NURS 1013 Lecture 4 B Fat-Soluble Vitamins PDF
Document Details
Uploaded by TriumphalSerenity
UWI School of Nursing, Mona
Tags
Summary
This document is a lecture on fat-soluble vitamins, including Vitamin A, D, and K. It discusses their functions, sources, deficiencies, and toxicity in the human body. The document includes review questions and a reference list.
Full Transcript
Fat soluble vitamins NURS 1013: Nutrition Objectives At the end of this presentation, students should be able to: ◼ List the chemical names of the fat soluble vitamins ◼ Outline the vitamers associated with each of the fat soluble vitamins ◼ Describe the difference with the pro and preformed vitamin...
Fat soluble vitamins NURS 1013: Nutrition Objectives At the end of this presentation, students should be able to: ◼ List the chemical names of the fat soluble vitamins ◼ Outline the vitamers associated with each of the fat soluble vitamins ◼ Describe the difference with the pro and preformed vitamin A ◼ Objectives cont’d Describe the role and function of water soluble vitamins ◼ Outline the deficiency and excess states associated with the water soluble vitamins ◼ List the RDA for Vitamins D and A ◼ Micronutrients ◼ vitamins and minerals needed by the body in very small amounts (micrograms or milligrams daily). WHO (2009) describes micronutrients as “magic wands” that facilitate the production of enzymes, hormones and other substances which are essential for growth and development. Micronutrients ◼ ◼ Micronutrient deficiencies are a major threat to health & development particularly in women & children in developing countries (WHO, 2009). Vitamins are organic compounds, classified as either water soluble or fat soluble based on their solubility. (Gallagher, 2008) Vitamin A ◼ “Vitamin A deficiency is a serious problem of public health nutrition…and is probably the most important cause of preventable blindness among children in developing countries…marginal deficiency is a factor in childhood susceptibility to infection and hence morbidity and mortality… The main physiologically active forms of vitamin A are retinaldehyde (in the visual system) and retinoic acid, which modulates gene expression and tissue differentiation.” (Bender, 2005 in Geissler & Powers pp.212). Vitamin A ◼ ◼ ◼ ◼ ◼ Vitamin A Retinol, retinal/retinaldehyde and retinoic acid are three related compounds referred to as preformed vitamin A. Preformed vitamin A in animal foods is found in fat storage cells. Provitamin A found in plants is in the form of carotenoids which are converted by the body to retinol. Beta carotene is the most important of the carotenoids with significant vitamin A activity (WHO/FAO, 2004, Gallagher, 2008). Vitamin A Present in the diet as either retinol (animal source) or carotenoids (ß-carotene, plant sources) Transported as retinol binding protein, stored in the liver and not easily depleted Also stored in adipose tissue, lung, testes, bone marrow, eye & kidney ◼ Vitamin A ◼ Active form: 11 cis-retinal is necessary for rod division in the eye ◼ Rhodopsin is the glycoprotein opsin of the rods of the retina; combines with retinal to form functional photo pigment responsive to light Vitamin A Retinoic acid induces differentiation of epithelial cells ◼ Important antioxidant ◼ Necessary for embryogenesis, reproduction & growth ◼ Vitamin A Deficiency causes night blindness. ◼ Severe deficiency can lead to keratinization of the cornea, corneal ulceration & blindness: ◼ Xerophthalmia (hardening of eye tissue) ◼ 350,000 pre-school children become blind each year. Bitot’s spots are early signs ◼ Vitamin A Deficiency: ◼ Plasma levels decreased with severe malnutrition due to lack of carrier proteins, poor growth ◼ Reduced immunity leads to many deaths from infection in malnourished children worldwide Vitamin A ◼ Major focus of public health programmes worldwide ◼ Inadequate status assoc. with PEM, low fat intake, malabsorption & febrile diseases ◼ Low plasma levels associated with increased risk of developing cancer Vitamin A Sources: Animal: liver, oily fish e.g. herring, sardines, tuna, liver oils of cod & halibut Milk & cheese Provitamin A carotinoids: carrots, pumpkin, green leafy vegetables, corn, tomatoes, papaya ◼ Vitamin A ◼ Both a deficiency and an excess of retinoic acid can cause severe developmental abnormalities. Vitamin A is both acutely and chronically toxic. Symptoms of toxicity are nausea, vomiting and headache, itching and exfoliation of the skin. ◼ The RDA for vitamin A is 6.7μg/kg body weight. (Bender, 2005). Vitamin A Chronic toxicity: Headache, alopecia, cracking of lips, dry, itchy skin, hepatomegaly, bone & joint pain ◼ Permanent damage to liver, bone & vision may result. ◼ Teratogenic effects: fetal resorption, birth defects etc ◼ Vitamin A Carotenoid actions: ◼ Hypercarotenosis: jaundice-like yellowing of the skin, high plasma carotenoids due to ingestion of large amounts of beta-carotene in food or supplements Vitamin D – 1:25 dihydroxycholecalciferol ◼ “Vitamin D is not strictly a vitamin, rather it is the precursor of one of the hormones involved in calcium homeostasis and the regulation of cell proliferation and differentiation. Dietary sources are relatively unimportant compared with endogenous synthesis in the skin; problems of a deficiency arise when there is inadequate exposure to sunlight.” (Bender, 2005 in Geissler & Powers pp.217). Vitamin D Vitamin D3 (cholecalciferol) is synthesized by the action of sunlight on its precursor : 7-dehydrocholesterol, in the skin Vitamin D ◼ The main body reserve of vitamin D is circulating cholecalciferol (calcitriol). The main function of vitamin D is in maintenance of calcium homeostasis. Vitamin D2 & D3 ◼ D3 is ◼ D2 present naturally in fish oils is added to margarine Vitamin D Vitamin D deficiency can develop if exposure to sunlight is inadequate or if diet is inadequate ◼ Metabolism occurs in the liver (25-HCC) ◼ & the kidney with production of the most active form (1:25DHCC) ◼ Vitamin D 1:25-DHCC is increased by low plasma Ca & P and high PTH ◼ Principal action of 1:25-DHCC is to induce absorption of Ca from the small intestine & increase resorption of Ca from bone Increased Ca in ECF permits bone formation ◼ ◼ Regulates immune cells in ECF (immunohaemopoiesis) Vitamin D deficiency Poorly mineralized skeleton ◼ Ricketts in children ◼ Osteomalacia in adults ◼ RDA 50µg day (max. 2000 IU) 25μg day for infants ◼ Vitamin D toxicity ◼ Vitamin D toxicity may cause weakness, nausea, loss of appetite, headache, abdominal pains, cramps and diarrhoea. It also may cause serious hypercalcaemia, renal calculi and calcification of vital organs. (Toxic adult dose >4000 IU) ◼ (Bender, 2005) Vitamin D ◼ Supplements are recommended for young children, pregnant women, elderly persons and anyone who is housebound or gets little or no sunlight Vitamin E -tocopherol First isolated as an antisterility factor in rats, ◼ Tocopherol from the Greek words “tokos” & “pherin” meaning “to bring forth children” ◼ 8 naturally occurring vitamin E compounds synthesized from plants ◼ Vitamin E ◼ Vitamin E is a major lipid-soluble antioxidant in cell membranes and plasma lipoproteins. The 8 vitamers have differing biological activity and antioxidant action. αtocopherol has actions in regulating platelet coagulability and vascular smooth muscle proliferation, and gene expression. The tocotrienols down regulate cholesterol synthesis. Vitamin E Important antioxidant ◼ Major role in protecting lipid cell membrane integrity from free radicals ◼ Anti-inflammatory effects ◼ Vitamin E ◼ DNA synthesis ◼ Stimulates immune response ◼ Regulating of intercellular signaling & cell proliferation Vitamin E ◼ Transported in blood by plasma lipoproteins & rbcs Deficiency: premature infants (susceptible to haemolytic anaemia) adults with severe fat malabsorption ◼ Low intake is associated with several cancers & heart disease ◼ Vitamin E Severe deficiency leads to leakage of cell contents ◼ Myopathies, neuropathies & liver necrosis RDA 15mg ◼ Sources: vegetable oils (e.g. coconut oil), fruits, nuts, cereals, whole grains ◼ (Bender, 2005) Vitamin K –phylloquinone & menaquinones Group of compounds ◼ Classified in 2 groups according to whether they are synthesized by plants or bacteria ◼ Phylloquinone (vitamin K1) synthesized by plants – main dietary source ◼ Vitamin K ◼ 2 types: K1 phylloquinone found in liver & green leafy vegetables K2 menaquinone synthesized by colonic bacteria Vitamin K ◼ The synthetic compounds menadione and menadiol (vitamin K3) are used for administration of the vitamin by injection to patients with malabsorption and to new born babies Vitamin K ◼ Widely distributed in food esp. liver, green leafy vegetables, vegetable oils e.g. soybean oil ◼ Absorption enhanced by bile ◼ Metabolized in liver Vitamin K Important for hepatic synthesis of prothrombin (factor II) & clotting factors VII, IX& X ◼ Bone matrix protein: osteocalcin (bone metabolism) ◼ Deficiency in mother may result in bone defects in fetus ◼ Deficiency may play a role in osteoporosis ◼ Vitamin K Not stored. Excreted through kidney & in faeces ◼ Dietary deficiency is rare ◼ Deficiency most often due to treatment with anticoagulants ◼ Prolonged antibiotic therapy ◼ Obstructive jaundice ◼ Low levels in newborn ◼ Lab dx: prothrombin time ◼ Vitamin K Risk of bleeding in the newborn baby in first week of life due to deficiency of vit K due to poor placental transfer ◼ Vitamin K low in breast milk ◼ Vitamin K injection given to baby at birth RDA: 0.5-1mg for adults (CFNI 1994) ◼ Review Questions What are the chemical names for each water soluble vitamin? ◼ What are the vitamers of each of the water soluble vitamins? ◼ Outline the preformed and provitamin formulations of Vitamin A ◼ Explain the functions of the fat soluble vitamins ◼ Review Questions Describe 2 conditions in which water soluble vitamins may be deficient ◼ Review the RDA for water soluble vitamins ◼ Outline the symptoms associated with the deficiency and excess of water soluble vitamins. ◼ References ◼ ◼ ◼ ◼ ◼ ◼ 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. & Sinha, D.P (Eds.).(2006). Nutrition Made Simple (4rd ed. pp.50-73). Kingston: Caribbean Food and Nutrition Institute. CFNI. (1994). Dietary Allowances for the Caribbean. Kingston: Caribbean Food and Nutrition Institute Gallagher, M.L. (2008). The nutrients and their metabolism. In Mahan, L. K., & Escott-Stump, S. (2008). Krause’s food, nutrition and diet therapy. (12th ed.). Philadelphia: Saunders. Huang, Z., Liu, Y., Qi, G., Brand, D., & Zheng, S. G. (2018). Role of vitamin A in the immune system. Journal of clinical medicine, 7(9), 258. Olson, J.A., Loveridge, N., Duthie, G.G., Shearer, M.J. (2002). Fat soluble vitamins. In Human Nutrition and Dietetics (10th ed. Ch. 13) Eds: J.S.Garrow, W.P.T.James, & A. Ralph. Edinburgh, Churchill Livingstone References ◼ ◼ ◼ ◼ ◼ ◼ Manson, J. E., Cook, N. R., Lee, I. M., Christen, W., Bassuk, S. S., Mora, S.,... & Buring, J. E. (2019). Vitamin D supplements and prevention of cancer and cardiovascular disease. New England Journal of Medicine, 380(1), 33-44. Meléndez‐Martínez, A. J. (2019). An Overview of Carotenoids, Apocarotenoids, and Vitamin A in Agro‐Food, Nutrition, Health, and Disease. Molecular nutrition & food research, 63(15), 1801045. Sassi, F., Tamone, C., & D’Amelio, P. (2018). Vitamin D: nutrient, hormone, and immunomodulator. Nutrients, 10(11), 1656. Smith, A.F., Beckett, G.J., Walker, S.W., Wray, P.W.H.(1999). Clinical Biochemistry (6th Ed.). Blackwell Science, Cambridge WHO (2009). Micronutrients. Retrieved on October 6, 2009 from: http://www.who.int/nutrition/topics/micronutrients /en/ Zinder, R., Cooley, R., Vlad, L. G., & Molnar, J. A. (2019). Vitamin A and wound healing. Nutrition in Clinical Practice, 34(6), 839-849.