Talk:Nutrition: Difference between revisions
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===Vitamin A supplements for preventing mortality, illness, and blindness in children aged under 5: systematic review and meta-analysis=== | |||
BMJ. 2011 Aug 25;343:d5094. doi: 10.1136/bmj.d5094. | |||
Mayo-Wilson E, Imdad A, Herzer K, Yakoob MY, Bhutta ZA. | |||
Source | |||
Centre for Evidence-Based Intervention, Department of Social Policy and Intervention, University of Oxford, Barnett House, Oxford OX1 2ER, UK. | |||
Abstract | |||
OBJECTIVE: | |||
To determine if vitamin A supplementation is associated with reductions in mortality and morbidity in children aged 6 months to 5 years. | |||
DESIGN: | |||
Systematic review and meta-analysis. Two reviewers independently assessed studies for inclusion. Data were double extracted; discrepancies were resolved by discussion. Meta-analyses were performed for mortality, illness, vision, and side effects. | |||
DATA SOURCES: | |||
Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library, Medline, Embase, Global Health, Latin American and Caribbean Health Sciences, metaRegister of Controlled Trials, and African Index Medicus. Databases were searched to April 2010 without restriction by language or publication status. Eligibility criteria for selecting studies Randomised trials of synthetic oral vitamin A supplements in children aged 6 months to 5 years. Studies of children with current illness (such as diarrhoea, measles, and HIV), studies of children in hospital, and studies of food fortification or β carotene were excluded. | |||
RESULTS: | |||
43 trials with about 215 633 children were included. Seventeen trials including 194 483 participants reported a 24% reduction in all cause mortality (rate ratio=0.76, 95% confidence interval 0.69 to 0.83). Seven trials reported a 28% reduction in mortality associated with diarrhoea (0.72, 0.57 to 0.91). Vitamin A supplementation was associated with a reduced incidence of diarrhoea (0.85, 0.82 to 0.87) and measles (0.50, 0.37 to 0.67) and a reduced prevalence of vision problems, including night blindness (0.32, 0.21 to 0.50) and xerophthalmia (0.31, 0.22 to 0.45). Three trials reported an increased risk of vomiting within the first 48 hours of supplementation (2.75, 1.81 to 4.19). | |||
CONCLUSIONS: | |||
Vitamin A supplementation is associated with large reductions in mortality, morbidity, and vision problems in a range of settings, and these results cannot be explained by bias. Further placebo controlled trials of vitamin A supplementation in children between 6 and 59 months of age are not required. However, there is a need for further studies comparing different doses and delivery mechanisms (for example, fortification). Until other sources are available, vitamin A supplements should be given to all children at risk of deficiency, particularly in low and middle income countries. | |||
PMID 21868478 | |||
http://www.bmj.com/content/343/bmj.d5094.full | |||
===The supply of choline is important for fetal progenitor cells=== | ===The supply of choline is important for fetal progenitor cells=== | ||
Revision as of 13:49, 1 September 2011
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Cite this page: Hill, M.A. (2024, April 19) Embryology Nutrition. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Nutrition |
2011
Vitamin A supplements for preventing mortality, illness, and blindness in children aged under 5: systematic review and meta-analysis
BMJ. 2011 Aug 25;343:d5094. doi: 10.1136/bmj.d5094.
Mayo-Wilson E, Imdad A, Herzer K, Yakoob MY, Bhutta ZA. Source Centre for Evidence-Based Intervention, Department of Social Policy and Intervention, University of Oxford, Barnett House, Oxford OX1 2ER, UK.
Abstract
OBJECTIVE: To determine if vitamin A supplementation is associated with reductions in mortality and morbidity in children aged 6 months to 5 years.
DESIGN: Systematic review and meta-analysis. Two reviewers independently assessed studies for inclusion. Data were double extracted; discrepancies were resolved by discussion. Meta-analyses were performed for mortality, illness, vision, and side effects.
DATA SOURCES: Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library, Medline, Embase, Global Health, Latin American and Caribbean Health Sciences, metaRegister of Controlled Trials, and African Index Medicus. Databases were searched to April 2010 without restriction by language or publication status. Eligibility criteria for selecting studies Randomised trials of synthetic oral vitamin A supplements in children aged 6 months to 5 years. Studies of children with current illness (such as diarrhoea, measles, and HIV), studies of children in hospital, and studies of food fortification or β carotene were excluded.
RESULTS: 43 trials with about 215 633 children were included. Seventeen trials including 194 483 participants reported a 24% reduction in all cause mortality (rate ratio=0.76, 95% confidence interval 0.69 to 0.83). Seven trials reported a 28% reduction in mortality associated with diarrhoea (0.72, 0.57 to 0.91). Vitamin A supplementation was associated with a reduced incidence of diarrhoea (0.85, 0.82 to 0.87) and measles (0.50, 0.37 to 0.67) and a reduced prevalence of vision problems, including night blindness (0.32, 0.21 to 0.50) and xerophthalmia (0.31, 0.22 to 0.45). Three trials reported an increased risk of vomiting within the first 48 hours of supplementation (2.75, 1.81 to 4.19).
CONCLUSIONS: Vitamin A supplementation is associated with large reductions in mortality, morbidity, and vision problems in a range of settings, and these results cannot be explained by bias. Further placebo controlled trials of vitamin A supplementation in children between 6 and 59 months of age are not required. However, there is a need for further studies comparing different doses and delivery mechanisms (for example, fortification). Until other sources are available, vitamin A supplements should be given to all children at risk of deficiency, particularly in low and middle income countries.
PMID 21868478
http://www.bmj.com/content/343/bmj.d5094.full
The supply of choline is important for fetal progenitor cells
Semin Cell Dev Biol. 2011 Jun 12.
Zeisel SH. Source Nutrition and Pediatrics, Nutrition Research Institute, School of Public Health and School of Medicine, The University of North Carolina at Chapel Hill, Kannapolis, NC 28081, United States.
Abstract
Fetal progenitor cells proliferate, migrate, differentiate and undergo apoptosis at specific times during fetal development. Choline is needed by these cells for membrane synthesis and for methylation. There is growing evidence that this nutrient also modulates epigenetic regulation of gene expression in both neuronal and endothelial progenitor cells, thereby modifying brain development. It is likely that these mechanisms explain why, in rodent models, maternal dietary intake of choline influences both angiogenesis and neurogenesis in fetal hippocampus, and results in life-long changes in memory function. This also may explain why women eating diets low in choline have a greater risk of having a baby with a birth defect. Choline is mainly found in foods that contain fat and cholesterol, and intake of such foods has diminished in response dietary advice from nutritionists and physicians. Forty years ago, diets commonly contained choline-rich foods but now women in the USA tend to eat diets low in choline content. Premenopausal women normally may require less choline in their diet than do men and postmenopausal women, because estrogen induces the gene for the enzyme catalyzing endogenous biosynthesis of the choline-containing phospholipid phosphatidylcholine. However, many women have a single nucleotide polymorphism (SNP) that blocks the induction of endogenous biosynthesis, thereby making them require more dietary choline. When these women eat diets low in choline, the supply of this nutrient to the fetus is likely to be inadequate, and may perturb progenitor cell proliferation, migration, differentiation and apoptosis.
Copyright © 2011 Elsevier Ltd. All rights reserved.
PMID 21693194
Does prenatal micronutrient supplementation improve children's mental development? A systematic review
Leung BM, Wiens KP, Kaplan BJ. BMC Pregnancy Childbirth. 2011 Feb 3;11:12. Review.
PMID 21291560 http://www.ncbi.nlm.nih.gov/pubmed/21291560
Vitamin D dependent rickets type I
Korean J Pediatr. 2011 Feb;54(2):51-4. Epub 2011 Feb 28.
Kim CJ. Source Department of Pediatrics, Chonnam National University Medical School, Gwangju, Korea.
Abstract
Vitamin D is present in two forms, ergocalciferol (vitamin D(2)) produced by plants and cholecalciferol (vitamin D(3)) produced by animal tissues or by the action of ultraviolet light on 7-dehydrocholesterol in human skin. Both forms of vitamin D are biologically inactive pro-hormones that must undergo sequential hydroxylations in the liver and the kidney before they can bind to and activate the vitamin D receptor. The hormonally active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)(2)D], plays an essential role in calcium and phosphate metabolism, bone growth, and cellular differentiation. Renal synthesis of 1,25(OH)(2)D from its endogenous precursor, 25-hydroxyvitamin D (25OHD), is the rate-limiting and is catalyzed by the 1α-hydroxylase. Vitamin D dependent rickets type I (VDDR-I), also referred to as vitamin D 1α-hydroxylase deficiency or pseudovitamin D deficiency rickets, is an autosomal recessive disorder characterized clinically by hypotonia, muscle weakness, growth failure, hypocalcemic seizures in early infancy, and radiographic findings of rickets. Characteristic laboratory features are hypocalcemia, increased serum concentrations of parathyroid hormone (PTH), and low or undetectable serum concentrations of 1,25(OH)(2)D despite normal or increased concentrations of 25OHD. Recent advances have showed in the cloning of the human 1α-hydroxylase and revealed mutations in its gene that cause VDDR-I. This review presents the biology of vitamin D, and 1α-hydroxylase mutations with clinical findings.
PMID: 21503197 [PubMed] PMCID: PMC3077501
http://www.ncbi.nlm.nih.gov/pubmed/21503197/
2010
Nutritional status of children with attention deficit hyperactivity disorder: a pilot study
Int J Pediatr. 2010;2010:767318. Epub 2010 Jun 28.
Kiddie JY, Weiss MD, Kitts DD, Levy-Milne R, Wasdell MB. Source Food Nutrition and Health, University of British Columbia, Vancouver, BC, Canada V6T 1Z4. Abstract Objectives. This is a pilot study of the dietary intake and nutrient status of children with Attention Deficit Hyperactivity Disorder (ADHD). Method. Nutritional assessment of 43 children aged 6-12 with ADHD was performed using a 3-day food record, 24-hour recall, and serum assessors. Results. Macronutrient intake and consumption of Low-Nutrient Foods were comparable to population norms; however, 66% were found to be deficient in zinc and 23% in copper. Conclusions. This pilot study reports the food intake and nutrient status of children with ADHD and shows a predisposition for low zinc and copper status in ADHD.
PMID 20652039 PMCID: PMC2905905
2006
Nutrient Reference Values for Australia and New Zealand Including Recommended Dietary Intakes
- The Nutrient Reference Values outline the levels of intake of essential nutrients considered to be adequate to meet the known nutritional needs of practically all healthy people for prevention of deficiency states. The document can be used by health professionals to assess the likelihood of inadequate intake in individuals or groups of people.
- Report used to prepare some content on topic page.
2002
http://www.scielosp.org/scielo.php?pid=S0042-96862002000800007&script=sci_arttext
