NURS 1013 Lecture 4A Water-Soluble Vitamins PDF

Water-soluble vitamins The UWI School of Nursing, Mona NURS1013 Nutrition Objectives  At the end of this presentation, students should be able to:  Define concepts related to micronutrients and vitamins  Outline the role and function of water soluble vitamins  List sources of water soluble vitam...

Water-soluble vitamins The UWI School of Nursing, Mona NURS1013 Nutrition Objectives  At the end of this presentation, students should be able to:  Define concepts related to micronutrients and vitamins  Outline the role and function of water soluble vitamins  List sources of water soluble vitamins ‘  Describe the deficiency and toxicity associated with water soluble vitamins. Vitamin deficiency/ Hypovitaminosis Sub-clinical deficiency – some depletion of body stores  Overt deficiency – usually accompanied by other evidence of malnutrition e.g. protein energy malnutrition (PEM) VITAMINS  Vitamins      are:- Organic substances Made of molecules such as- H, O, C Needed for normal metabolism Referred to as micronutrients because they are needed in small quantities Some can be manufactured from substrates that are available  e.g. vitamin D from cholesterol (& sunlight)  e.g. niacin from the essential amino acid, tryptophan Causes of deficiency  Fad diets  Inadequate diet e.g. alcoholism or metabolic disorders  Impaired absorption e.g. lack of intrinsic factor for B12  Inefficient utilization e.g. lack of vitamin C for folic acid metabolism  Increased requirements e.g. pregnancy, HIV  Increased rate of excretion e.g. trace elements lost in diarrhoea  (Duggan & Golden, 2005) Vitamin Related Terms  ProVitamin- inactive form of a vitamin which requires conversion to be active  Preformed Vitamin- metabolically active form of a vitamin  Vitamer:- One of two or more related chemical substances that fulfill the same specific vitamin function. “B” Vitamins B1 - Thiamin  Named B1 as it was the first identified  Essential coenzyme for many reactions in carbohydrate and amino acid metabolism (therefore essential for energy production). Beriberi  Deficiency of thiamin: Beriberi ❑ GI: anorexia, indigestion ❑ CNS: chronic peripheral neuritis, ❑ encephalopathy (assoc. alcoholism, narcotic abuse & HIV/AIDS ❑ CV: cardiac failure with peripheral vasodilation & oedema of extremeties ❑ Endocrine: Impaired Glucose metabolism B1 – Thiamin  Deficiency: common in alcoholics, neglected persons, persons who eat mainly polished rice, elderly. Patients on diuretics.  Symptoms may be induced by excessive carbohydrate intake in a malnourished state  will be depleted when used a coenzyme for Carb metabolism. (Bender, 2005) Thiamin  Not stored in liver, daily intake required proportional to the intake of carbohydrate.  It is destroyed by heat, sulphites & thiaminase (in raw fish e.g. sushi meal)  RDA: 0.3-0.5mg/1000kcal/day or ≈1.0mg/d in adults  Sources : Pork, beef, whole or enriched grains, legumes, nuts, yeast  (Bender, 2005) Thiamin  Hypervitaminosis of B1  Chronic intakes of thiamin >3g/day are toxic to adults  Signs include headache, irritability, insomnia, rapid pulse, weakness, dermatitis  The incidence of toxicity is very low B2 - Riboflavin  Coenzyme in protein & energy metabolism (production of flavoproteins, e.g. FAD- flavin adenine dinucleotide and NADnicotinamide adenine dinucleotide)  Plays  Is a role oxidation/reduction reactions heat stable B2-Riboflavin  Deficiency: ❑ Called ariboflavinosis ❑ Associated with hypochromic anaemia, wound aggravation, cheilosis, glossitis, conjunctivitis, photophobia, seborrhea dermatitis, hair loss, failure to grow. ❑ Certain drugs may inhibit flavokinase (important enzyme in the reversible conversion of B2 to FAD) leading to functional deficiency ❑ Normally associated with other deficiencies such as PEM B2-Riboflavin  Deficiency: ❑ Antidepressants may interfere with B2 metabolism ❑ Requirements lactation ❑ Needed milk ❑ are higher in pregnancy and for fetal tissue synthesis and is lost in breast There is limited evidence supporting development of an upper limit for this vitamin the Riboflavin  Persons with low intake at increased risk of ackee poisoning  RDA: 1.2-1.8 mg  Sources: ❑ Milk, kidney, liver, cheeses, whole cereals, pulses, beef, mutton, pork, green vegetables.  (Bender, 2005) Niacin (nicotinic acid)  Coenzyme in tissue oxidation and reduction reactions (e.g. nicotinamide adenine dinucleotide (NAD, NADP).  Important in energy production Niacin (B3)  Endogenous synthesis from the amino acid, tryptophan is more important than the dietary intake of the vitamin  (60-80mg  High of tryptophan =1mg of niacin) intakes of niacin may cause liver damage- B3 is stored in the liver. Niacin deficiency- Pellagra  Pellagra- Italian word meaning sour skin  A deficiency of niacin was first recognized in persons subsisting on corn-based diets. ❑ Limiting amino acid in corn/maize is tryptophan  B6 deficiency may cause a B3 deficiency as B6 is needed for amino acid metabolism  Symptoms of pellagra include weakness, lassitude, anorexia, scaly dermatitis (exposed skin), neuritis and confusion. Niacin  RDA: 5.5mg/1000kcal  Sources, liver, heart, kidney meat, fish, peanuts, yeast.  (Bender, 2005) Pyridoxine – B6  Coenzyme in amino acid metabolism: ❑ decarboxylation, ❑ deamination, ❑ transamination, transsulfuration, ❑ amino acid absorption. ❑  Coenzyme ❑ haeme activity in RBC formation formation, Pyridoxine  Deficiency of pyridoxine is rare  May be associated with a deficiency of riboflavin and protein deficiency - manifested as a hypochromic macrocytic anaemia or pregnancy anaemia.  Izoniazid and penicillamine (Tb drugs)are B6 antagonists- impair B6 absorption  B6 is destroyed by alcoholic beverages Pyridoxine  The RDA is 15µg/g protein/day (approx.1-2 mg).  Very high doses of pyridoxine may cause sensory nerve damage.  Food sources are fruits (especially ripe bananas), meat, fish, liver, nuts, beans, refined cereals, and leafy vegetables.  (CFNI, 1993) Cyanocobalamin – B12  Functions: ❑ Coenzyme in protein synthesis ❑ Important for the formation of nucleic acid & cell proteins ❑ Forms RBCs with folic acid ❑ Necessary for transmethylation ❑ Formation of myelin sheath ❑ Extrinsic factor in pernicious anaemia B12  In the centre of the molecule of cyanocobalamin is the trace metallic element cobalt (Co) B12  Dietary deficiency occurs only in strict vegans as there are no plant sources of the vitamin.  Nitrous oxide exposure may precipitate overt deficiency where there is sub clinical deficiency. ❑ Nitrous oxide inactivates the cobalamin form of vitamin B12 by oxidation  Deficiency may be due to atrophic gastritis in an elderly person.  Symptoms include paralysis and macrocytic anaemia  (Bender, 2005) B12- deficiency  “Pernicious anaemia is the megaloblastic anaemia due to vitamin B12 deficiency, commonly as a result of failure of intrinsic factor secretion, in which there is also spinal cord degeneration and peripheral neuropathy.…  Failure of intrinsic factor secretion is often due to autoimmune disease…”  (Bender, 2005 in Giessler & Powers pp.202). B12- deficiency  High intakes of folate prevent the development of megaloblastic anaemia, and in up to one-third of patients the (irreversible) neurological signs develop without megaloblastosis  (Bender, 2005 in Giessler & Powers pp.202). B12- Requirements RDA: 1- 2-5μg Sources: ❑Liver, meat, milk, egg, cheese, shell fish, fermented foods.  (Bender, 2005) Pantothenic Acid A vitamin of the B complex group widely distributed in nature (yeast, salmon, liver, heart, eggs, milk, grains)  RDA: 4-7 mg Pantothenic acid  Constituent ❑ of acetyl CoA, (Krebs cycle). Contributes to fatty acid metabolism, steroid hormone synthesis & gluconeogenesis  Spontaneous human deficiency has never been described. Biotin  “B” vitamin, essential cofactor for the metabolism of fats, carbohydrates, and Amino Acids.  Deficiency in children results in : retarded mental & physical development, alopecia, impaired immunity, fatigue, nausea, and anaemia. Biotin Deficiency: ❑May be due to ingestion of antagonist: raw egg white (avidin) or a deficiency in patients on Total Parenteral Nutrition (TPN) ❑is very rare- bacterial production of Biotin occurs in the large intestine Biotin  Deficiency:  Dry scaly dermatitis of biotin deficiency is similar to that of essential fatty acid deficiency  Sources: cereals. liver, kidney, milk, egg yolks, yeast, soy, Folic Acid- Folate  Vitamin in the B complex group  Occurs naturally in green plant tissue, liver, & yeast.  Easily destroyed by food processing.  Depends on the presence of Vitamin C, B6, B12, & methionine for its complex metabolism  Vitamin C & folate are lost during cooking Functions of Folate  Essential for nucleic acid & DNA synthesis.  Red cell maturation.  Prevention of neural tube defects.  Prevention of homocysteinemia.  Reduced CV risk- by reducing homocysteine levels.  RDA: 4 mg  (Tabers ,1997) Increased Requirements  Pregnancy,  Oral contraceptive use.  Steroids, etc. especially in the first 28 days. metformin, theophylline, thiazides Increased Requirements  Anti-epileptic medications -(e.g. phentoin).  Anti-cancer medications such as methotrexate (antagonist).  Stress, trauma, fevers  Rapid rate of erythropoiesis (e.g. Sickle cell-SS patients).  Haemotology disorders  Intestinal disorders  Ureamia  Alcoholics Hurricane Gilbert Deficiency  Scarcity of fresh produce.  Population deficiency manifested in SS patients: megaloblastosis. 9 - 10m later: significant increase in babies born with (nutritional deficiency) NTDs.  (Duff et al. Lancet 1991)  (Duff et al. Am J Public Health 1994) Choline  Important role in synthesis of acetylcholine  Phosphatidylcholine membranes  Maintenance a major component of cell of normal triglyceride levels & Normal plasma homocysteine concentrations Choline  Choline is an amine which was previously classified as a non-essential nutrient (some synthesized in the liver)  Now classified as a “vitamin-like” nutrient  Essential for normal fat and charbohydrate metabolism.  Deficiency loss may cause liver cell death, memory Choline  RDA: ❑ Men 550mg, ❑ Women 425 mg, ❑ Pregnant woman 450 mg  Sources: ❑ eggs, liver, chicken, fish, legumes, cruciferous vegetables, milk & soy (contain lecithin). (Institute of Medicine & National Academy of Sciences USA 1998; Westermark & Antila, 2002) Vitamin C-Ascorbic acid  Functions: ❑ ❑ ❑ ❑ ❑ ❑ ❑ ❑ Collagen formation Firm capillary walls Makes Fe available Required for metabolism of folic acid Antioxidant Neural support Fat metabolism (reactions with carnitine) Bile synthesis Ascorbic acid  Deficiency: Scurvy – haemorrhagic disease: ❑ Capillary walls, bone matrix, cartilage not properly formed: profuse tissue bleeding, limbs & joints painful & swollen, subperiosteal haemorrhage. ❑ Bones fracture easily, wounds fail to heal, gums swollen & bleeding, teeth loosen Ascorbic acid  Sources: ❑ citrus fruits, guavas, garden cherries, tomatoes, grapes, peppers, strawberries, bananas. ❑ Many fresh fruits & vegetables ❑ RDA 60 mg Vitamin C  Excessive intake (>2g/day) causes ascorbic acid to be excreted as oxalates in urine (may cause kidney stones)  Destroyed by cooking Review questions  Examine the chemical names for each of the water soluble vitamins  List the RDA for key water soluble vitaminsVitamin C, B12, B9, and B3  Classify the B vitamins as energy producing or erythropoietic  Summarize the functions of key water soluble vitamins- C, B12, B9, and B3  Identify the deficiency disease associated with key water soluble vitamins-C, B12, B9, and B3 References  Bender, D.A. (2005).Water soluble vitamins. In C. Geissler & H. Powers (Eds.). Human Nutrition (11th ed. pp.185-210). Edinburgh: Elservier Churchill Livingstone.  Bender, D.A. (2005).Fat soluble vitamins. In C. Geissler & H. Powers (Eds.). Human Nutrition (11th ed. pp.211-230). Edinburgh: Elservier Churchill Livingstone.   Campbell, V.S.& Sinha, D.P.(2006) Nutrition Made Simple. Kingston: CFNI, PAHO Carr, A. C., & McCall, C. (2017). The role of vitamin C in the treatment of pain: new insights. Journal of translational medicine, 15(1), 77.  CFNI. (1994). Dietary Allowances for the Caribbean. Kingston: Caribbean Food and Nutrition Institute References  Duff, E.M.W.& Cooper, E.S. (1994). Neural tube defects in Jamaica following Hurricane Gilbert. American Journal of Public Health, 84(3), 473-476  Duff, E.M.W., Cooper, E.S., Danbury, C.M., Johnson, B.E.& Sergeant, G.R. (1991). Neural tube defects in hurricane aftermath. Lancet,337,120-121  Garrow, J.S., James, W.P.T.& Ralph, A. (2002) (Eds.). Human Nutrition and Dietetics. Edinburgh, Churchill Livingstone.  Hemilä, H., & Chalker, E. (2020). Vitamin C as a possible therapy for COVID-19. Infection & chemotherapy.  Mitchell, M. (2003). Nutrition across the life span. Philadelphia: W.B. Saunders Company  Skeaff, M. (2007). Vitamins C & E. In J. Mann & S. Truswell. Essential of Human Nutrition. (3rd Ed. pp.201-213). Oxford: University Press. References  Truswell, T. (2007). The B. Vitamins. In J. Mann & S. Truswell. Essential of Human Nutrition. (3rd Ed. pp.184-200). Oxford: University Press.  Tucker, S., & Dauffenbach, V. (2011). Nutrition and Diet for Nurses. (1st Ed.). Boston: Pearson Press.  Van Gorkom, G. N., Klein Wolterink, R. G., Van Elssen, C. H., Wieten, L., Germeraad, W. T., & Bos, G. M. (2018). Influence of vitamin C on lymphocytes: an overview. Antioxidants, 7(3), 41.  Venes, D., Thomas, C.L. (1997) (Eds).Taber’s Cyclopedic Medical Dictionary 19th Edition., Philadelphia, FA Davis Company  Westermarck, T. & Antila, E. (2002). Diet in relation to the nervous system. In J.S. Garrow, W.P.T. James, & A. Ralph (Eds.), Human Nutrition and Dietetics (10th ed.pp.715-730). Edinburgh: Churchill Livingstone.