author(s):

Li Zhang ◽

Lin Feng ◽

Wei-Dan Jiang ◽

Yang Liu ◽

Pei Wu ◽

...

Keyword(s):

Vitamin A ◽

Immune Function ◽

Intestinal Inflammation ◽

Vitamin A Deficiency ◽

Challenge Test ◽

Signalling Pathway ◽

Fish Growth ◽

Ctenopharyngodon Idella ◽

Dietary Vitamin ◽

Mitogen Activated Protein

AbstractThe present study investigated the effects of dietary vitamin A on immune function in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) of young grass carp (Ctenopharyngodon idella). Fish were fed graded levels of dietary vitamin A for 10 weeks, and then a challenge test using an injection ofAeromonas hydrophilawas conducted for 14 d. The results showed that, compared with the optimum vitamin A level, vitamin A deficiency significantly decreased fish growth performance, increased enteritis morbidity, decreased intestinal innate humoral immune response and aggravated intestinal inflammation. However, liver-expressed antimicrobial peptide 2A/B mRNA in the DI andIL-6,IL-17D,IL-10, transforming growth factor (TGF)-β1andTGF-β2mRNA in the PI were not affected by vitamin A levels. Meanwhile, vitamin A deficiency disturbed inflammatory cytokines in the PI, MI and DI, which might be partly linked to p38 mitogen-activated protein kinase (p38MAPK) signalling andNF-κBcanonical signalling pathway (IκB kinaseβ(IKKβ),IKKγ, inhibitor ofκBα,NF-κB p65andc-Rel) rather thanNF-κBnon-canonical signalling pathway (NF-κB p52andIKKα). However, the signalling moleculesNF-κB p65andp38MAPKdid not participate in regulating cytokines in the PI. These results suggested that vitamin A deficiency decreased fish growth and impaired intestinal immune function, and that different immune responses in the PI, MI and DI were mediated partly byNF-κBcanonical signalling andp38MAPKsignalling pathways. On the basis of percentage of weight gain, to protect fish against enteritis morbidity and acid phosphatase activity, the optimum dietary vitamin A levels were estimated to be 0·664, 0·707 and 0·722 mg /kg, respectively.

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Effects of dietary vitamin A intake on acrosin- and plasminogen-activator activity of ram spermatozoa

Reproduction ◽

10.1530/rep.1.00182 ◽

2005 ◽

Vol 129 (6) ◽

pp. 707-715 ◽

Cited By ~ 5

Author(s):

I A Zervos ◽

M P Tsantarliotou ◽

G Vatzias ◽

P Goulas ◽

N A Kokolis ◽

...

Keyword(s):

Vitamin A ◽

Plasminogen Activator ◽

Proteolytic Enzymes ◽

Vitamin A Deficiency ◽

Plasminogen Activators ◽

The Body ◽

Dietary Vitamin ◽

Retinyl Acetate ◽

Plasminogen Activator Activity ◽

Group B

Acrosin and plasminogen activators are proteolytic enzymes of ram spermatozoa that play an essential role in the induction of the acrosome reaction, as well as the binding of spermatozoa to the oocyte and their penetration through the layers that surround the oocyte. Since vitamin A can alter gene expression in various tissues, testis included, this study was undertaken to evaluate the possible effect of vitamin A intake on acrosin- and plasminogen-activator activity. During a 20-week experiment, 15 rams of the Greek breed Karagouniki, divided to three groups, received different amounts of vitamin Aper osin retinyl acetate capsules (group A, controls, 12 500 iu/animal per day; group B, 50 000 iu/animal per day; group C, 0 iu/animal per day up to the 13th week, then 150 000 iu/animal per day until the end of the experiment). Acrosin- and plasminogen-activator activity were determined by spectrophotometric methods. Vitamin A was determined in blood plasma by HPLC. No statistical differences were detected regarding the body weight of the rams or the qualitative and quantitative parameters of their ejaculate throughout the whole experiment. No statistically significant alterations of enzyme activity were detected in group B. In group C, both enzyme activities started declining in week 9. Compared with controls, maximum reduction for acrosin was 49% on week 11 and for plasminogen activators 51% in week 14. Activities returned to normal rates after vitamin A resupplementation. To date, the main result of vitamin A deficiency was known to be arrest of spermatogenesis and testicular degeneration. A new role for vitamin A may be suggested, since it can influence factors related to male reproductive ability before spermatogenesis is affected.

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THE EFFECT OF DIETARY VITAMIN A DEFICIENCY ON THE CLINICAL CONDITION, BLOOD CONSTITUENTS AND INTERNAL ORGANS OF ADULT BUFFALOE

Assiut Veterinary Medical Journal ◽

10.21608/avmj.1982.191562 ◽

1982 ◽

Vol 9 (17.18) ◽

pp. 135-140

Keyword(s):

Vitamin A ◽

Clinical Condition ◽

Vitamin A Deficiency ◽

Dietary Vitamin ◽

Internal Organs ◽

Blood Constituents

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The effect of retinyl palmitate added to iron-fortified maize porridge on erythrocyte incorporation of iron in African children with vitamin A deficiency

British Journal Of Nutrition ◽

10.1079/bjn2003914 ◽

2003 ◽

Vol 90 (2) ◽

pp. 337-343 ◽

Cited By ~ 15

Author(s):

Lena Davidsson ◽

Pierre Adou ◽

Christophe Zeder ◽

Thomas Walczyk ◽

Richard Hurrell

Keyword(s):

Single Dose ◽

Vitamin A ◽

Test Meal ◽

Vitamin A Deficiency ◽

Geometric Mean ◽

Retinyl Palmitate ◽

Dietary Vitamin ◽

Vitamin A Supplementation ◽

Vitamin A Status ◽

Before And After

Retinyl palmitate added to Fe-fortified maize bread has been reported to enhance Fe absorption in adult Venezuelan subjects but not in Western Europeans. It is not known to what extent these results were influenced by differences in vitamin A status of the study subjects. The objective of the present study was to evaluate the influence of retinyl palmitate added to Fe-fortified maize porridge on erythrocyte incorporation of Fe in children with vitamin A deficiency, before and after vitamin A supplementation. Erythrocyte incorporation of Fe-stable isotopes was measured 14 d after intake of maize porridge (2·0 mg Fe added as ferrous sulfate) with and without added retinyl palmitate (3·5 μmol; 3300 IU). The study was repeated 3 weeks after vitamin A supplementation (intake of a single dose of 210 μmol retinyl palmitate; ‘vitamin A capsule’). Vitamin A status was evaluated by the modified relative dose–response (MRDR) technique. Retinyl palmitate added to the test meal reduced the geometric mean erythrocyte incorporation of Fe at baseline from 4·0 to 2·6 % (P=0·008, n 13; paired t test). At 3 weeks after vitamin A supplementation, geometric mean erythrocyte incorporation was 1·9 and 2·3 % respectively from the test meal with and without added retinyl palmitate (P=0·283). Mean dehydroretinol:retinol molar ratios were 0·156 and 0·125 before and after intake of the single dose of 210 μmol retinyl palmitate; ‘vitamin A capsule’ (P=0·15). In conclusion, retinyl palmitate added to the labelled test meals significantly decreased erythrocyte incorporation of Fe in children with vitamin A deficiency at baseline but had no statistically significant effect 3 weeks after vitamin A supplementation. The difference in response to retinyl palmitate added to Fe-fortified maize porridge on erythrocyte incorporation of Fe before and after intake of the vitamin A capsule indicates, indirectly, changes in vitamin A status not measurable by the MRDR technique. The lack of conclusive data on the effect of retinyl palmitate on Fe absorption indicates the complexity of the interactions between vitamin A status, dietary vitamin A and Fe metabolism.

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