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Książki na temat „Folic acid deficiency”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lutego 2023

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1

Frances, Picciano Mary, Stokstad E. L. Robert, Gregory Jesse F i American Chemical Society. Food and Nutritional Biochemistry Subdivision., red. Folic acid metabolism in health and disease. New York: Wiley-Liss, 1990.

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Bailey, Lynn B. Folate in health and disease. Wyd. 2. Boca Raton: Taylor & Francis, 2010.

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1948-, Bailey Lynn B., red. Folate in health and disease. New York: M. Dekker, 1995.

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Kurtzweil, Paula. How folate can help prevent birth defects. [Rockville, MD: Dept. of Health and Human Services, Public Health Service, Food and Drug Administration, 1996.

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Kurtzweil, Paula. How folate can help prevent birth defects. [Rockville, MD: Dept. of Health and Human Services, Public Health Service, Food and Drug Administration, 1997.

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6

Folic acid and the prevention of disease: Report of the Committee on Medical Aspects of Food and Nutrition Policy. London: Stationery Office, 2000.

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7

J, Massaro Edward, i Rogers John M, red. Folate and human development. Totowa, N.J: Humana Press, 2002.

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8

World Health Organization. Regional Office for South-East Asia. Prevention of iron deficiency anaemia in adolescents: Role of weekly iron and folic acid supplementation. New Delhi, India: World Health Organization, Regional Office for South-East Asia, 2011.

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9

Amouzou, Kou'santa Sabiba. Evaluation des marqueurs nutritionnels et génétiques du statut en coenzymes B (cobalamines et folates) et de l'homocystéinemie plasmatique dans une population d'Afrique de l'Ouest (Benin-Togo). Lomé: [s.n., 2003.

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10

Folate in health and disease. Wyd. 2. Boca Raton: Taylor & Francis, 2010.

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11

1938-, Zittoun J., i Cooper B. A. 1928-, red. Folates and cobalamins. Berlin: Springer-Verlag, 1989.

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Folate in Health and Disease. Wyd. 2. CRC, 2009.

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13

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 1994.

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14

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 2009.

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15

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 2009.

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16

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 2009.

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17

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 2009.

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18

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 1994.

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19

D, Wright Jacqueline, i National Center for Health Statistics (U.S.), red. Blood folate and vitamin B12: United States, 1988-95. Hyattsville, Md: U.S. Dept of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics, 1998.

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20

Serge, Hercberg, Galan P i Dupin Henri professeur, red. Aspects actuels des carences en fer et en folates dans le monde: Colloque international, Paris 11-13 juillet 1989. Paris: Editions de l'Institut national de la santé et de la recherche médicale, 1990.

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21

Folsäureversorgung der deutschen Bevölkerung: Abschlussbericht zum Forschungsvorhaben. Berlin: BfR, Bundesinstitut für Risikobewertung, Pressestelle, 2005.

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22

Assessment of folate methodology used in the Third National Health and Nutrition Examination Survey (NHANES III, 1988-1994). Bethesda, Md: Life Sciences Research Office, Federation of American Societies for Experimental Biology, 1994.

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23

Bradshaw, Spencer D. Folic Acid (Pteroylglutamic Acid) in Health, Deficiency & Therapy: Index of New Information With Authors, Subjects & References. Abbe Pub Assn of Washington Dc, 1996.

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24

Changing Preconception. Health Education Authority, 1998.

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25

Bunch, Chris. Deficiency anaemias. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0279.

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This chapter addresses the diagnosis, investigation, and management of anaemia due to a deficiency in iron, vitamin B12, or folate. Erythropoiesis requires an adequate supply of iron for haem formation, as well as vitamin B12 and folic acid (folate) to support high levels of DNA synthesis, and a lack of any of these will result in anaemia. Iron-deficient anaemias are typically microcytic, while a deficiency in vitamin B12 or folate results in megaloblastic haemopoiesis and a macrocytic anaemia. Iron deficiency results from poor dietary iron intake, poor absorption, increased demands, blood loss, or combinations of these. The usual cause of severe vitamin B12 deficiency in Western countries is an autoimmune atrophic gastritis, in which there is a loss of gastric parietal cell numbers and an absence of intrinsic factor production, which effectively prevents vitamin B12 absorption. This is the classical pernicious anaemia, and it is often seen in association with other autoimmune disorders. Folate deficiency may result from poor diet, malabsorption, or when demand for folate is increased, for example, during pregnancy, or with increased haemopoiesis in haemolytic anaemias or myeloproliferative disorders.

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26

Rogers, John M., i Edward J. Massaro. Folate and Human Development. Humana Press, 2010.

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Rogers, John M., i Edward J. Massaro. Folate and Human Development. Humana Press, 2013.

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28

Rogers, John M., i Edward J. Massaro. Folate and Human Development. Humana Press, 2002.

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29

Usha, Ramakrishnan, red. Nutritional anemias. Boca Raton: CRC Press, 2000.

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30

Ramakrishnan, Usha. Nutritional Anemias. Taylor & Francis Group, 2000.

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31

Ramakrishnan, Usha. Nutritional Anemias. Taylor & Francis Group, 2000.

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32

Silva, Aminda De, J. A. Saunders i M. A. Stroud. Vitamin deficiencies. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0333.

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Vitamins are organic compounds required by the body in small amounts to perform specific cellular functions. Nine vitamins (thiamine (vitamin B1), riboflavin (vitamin B2), pyridoxine (vitamin B6), cyanocobalamin (vitamin B12), niacin (nicotinic acid; vitamin B3), pantothenic acid (vitamin B5), biotin (vitamin B7; vitamin H), folic acid (folate; vitamin B9), and ascorbic acid (vitamin C)) are water soluble, while four (vitamins A, D, E, and K) are fat soluble. The importance of vitamins was first appreciated through recognition of their clinical deficiency state. However, this approach has led to the concept that the primary purpose of a vitamin is to prevent the associated clinical deficiency state and, consequently, unless patients exhibit signs of a specific clinical deficiency state, they are thought to be replete in the corresponding vitamin. This is a misunderstanding. In reality, most vitamins have many different functions which are incompletely understood, and impaired biochemical function and even functional problems affecting metabolic, immunological, or cognitive status can occur with marginal vitamin depletion long before overt clinical deficiency becomes evident. A high index of suspicion is thus essential in all patients who have malnutrition or malabsorption, to ensure that levels that might compromise health, resistance to disease, and recovery from injury or illness are not left untreated.

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33

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng i Anne Bardsley. Vitamin B9 (folate) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0012.

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Folate is a coenzyme in multiple biochemical pathways involving one-carbon metabolism, including amino acid metabolism, DNA and RNA synthesis, homocysteine metabolism, and methylation of DNA. The most overt consequence of folate deficiency is megaloblastic anaemia caused by the inhibition of DNA synthesis in red blood cell production. Folate deficiency may also influence the ability to maintain DNA methylation patterns in replicating cells, resulting in lasting phenotypic changes. Embryogenesis and fetal growth require higher levels of folate, which must be supplied maternally during pregnancy. A link between low maternal folate levels and the occurrence of neural tube defects has long been recognized. Other effects in pregnancy include increased risks of pre-eclampsia and placental vascular disorders. The general recommendation is for supplementation prior to conception and throughout pregnancy with 400 #amp;#x03BC;g of folic acid in tablet form, in addition to dietary sources, which can reduce the risk of neural tube defects.

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34

Food Fortification: The Evidence, Ethics, and Politics of Adding Nutrients to Food. Oxford University Press, 2013.

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35

Lawrence, Mark. Food Fortification: The Evidence, Ethics, and Politics of Adding Nutrients to Food. Oxford University Press, 2013.

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