Talk:Nutrition: Difference between revisions
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==2015== | ==2015== | ||
===The phenomenon of vitamin D=== | |||
Postepy Hig Med Dosw (Online). 2015 Jan 23;69(0):127-39. | |||
Gruber BM1. | |||
Abstract | |||
The receptor of vitamin D (VDR) is present in most non-skeletal human cells, suggesting its role beyond the bone and calcium metabolism. The relationship between vitamin D and the respiratory tract is a consequence of its activity in the immune system. Some gastrointestinal diseases, such as inflammatory bowel disease, coeliac disease, liver, pancreas or cardiac diseases, lead to vitamin D deficiency. Many studies indicate a correlation between vitamin D and diabetes. VDR and 1α-hydroxylase have been detected in the cutaneous capillary vessels, endothelium, vascular smooth muscles, myocytes and cardiac fibroblasts. The influence of vitamin D on the expression of genes related to the vascular walls implies its role in the pathomechanisms of vascular diseases and the cardiovascular system. Due to the VDR detected in most immunocompetent cells, calcitriol can modulate the congenital and acquired immune system. The correlation between vitamin D and cancer development is also not surprising because of many functions which vitamin D has in the organism. The vitamin D-regulated genes encode the proteins which participate in differentiation, proliferation or apoptosis. This paper aims to focus on the less well known roles of vitamin D in the organism, especially considering that most "sun consumers" know only its antirachitic and bone reinforcing action. So, this article may be surprising, and first of all it should convince everyone to vitamin D supplemention. | |||
PMID 25614680 | |||
==2014== | ==2014== | ||
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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 |
2015
The phenomenon of vitamin D
Postepy Hig Med Dosw (Online). 2015 Jan 23;69(0):127-39.
Gruber BM1.
Abstract
The receptor of vitamin D (VDR) is present in most non-skeletal human cells, suggesting its role beyond the bone and calcium metabolism. The relationship between vitamin D and the respiratory tract is a consequence of its activity in the immune system. Some gastrointestinal diseases, such as inflammatory bowel disease, coeliac disease, liver, pancreas or cardiac diseases, lead to vitamin D deficiency. Many studies indicate a correlation between vitamin D and diabetes. VDR and 1α-hydroxylase have been detected in the cutaneous capillary vessels, endothelium, vascular smooth muscles, myocytes and cardiac fibroblasts. The influence of vitamin D on the expression of genes related to the vascular walls implies its role in the pathomechanisms of vascular diseases and the cardiovascular system. Due to the VDR detected in most immunocompetent cells, calcitriol can modulate the congenital and acquired immune system. The correlation between vitamin D and cancer development is also not surprising because of many functions which vitamin D has in the organism. The vitamin D-regulated genes encode the proteins which participate in differentiation, proliferation or apoptosis. This paper aims to focus on the less well known roles of vitamin D in the organism, especially considering that most "sun consumers" know only its antirachitic and bone reinforcing action. So, this article may be surprising, and first of all it should convince everyone to vitamin D supplemention.
PMID 25614680
2014
Vitamin C Depletion in Prenatal Guinea Pigs as a Model of Lissencephaly Type II
Vet Pathol. 2014 Dec 8. pii: 0300985814561270. [Epub ahead of print]
Capo I1, Hinić N2, Lalošević D2, Vučković N3, Stilinović N4, Marković J5, Sekulić S6.
Abstract
Humans and guinea pigs are unable to produce vitamin C, with deficiency resulting in a well-known disorder of collagen synthesis. Pial basement membrane structure preservation is essential in the proper migration of neurons. In our study, intrauterine deprivation of vitamin C in guinea pig fetuses led to a collagen synthesis disorder, weakness, and finally a breach of pial basement membrane. We found excessive migration of the external germinal layer cells into the subarachnoid space of the cerebellum through defects in the pial basement membrane. The changes ranged from focal rupture of pial basement membranes to their complete disintegration. The loss of proper folia formation resulted in macroscopically visible flattening of the cerebellar surface. Different grades of dysplastic changes in the folia of the cerebellar cortex were observed in 2 experimental groups assigned different limits to mark the time of commencement and duration of vitamin C deprivation. The most severe form of dysplastic changes was characterized by marked irregularity of the cerebellar cortex similar to that in lissencephaly type II. Thus, prenatal vitamin C deficiency represents a novel animal model to study the effects of collagen synthesis on development of breaches in the pial basement membrane, disordered migration of neurons, dysplasia of cerebellar cortex, and the pathogenesis of lissencephaly. © The Author(s) 2014. KEYWORDS: animal model; cerebellum; guinea pigs; lissencephaly; scurvy; vitamin c deficiency PMID 25487414
2013
CDC finds cluster of newborns in Tennessee with bleeding disorder
Report highlights importance of vitamin K shot at birth
http://www.cdc.gov/media/releases/2013/p1114-newborn-bleeding-disorder.html
American Academy of Pediatrics Report Of Committee On Nutrition - Vitamin K Compounds And The Water-Soluble Analogues (1961) PEDIATRICS Vol. 28 No. 3 September 1, 1961 pp. 501 -507
2011
The correlation between third-trimester maternal and newborn-serum 25-hydroxy-vitamin D in a selected South Australian group of newborn samples
BMJ Open. 2011 Jan 1;1(2):e000236. Thomas SD, Fudge AN, Whiting M, Coates PS. Source Department of Chemical Pathology, SA Pathology, Adelaide, South Australia, Australia. devika.thomas@health.sa.gov.au Abstract BACKGROUND: Although vitamin D insufficiency is prevalent in the community, only a few population-based studies have measured serum 25-hydroxy-vitamin D (25OHD) levels during pregnancy and in newborns. Maternal vitamin D deficiency has been linked to pregnancy complications, as well as hypocalcaemia and rickets in the newborn. Here, the authors report third-trimester maternal and newborn-serum 25OHD concentrations in 101 neonates whose serum samples were sent for testing. METHODS: The newborn 25OHD levels were correlated with the third-trimester maternal serum 25OHD levels using a least-square regression analysis. All samples were measured using an enzyme immunoassay (EIA). Ten randomly selected newborn serum samples were also measured using liquid chromatography/tandem mass spectrometry LC-MSMS, and correlated with the EIA method. RESULTS: Out of 99 mothers of the newborns, only 19, 42 and 68 had their 25OHD level measured in the first, second and third trimester respectively. The mean maternal age was 30 years, while the mean maternal third-trimester 25OHD concentration was 48 nmol/l. Of the newborns, 53% were female, and 85% were term deliveries. The mean newborn-serum 25OHD was 68 nmol/l. Neonatal 25OHD was related to maternal third-trimester levels measured by EIA (r=0.3; newborn 25OHD=0.42(maternal 25OHD)+44.2; p=0.02). EIA and LC-MSMS concentrations for newborns correlated significantly over a range between 20 and 103 nmol/l by EIA (r=0.9; EIA=1.04(LCMSMS)+10.1; p<0.00 (slope); p=0.18 (intercept)). The mean 25OHD concentration in women who suffered pre-eclampsia and premature rupture of membranes were 45 and 39 nmol/l respectively. CONCLUSIONS: Newborn-serum 25OHD concentrations depend on the maternal circulating plasma 25OHD level at least during the third trimester. Neonatal 25OHD levels obtained by EIA correlated well with LC-MSMS. Although the EIA values for neonates were greater than LC-MSMS values, this difference was not statistically significant.
PMID 22021888
Vitamin A in reproduction and development
Nutrients. 2011 Apr;3(4):385-428. Epub 2011 Mar 29.
Clagett-Dame M, Knutson D. Source Department of Biochemistry, University of Wisconsin-Madison, 433 Babcock Drive, Madison, WI 53706, USA. dame@biochem.wisc.edu
Abstract
The requirement for vitamin A in reproduction was first recognized in the early 1900's, and its importance in the eyes of developing embryos was realized shortly after. A greater understanding of the large number of developmental processes that require vitamin A emerged first from nutritional deficiency studies in rat embryos, and later from genetic studies in mice. It is now generally believed that all-trans retinoic acid (RA) is the form of vitamin A that supports both male and female reproduction as well as embryonic development. This conclusion is based on the ability to reverse most reproductive and developmental blocks found in vitamin A deficiency induced either by nutritional or genetic means with RA, and the ability to recapitulate the majority of embryonic defects in retinoic acid receptor compound null mutants. The activity of the catabolic CYP26 enzymes in determining what tissues have access to RA has emerged as a key regulatory mechanism, and helps to explain why exogenous RA can rescue many vitamin A deficiency defects. In severely vitamin A-deficient (VAD) female rats, reproduction fails prior to implantation, whereas in VAD pregnant rats given small amounts of carotene or supported on limiting quantities of RA early in organogenesis, embryos form but show a collection of defects called the vitamin A deficiency syndrome or late vitamin A deficiency. Vitamin A is also essential for the maintenance of the male genital tract and spermatogenesis. Recent studies show that vitamin A participates in a signaling mechanism to initiate meiosis in the female gonad during embryogenesis, and in the male gonad postnatally. Both nutritional and genetic approaches are being used to elucidate the vitamin A-dependent pathways upon which these processes depend.
PMID 22254103
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
