Vitamin D
Description
Vitamin D is a steroid hormone that exists in two molecular forms: vitamin D-3 (cholecalciferol) found in animal skin, and vitamin D-2 (ergocalciferol) found in yeast. These two forms are created by the action of the sun's ultraviolet rays on the biological precursors 7-dehydrocholesterol and ergosterol. Vitamin D is essential for calcium and phosphorus metabolism, and it is required for the normal development of bones and teeth.
Method of Action
Vitamin D can be acquired either by ingestion of preformed vitamin D or by the conversion of 7-dehydrocholesterol, after exposure to ultraviolet light.
Ingested vitamin D is absorbed with the aid of bile. Vitamin D is then transported to the liver and is converted to 25-hydroxycholecalciferol. This compound is transformed in the kidney into the physiologically active form 1,25-dihydroxycholecalciferol (1,25-DHCC). 1,25-DHCC is then transported to the intestinal mucosal cells, bone, and skeletal muscle where it is stored, regulating calcium absorption and mobilization.
Vitamin D aids the absorption of calcium from the intestinal tract by stimulating the synthesis of calcium-binding protein in the intestinal mucous membrane. It also aids the resorption of phosphate in the renal tube. Vitamin D mobilizes phosphate from the bone to maintain serum phosphate levels, and stimulates the active phosphate transport.
Vitamin A, choline, vitamin C, unsaturated fatty acids, and phosphorus assist absorption of vitamin D. Mineral oil or insufficient sunlight can prevent vitamin D absorption.
Properties & Uses
Vitamin D's clinical application is in the treatment of rickets and osteomalacia.
Rickets can be prevented in newborns by administering vitamin D in proper amounts early in, and throughout the growth period. If rickets do occur, large doses of the vitamin are given.
Osteomalacia is prevented by adequate vitamin D, calcium, and phosphorus in the diet. Vitamin D must come from food, adequate sunlight, or concentrated supplements. The pain and weakness associated with vitamin D deficiency will usually disappear after one to two months of treatment.
Consequence of Deficiency
Vitamin D deficiency creates a deficient deposition of hydroxyapatite in the bones. This is due to inadequate absorption of calcium from the intestinal tract, and from the retention of phosphorus in the kidney. This inadequate mineralization of the bones causes rickets in infants and children, and osteomalacia in adults. Rickets can cause delayed closure of the fontanelles, softening of the skull, soft fragile bones, enlargement of the wrist, knee, and ankle joints, poorly developed muscles, restlessness and nervous irritability. Also, delayed tooth development can be a sign of rickets. There are also children who develop rickets with vitamin D supplementation. This may be due to a genetic error in vitamin D metabolism, usually renal tubular dysfunction.
Insufficient sunlight can create vitamin D deficiency by preventing the conversion of 7-dehydrocholesterol to cholecalciferol. This type of deficiency is most common in countries with limited sunlight, or where the population dresses in a manner that reduces the sunlight exposure.
Toxicity Factors
Vitamin D taken in excess can cause pathological changes in the body. Signs of vitamin D toxicity include excessive calcification of bone, kidney stones, calcification of soft tissue, headaches, weakness, nausea, vomiting, constipation, polyuria and polydipsia.
Recommended Dietary Allowance
| age | RDA (mcg) | RNI (mcg) | |
| infants/children | |||
| 0-6 months | 7.5 | 8.5 | |
| 6-12 months | 10 | 7 | |
| 1-3 years | 10 | 7 | |
| 3-10 years | 10 | - | |
| males | |||
| 10-24 years | 10 | - | |
| 25-65 years | 5 | - | |
| 65+ years | 5 | 10 | |
| females | |||
| 10-24 years | 10 | - | |
| 25-65 years | 5 | - | |
| 65+ years | 5 | 10 | |
| pregnancy | 10 | 10 | |
| lactation | 10 | 10 |
Difficulties in establishing requirements for vitamin D arise from the limited number of food sources available, lack of knowledge of precise body needs, and degree of synthesis in the skin by irradiation. The amount needed can vary between winter and summer in northern climates.
In addition, lifestyle determines the degree of exposure to sunlight and would therefore influence individual need. This is especially true of the elderly and invalids who do not go outside and therefore may need supplementary vitamin D. Growth demands in childhood, during pregnancy, and during lactation necessitate increased intake.
The daily recommendation for young adults is 7.5 micrograms and older adults 5.0 micrograms. The Recommended Dietary Allowance (RDA) standard is 10 micrograms, or 400 international units (IU), of cholecalciferol daily for children and for women during pregnancy and lactation. One IU of vitamin D is equivalent to biologic activity of 0.025 micrograms of pure crystalline vitamin D-3 (cholecalciferol).
For over thirty years, Recommended Daily Amounts has existed in the United Kingdom. It has been used to measure the adequacy of an individual's diet. However, in 1991 the Committee on Medical Aspects of Food Policy (COMA) gave forth a whole new set of figures upon the request of the Department of Health's Chief Medical Officer. Reference Nutrient Intake (RNI) is one of these sets collectively known as "Dietary Reference Values." RNI is an amount of a nutrient that is enough for almost every individuals, even someone who has high needs for the nutrient. This level of intake is, therefore, considerably higher than what most people would need. If individuals are consuming the RNI of a nutrient they are most unlikely to be deficient in that nutrient.
Adults over 22 years of age need only a small amount of vitamin D. Under normal circumstances their need is met by the vitamin D contained in an ordinary mixed diet and by exposure to sunlight. Adults who work at night and those whose clothing or living customs shield them from sunlight need somewhat more vitamin D in their diet.
No extra benefit is obtained from taking more than 400 IU daily except for therapeutic reasons; then, dosages can range from 1,500 to 2,800 IU daily.
Food Sources
Low: (10 - 100 IU/ 100 g)
| Beef | Grain oils |
| Butter | Halibut |
| Cheese | Horse meat |
| Cod roe | Milk |
| Cream | Veal |
| Egg | Vegetable oils |
Medium: (100 - 100 IU/ 100 g)
| Egg yolk | Pilchards |
| Herring | Salmon |
| Kippers | Sardines |
| Lard | Shrimp |
| Mackerel | Tuna |
| Margarine |
High: (1,000-25 x 10 6 IU/100 g) Liver oils of:
| Bass | Sable |
| Bonito | Sardines (canned) |
| Cod | Shark |
| Halibut | Swordfish |
| Herring | Tuna |
| Lingcod |
References
Beaty, M., Lee, E., Glauart, H. FASEB J., 1991; 5: 926A.
Blomhoff-R & Drevon-CA: [Fat-soluble vitamins in clinical practice]. Tidsskr-Nor-Laegeforen. 1995 Feb 10; 115(4): 481-5.
Borrman, W.R. 1979. Comprehensive Guide to Nutrition. New Horizons Pub Corp. Chicago, Illinois.
Chapny, M.C., Chapny, P., Mennier, P.J. Am J Clin Nutr., 1987; 46: 324- 328.
Crombie, I.K. Brit J Cancer, 1981; 43: 842-849.
Fogelman-Y et al: High prevalence of vitamin D deficiency among Ethiopian women immigrants to Israel: exacerbation during pregnancy and lactation [see comments] Isr-J-Med-Sci. 1995 Apr; 31(4): 221-4.
Gaby, S.K., Singh, V.N. In: Vitamin Intake and Health: A Scientific Review, Marcel Dekker: Ner York, 1991, pp. 59-70.
Garland, C., Garland, F. Int J Epidemiol., 1980; 9: 227-231.
Garland, F.C., et al. Prevent Med., 1990; 19: 614-622.
Garland, F.C., et al. Arch Environ Health, 1990; 45: 261-267.
Garland, C., et al. Lancet, 1985; 1: 307-309.
Garland, C.F., et al. Lancet, 1989; 2: 1176-1178.
Gureter, J., et al. Lancet, 1987; 1: 306-307.
Jensen-JE: [Severe vitamin D deficiency in an immigrant family]. Ugeskr-Laeger. 1995 Jan 30; 157(5): 595-6.
Kirschmann, John D.. Nutrition Almanac: Nutrition Search Inc. New York: McGraw-Hill, 1975.
Kirschmann, J.D. Nutrition Almanac: Nutrition Search. McGrew-Hill: New York. 1990.
Koh, H.K., Kligler, B.E., Lew, R.A. Photochem Photobiol., 1990; 19: 614- 622.
Krause, M.V. & L.K. Mahan. 1979. Food, Nutrition and Diet Therapy. 6th ed. W.B. Saunders Company, Philadelphia. 963.
Kutsky, R.J. 1973. Handbook of Vitamins and Hormones. Van Nostrand Reinhold, Co. New York, New York. 278.
Lips, P., et al. Am J Clin Nutr., 1987; 46: 1005-1010.
MacLaughlin, J., Holick , M.F., J Clin Invest., 1985; 76: 1536-1538.
Murray, M.T. & Pizzorno, J.E. Encyclopedia of Natural Medicine. Rocklin, CA: Prima Publishing,1991.
Omdahl, J.L. et al. Am J Clin Nutr., 1982; 1982; 36: 1225-1233.
Osol, Arthur. 1980. Remington's Pharmaceutical Sciences. Mack Publishing Company, Pennsylvania. 1928.
Parfitt, A.M., et al. Am J Clin Nutr., 1982; 36: 1014-1031.
Recommended Dietary Allowances. 1989. National Academy of Science, National Academy Press, Washington, D.C.
Sowers, M.R., Wallace, R.B., Lemke, J.H. Am J Clin Nutr., 1985; 42: 135-142.
Sowers, M.R., et al. Am J Clin Nutr., 1988; 48: 1053-1056.
Vagero, R., Ringback, G., Kiveranta, H. Brit J Cancer, 1986; 53: 507- 512.
Walji, H., Vitamin Guide: Essential nutrients for healthy living., Element: Dorset, U.K. 1992.
Walji, H., Vitamin Minerals & Dietary Supplements., Hodder Headline Plc.: London, U.K. 1994.
Webb, A.R., Holick, M.F. Ann Rev Nutr., 1988; 8: 375-399.
Wiedman, K.H., et al. Lancet, 1985; 1: 307-309.
Williams, R.D, Mason, H.L., Power, M.H., And Wilder, R.M. Induced Thiamine (Vitamin B1) Deficiency In Man; Relation Of Depletion Of Thiamine To Development Of Biochemical Defect And Of Polyneuropathy. Arch. Int. Med. 71:38-53,1943.
Williams, Sue Rodwell. Nutrition And Diet Therapy. 5th edition. St Louis: Times Mirror Mosby, 1985.
Wyngaarden, J.B. & L.H. Smith. 1985. Cecil's Textbook of Medicine. Saunders Pub Co., Philadelphia. 2341.
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