• Home   /  
  • Archive by category "1"

Essay On Water Soluble Vitamins

  • Abdel-Galil, A.M. 1986. Preventive effect of vitamin C (L-ascorbic acid) on methylcholanthrene-induced soft tissue sarcomas in mice. Oncology 43:335-337. [PubMed: 3763128]

  • Abul-Hajj, Y.J., and M. Kelliher. 1982. Failure of ascorbic acid to inhibit growth of transplantable and dimethylbenzanthracene induced rat mammary tumors. Cancer Lett. 17:67-73. [PubMed: 6817914]

  • Ahmann, F.R., and B.G.M. Durie. 1984. Acute myelogenous leukaemia modulated by B12 deficiency: a case with bone marrow blast cell assay corroboration. Br. J. Haematol. 58:91-94. [PubMed: 6590092]

  • Alpers, D.H., R.E. Clouse, and W.F. Stenson. 1983. Manual of Nutritional Therapeutics. Little, Brown and Company, Boston. 457 pp.

  • Altman, R.F., G.M. Schaeffer, C.A. Salles, A.S. Ramos de Souza, and P.M. Cotias. 1980. Phospholipids associated with vitamin C in experimental atherosclerosis. Arzneim. Forsch. 30:627-630. [PubMed: 7190404]

  • Anderson, B.B., H. O'Brien, G.E. Griffin, and D.L. Mollin. 1980. Hydrolysis of pyridoxal 5'-phosphate in plasma in conditions with raised alkaline phosphate. Gut 21:192-194. [PMC free article: PMC1420355] [PubMed: 7399318]

  • APA (American Psychiatric Association). 1973. Megavitamin and Orthomolecular Therapy in Psychiatry. A Report of the Task Force on Vitamin Therapy in Psychiatry. American Psychiatric Association, Washington, D.C. 54 pp.

  • Areekul, S., P. Hathirat, and K. Churdchu. 1986. Folic acid, vitamin B12, and vitamin B12 binding proteins in patients with neuroblastoma. Southeast Asian J. Trop. Med. Public Health 17:184-188. [PubMed: 3787306]

  • Arvanitakis, C., F.F. Holmes, and E. Hearne III. 1979. A possible association of pernicious anemia with neoplasia. Oncology 36:127-129. [PubMed: 471423]

  • Baker, H., O. Frank, H. Ziffer, S. Goldfarb, C.M. Leevy, and H. Sobotka. 1964. Effect of hepatic disease on liver B-complex vitamin titers. Am. J. Clin. Nutr. 14:1-6. [PubMed: 14106867]

  • Baker, H., O. Frank, and M.F. Sorrell. 1976. Nicotinic acid and alcoholism. Bibl. Nutr. Dieta. 24:32-39. [PubMed: 12737]

  • Baker, H., O. Frank, T. Chen, S. Feingold, B. DeAngelis, and E.R. Baker. 1981. Elevated vitamin levels in colon adenocarcinoma as compared with metastatic liver adenocarcinoma from colon primary and normal adjacent tissue. Cancer 47:2883-2886. [PubMed: 7260874]

  • Banic, S. 1981. Vitamin C acts as a cocarcinogen to methylcholanthrene in guinea-pigs. Cancer Lett. 11:239-242. [PubMed: 7248928]

  • Beetens, J.R., M.C. Coene, A. Verheyen, L. Zonnekeyn, and A.G. Herman. 1984. Influence of vitamin C on the metabolism of arachidonic acid and the development of aortic lesions during experimental atherosclerosis in rabbits. Biomed. Biochim. Acta 43:S273-S276. [PubMed: 6440540]

  • Beetens, J.R., M.C. Coene, A. Verheyen, L. Zonnekeyn, and A.G. Herman. 1986. Vitamin C increases the prostacyclin production and decreases the vascular lesions in experimental atherosclerosis in rabbits. Prostaglandins 32:335-352. [PubMed: 3538204]

  • Bell, E. 1980. The excretion of a vitamin B6 metabolite and the probability of recurrence of early breast cancer. Eur. J. Cancer 16:297-298. [PubMed: 7371685]

  • Bidlack, W.R., R.C. Brown, and C. Mohan. 1986. Nutritional parameters that alter hepatic drug metabolism, conjugation, and toxicity. Fed. Proc. 45:142-148. [PubMed: 3510912]

  • Bjelke, E. 1978. Dietary factors and the epidemiology of cancer of the stomach and large bowel. Aktuel. Ernaehrungsmed. Klin. Prax. Suppl. 2:10-17.

  • Böing, H., L. Martinez, R. Frentzel-Beyme, and U. Oltersdorf. 1985. Regional nutritional pattern and cancer mortality in the Federal Republic of Germany. Nutr. Cancer 7:121-130. [PubMed: 4080563]

  • Bonjour, J.P. 1980. Vitamins and alcoholism. III. Vitamin B6. Int. J. Vitam. Nutr. Res. 50:215-230. [PubMed: 6249768]

  • Brown, J.P., G.E. Davidson, J.M. Scott, and J. Weir. 1973. Effect of diphenylhydantoin and ethanol feeding on the synthesis of rat liver folates from exogenous pteroylglutamate (3H). Biochem. Pharmacol. 22:3287-3289. [PubMed: 4769600]

  • Bulovskaia, L.N. 1976. Acetylation reaction in mice in the normal state and in tumors. Vopr. Onkol. 22:59-63. [PubMed: 1274265]

  • Burch, H.B., F.E. Hunter, Jr., A.M. Combs, and B.A. Schutz. 1960. Oxidative enzymes and phosphorylation in hepatic mitochondria from riboflavin-deficient rats. J. Biol. Chem. 235:1540-1544. [PubMed: 13805983]

  • Butterworth, C.E., Jr., K.D. Hatch, H. Gore, H. Mueller, and C.L. Krumdieck. 1982. Improvement in cervical dysplasia associated with folic acid therapy in users of oral contraceptives. Am. J. Clin. Nutr. 35:73-82. [PubMed: 7064879]

  • Cameron, E., and L. Pauling. 1979. Cancer and Vitamin C. Linus Pauling Institute of Science and Medicine, Menlo Park, Calif. 238 pp.

  • Carmel, R. 1975. Extreme elevation of serum transcobalamin I in patients with metastatic cancer. N. Engl. J. Med. 292:282-284. [PubMed: 1053806]

  • Carmel, R., and L. Eisenberg. 1977. Serum vitamin B12 and transcobalamin abnormalities in patients with cancer. Cancer 40:1348-1353. [PubMed: 902243]

  • Chabner, B.A., V.T. DeVita, D.M. Livingston, and V.T. Oliverio. 1970. Abnormalities of tryptophan metabolism and plasma pyridoxal phosphate in Hodgkin's disease. N. Engl. J. Med. 282:838-843. [PubMed: 5418547]

  • Chen, C., and T. Liao. 1960. Histochemical study on riboflavin. J. Vitaminol. Osaka 6:171-195. [PubMed: 13692756]

  • Clamon, G.H., R. Feld, W.K. Evans, R.S. Weiner, B.S. Kramer, LL. Lininger, LB. Gardner, E.C. Wolfe, W.D. DeWys, and F.A. Hoffman. 1984. Serum folate and vitamin B12 levels in patients with small cell lung cancer. Cancer 53:306-310. [PubMed: 6317162]

  • Cole, M., A. Turner, O. Frank, H. Baker, and C.M. Leevy. 1969. Extraocular palsy and thiamin therapy in Wernicke's encephalopathy. Am. J. Clin. Nutr. 22:44-51. [PubMed: 5764630]

  • Cook-Mozaffari, P. 1979. The epidemiology of cancer of the oesophagus. Nutr. Cancer 1:51-60.

  • Cook-Mozaffari, P.J., F. Azordegan, N.E. Day, A. Ressicaud, C. Sabai, and B. Aramesh. 1979. Oesophageal cancer studies in the Caspian Littoral of Iran: results of a case-control study. Br. J. Cancer 39:293-309. [PMC free article: PMC2009866] [PubMed: 465299]

  • Coronary Drug Project Research Group. 1975. Clofibrate and niacin in coronary artery disease. J. Am. Med. Assoc. 231:360-381. [PubMed: 1088963]

  • Dancy, M., G. Evans, M.K. Gaitonde, and J.D. Maxwell. 1984. Blood thiamine and thiamine phosphate ester concentrations in alcoholic and non-alcoholic liver diseases. Br. Med. J. 289:79-82. [PMC free article: PMC1441909] [PubMed: 6428686]

  • De Reuck, J.L., G.J. Sieben, M.R. Sieben-Praet, P. Ngendahayo, W.J. De Coster, and H.M. Vander Eecken. 1980. Wernicke's encephalopathy in patients with tumors of the lymphoid-hemopoietic systems. Arch. Neurol. 37:338-341. [PubMed: 7387463]

  • DHHS-USDA (Department of Health and Human Services and U.S. Department of Agriculture). 1986. Nutrition Monitoring in the United States—A Progress Report from the Joint Nutrition Monitoring Evaluation Committee. DHHS Pub. No. (PHS) 86-1255, Public Health Service, National Center for Health Statistics, Department of Health and Human Services, Hyattsville, Md. 356 pp.

  • DiPalma, J.R., and D.M. Ritchie. 1977. Vitamin toxicity. Annu. Rev. Pharmacol. Toxicol. 17:133. [PubMed: 326160]

  • DiSorbo, D.M., R. Wagner, Jr., and L. Nathanson. 1985. In vivo and in vitro inhibition of B16 melanoma growth by vitamin B6. Nutr. Cancer 7:43-52. [PubMed: 4070008]

  • Dubick, M.A., G.C. Hunter, S.M. Casey, and C.L. Keen. 1987. Aortic ascorbic acid, trace elements, and superoxide dismutase activity in human aneurysmal and occlusive disease. Proc. Soc. Exp. Biol. Med. 184:138-143. [PubMed: 3809168]

  • Dunham, W.B., E. Zuckerkandl, R. Reynolds, R. Willoughby, R. Marcuson, R. Barth, and L. Pauling. 1982. Effects of intake of L-ascorbic acid on the incidence of dermal neoplasms induced in mice by ultraviolet light. Proc. Natl. Acad. Sci. U.S.A. 79:7532-7536. [PMC free article: PMC347374] [PubMed: 6961430]

  • Du Vigneaud, V., J.M. Spangler, D. Burk, C.J. Kensler, K. Sugiura, and C.P. Rhoades. 1942. The procarcinogenic effect of biotin in butter yellow tumor formation. Science 95:174-176. [PubMed: 17818886]

  • Eichner, E.R., and R.S. Hillman. 1971. The evolution of anemia in alcoholic patients. Am. J. Med. 50:218-232. [PubMed: 5545458]

  • Eichner, E.R., B. Buchanan, J.W. Smith, and R.S. Hillman. 1972. Variations in the hematologic and medical status of alcoholics. Am. J. Med. Sci. 263:35-42. [PubMed: 5057850]

  • Einstein, N., A. Baker, J. Galper, and H. Wolfe. 1975. Jaundice due to nicotinic acid therapy. Am. J. Dig. Dis. 20:282-286. [PubMed: 1124751]

  • Fass, S., and R.S. Rivlin. 1969. Regulation of riboflavin-metabolizing enzymes in riboflavin deficiency. Am. J. Physiol. 217:988-991. [PubMed: 4309977]

  • Foy, H., and A. Kondi. 1984. The vulnerable esophagus: riboflavin deficiency and squamous cell dysplasia of the skin and the esophagus. J. Natl. Cancer Inst. 72:941-948. [PubMed: 6584669]

  • Foy, H., and V. Mbaya. 1977. Riboflavin. Prog. Food Nutr. Sci. 2:357-394. [PubMed: 404669]

  • Foy, H., A. Kondi, J.N. Davies, B. Anderson, A. Parker, J. Preston, and F.J. Peers. 1974. Histologic changes in livers of pyridoxine-deprived baboons—relation to alpha l-fetoprotein and liver cancer in Africa. J. Natl. Cancer Inst. 53:1295-1311. [PubMed: 4139278]

  • Frank, O., A. Luisada-Opper, M.F. Sorrell, A.D. Thomson, and H. Baker. 1971. Vitamin deficits in severe alcoholic fatty liver of man calculated from multiple reference units. Exp. Mol. Pathol. 15:191-197. [PubMed: 5111801]

  • Fukushima, S., K. Imaida, T. Sakata, T. Okamura, M.A. Shibata, and N. Ito. 1983. Promoting effects of sodium L-ascorbate on two-stage urinary bladder carcinogenesis in rats. Cancer Res. 43:4454-4457. [PubMed: 6871876]

  • Fukushima, S., Y. Kurata, M.A. Shibata, E. Ikawa, and N. Ito. 1984. Promotion by ascorbic acid, sodium erythorbate and ethoxyquin of neoplastic lesions in rats initiated with N-butyl-N-(4-hydroxybutyl)nitrosamine. Cancer Lett. 23:29-37. [PubMed: 6744233]

  • Ghoshal, A.K., and E. Farber. 1984. The induction of liver cancer by dietary deficiency of choline and methionine without added carcinogens. Carcinogenesis 5:1367-1370. [PubMed: 6488458]

  • Ghoshal, A.K., M. Ahluwalia, and E. Farber. 1983. The rapid induction of liver cell death in rats fed a choline-deficient methionine-low diet. Am. J. Pathol. 113:309-314. [PMC free article: PMC1916365] [PubMed: 6650660]

  • Giambarresi, L.I., S.L. Katyal, and B. Lombardi. 1982. Promotion of liver carcinogenesis in the rat by a choline-devoid diet: role of liver cell necrosis and regeneration. Br. J. Cancer 46:825-829. [PMC free article: PMC2011142] [PubMed: 7171459]

  • Graham, S., C. Mettlin, J. Marshall, R. Priore, T. Rzepka, and D. Shedd. 1981. Dietary factors in the epidemiology of cancer of the larynx. Am. J. Epidemiol. 113:675-680. [PubMed: 7234856]

  • Grassetti, D.R. 1986. The antimetastatic and tumor growth retarding effects of sulfur containing analogs of nicotinamide. Cancer Lett. 31:187-195. [PubMed: 2938726]

  • Ha, C., N.I. Kerkvliet, and L.T. Miller. 1984. The effect of vitamin B6 deficiency on host susceptibility to Moloney sarcoma virus-induced tumor growth in mice. J. Nutr. 114:938-945. [PubMed: 6726463]

  • Haenszel, W., and P. Correa. 1975. Developments in the epidemiology of stomach cancer over the past decade. Cancer Res. 35:3452-3459. [PubMed: 1104154]

  • Halsted, C.H., and T. Tamura. 1979. Folate deficiency in liver disease. Pp. 91-100 in C.S. Davidson, editor. , ed. Problems in Liver Diseases. Stratton, New York.

  • Halsted, C.H., E.A. Robles, and E. Mezey. 1971. Decreased jejunal uptake of labeled folic acid (3H-PGA) in alcoholic patients: roles of alcohol and nutrition. N. Engl. J. Med. 285:701-706. [PubMed: 5571128]

  • Halsted, C.H., E.A. Robles, and E. Mezey. 1973. Intestinal malabsorption in folate-deficient alcoholics. Gastroenterology 64:526-532. [PubMed: 4700768]

  • Harada, T., T. Kitazawa, K. Maita, and Y. Shirasu. 1985. Effects of vitamin C on tumor induction by diethylnitrosamine in the respiratory tract of hamsters exposed to cigarette smoke. Cancer Lett. 26:163-169. [PubMed: 3978606]

  • Henderson, J.M., M.A. Codner, B. Hollins, M.H. Kutner, and A.H. Merrill. 1986. The fasting B6 vitamer profile and response to a pyridoxine load in normal and cirrhotic subjects. Hepatology 6:464-471. [PubMed: 3710434]

  • Herbert, V., R. Zalusky, and C.S. Davidson. 1963. Correlation of folate deficiency with alcoholism and associated macrocytosis, anemia, and liver disease. Ann. Intern. Med. 58:977-998. [PubMed: 13953905]

  • Higginson, J. 1966. Etiological factors in gastrointestinal cancer in man. J. Natl. Cancer Inst. 37:527-545. [PubMed: 5923503]

  • Hillman, R.S. 1975. Alcohol and hematopoiesis. Ann. N.Y. Acad. Sci. 252:297-306. [PubMed: 1056731]

  • Hillman, R.S. 1980. Vitamin B12, folic acid, and the treatment of megaloblastic anemias. Pp. 1331-1346 in A.G. Gilman, editor; , L.S. Goodman, editor; , and A. Gilman, editor. , eds. The Pharmacological Basis of Therapeutics. Macmillan, New York.

  • Hinds, M.W., L.N. Kolonel, J.H. Hankin, and J. Lee. 1984. Dietary vitamin A, carotene, vitamin C and risk of lung cancer in Hawaii. Am. J. Epidemiol. 119:227-237. [PubMed: 6695902]

  • Hormozdiari, H., N.E. Day, B. Aramesh, and E. Mahboubi. 1975. Dietary factors and esophageal cancer in the Caspian Littoral of Iran. Cancer Res. 35:3493-3498. [PubMed: 1242686]

  • Hoover, K.L., P.H. Lynch, and L.A. Poirier. 1984. Profound postinitiation enhancement by short-term severe methionine, choline, vitamin B12, and folate deficiency of hepatocarcinogenesis in F344 rats given a single low-dose diethylnitrosamine injection. J. Natl. Cancer Inst.

  • As the name suggests, fat-soluble vitamins are a type of vitamin that is absorbed into the body through fatty tissue.

    The human body requires a variety of vitamins to keep working properly. There are two types of vitamins: water-soluble and fat-soluble vitamins.

    Vitamins are often obtained through regular food intake. Some people require or want additional vitamins provided through supplements.

    Though both types of vitamin are important to the body, this article focuses on the types, functions, and sources of fat-soluble vitamins.

    What are fat-soluble vitamins?

    Fat-soluble vitamins provide the most benefit when consumed alongside foods that contain fat.

    Fat-soluble vitamins will not dissolve in water. Instead, fat-soluble vitamins absorb best when taken with higher-fat foods.

    Once absorbed into the body, fat-soluble vitamins are stored in fatty tissues and liver. The body can use these stores for future use. The water-soluble vitamins are vitamins B and C.

    There are four types of fat-soluble vitamins:

    Each type of fat-soluble vitamin promotes different functions in the body. People deficient in the fat-soluble vitamins may require supplements to boost their supply.

    However, it is possible to take in too much of a fat-soluble vitamin, which could lead to toxicity and adverse reactions.

    Vitamin A

    Vitamin A plays an important role in maintaining healthy vision. Without vitamin A, a person would suffer from severe vision issues.


    Vitamin A does not refer to one single vitamin but is a collection of compounds known as retinoids. Retinoids can be found both in the human body and in some food sources.


    Vitamin A supports several functions throughout the body. Some of the most important functions it supports include vision and the immune system.

    Dietary sources

    Vitamin A can be obtained through natural sources. Some sources include:

    • fish liver oil
    • liver of animals
    • butter

    Animal sources provide the active components to help create retinols within the human body.

    Some plants also provide pro-vitamin A compounds known as carotenoid antioxidants. The most common is called beta carotene, which can be found in foods such as:

    Recommended intake

    The recommended intake of vitamin A varies by age and gender. The following are some recommended daily allowance values:

    • infants (0–12 months): 400–500 micrograms (mcg)
    • children aged 1–3: 300 mcg
    • children aged 4–8: 400 mcg
    • children aged 9–13: 600 mcg
    • adult women: 700 mcg
    • adult men: 900 mcg


    Vitamin A deficiency is not common in developed countries. However, vegetarians are at a higher risk of a deficiency because they do not get some kinds of vitamin A through their normal diet.

    Similarly, people in developing countries with limited food sources or people whose diet is low in meat intake may also suffer from vitamin A deficiencies.

    Some signs of vitamin A deficiency include:


    It is possible to reach toxic levels of vitamin A. This condition is called hypervitaminosis. People who take vitamin A supplements or eat copious amounts of fish liver oils are at the highest risk.

    Pregnant women should not double up on their prenatal vitamins. High levels of vitamin A are harmful to a growing fetus.

    If a person experiences an overdose, they may experience symptoms ranging from headaches and fatigue. In severe cases, hypervitaminosis in a pregnant woman may result in a baby with birth defects.

    Vitamin D

    Vitamin D is produced by the body when the skin is exposed to sunlight.

    Vitamin D is produced naturally in the human body when the skin is exposed to the sun. Vitamin D aids in bone health and development.


    Similar to vitamin A, vitamin D is a collective term used to describe a collection of compounds. Collectively, these are often referred to as calciferol.

    There are two types found naturally:

    • vitamin D-3, found in animal fats
    • vitamin D-2, found in plants, such as mushrooms


    Once vitamin D is absorbed into the bloodstream, the liver and kidneys change calciferol into calcitriol, the biologically active form of vitamin D.

    When used in the body, vitamin D performs two major roles:

    • bone maintenance
    • immune system support

    Dietary sources

    Vitamin D absorption is one of the only arguments for a person exposing large, unprotected areas of skin to the sun. When exposed regularly, people can actually absorb enough rays to produce vitamin D to function properly, without need for supplements.

    However, many people do not spend hours in the sun. When people do, they are also often covered in sunscreen and clothing. As a result, a person is not likely to absorb as much vitamin D through sunlight alone.

    Instead, people can obtain vitamin D through some food sources, including:

    • fish oil
    • fatty fish
    • mushrooms exposed to ultraviolet light
    • fortified dairy products

    Recommended intake

    Recommended daily values of vitamin D vary by age, though not by much. Some general guidelines indicate the following daily values:

    • infants (0–12 months): 10 mcg
    • 1–70 years of age: 15 mcg
    • above age 70: 20 mcg


    It is not very common for a person to develop vitamin D deficiency. When it happens, most cases involve older adults or people who have been admitted to the hospital for extended amounts of time.

    Some people are at a higher risk of developing a vitamin D deficiency. These include:

    • obese people
    • people with dark skin tones
    • older adults
    • those who get limited sun exposure
    • people with chronic conditions

    Some of the most common signs and symptoms of vitamin D deficiency include:

    • increased bone fractures
    • weakend immune system
    • weakened muscles
    • impaired healing
    • soft bones
    • hair loss
    • more prone to infections
    • tiredness


    Toxic levels of vitamin D rarely occur. They are most likely to occur in people who take too many vitamin D supplements.

    An overabundance of vitamin D in the body can lead to a condition called hypercalcemia. This condition is marked by excessive levels of calcium in the blood.

    When hypercalcemia occurs, a person may experience:

    Vitamin E

    Vitamin E is an antioxidant that can help the body destroy free radicals. Free radicals are unstable atoms that may cause the formation of cancer cells. As such, vitamin E could play an important part in preventing cancer.


    Vitamin E is broken down into eight different types, with the two main kinds being tocopherols and tocotrienols. Tocopherol contains the most abundant form of vitamin E.


    As an antioxidant, vitamin E protects fatty tissues from free radicals that can cause cancer. Some water-soluble vitamins, such as C and B, help aid vitamin E's functions.

    In higher doses, vitamin E can also function as a blood thinner.

    Dietary sources

    Vitamin E is most abundant in seeds, vegetable oils, and nuts. Some of the best sources of vitamin E include:

    • wheat germ oil
    • sunflower seeds or oil
    • hazelnuts
    • almonds

    Recommended intake

    Similar to vitamin D, recommended daily values for vitamin E vary by age.

    Here are some of the breakdowns of recommended daily values:

    • infants aged 0–6 months: 4 milligrams (mg)
    • infants aged 7–12 months: 5 mg
    • children aged 1–3 years: 6 mg
    • children aged 4–8 years: 7 mg
    • boys aged 9–13 years: 11 mg
    • 14 years old and above: 15 mg
    • during lactation: 19 mg


    Vitamin E deficiency is extremely rare in otherwise healthy individuals. Those with specific illnesses that block the liver from absorbing vitamin E are most at risk.

    Symptoms of deficiency include:

    • trouble walking
    • muscle weakness or tremors
    • vision issues
    • numbness

    There are also several long-term health issues that can result from vitamin E deficiency, including anemia and heart disease.


    It is nearly impossible for a person to overdose on vitamin E through natural sources. Most people who experience an overdose do so because of taking vitamin E supplements.

    However, people taking blood thinners may be more prone to overdose. In high doses, vitamin E may actually increase the risk of a person developing cancer.

    Vitamin K

    Kale, spinach, and parsley all contain vitamin K.

    Vitamin K helps the body form blood clots. This necessary function prevents a person from bleeding out from small scratches.


    Vitamin K has a variety of types. The two most common groups are:

    • vitamin K-1, found in plant sources
    • vitamin K-2, found in animal sources

    There are additional man-made types of vitamin K.


    The main role that vitamin K plays in the body is blood clotting. However, vitamin K can also help with:

    • reducing risk of heart disease
    • bone health
    • reducing the buildup of calcium in the blood

    Dietary sources

    Vitamin K-1 and K-2 are found in a variety of sources. Some of these sources include:

    • kale
    • liver
    • spinach
    • parsley
    • butter
    • egg yolks

    Recommended intake

    Unlike the other vitamins mentioned, vitamin K recommended values are thought of as adequate intake.

    When a supplement is measured in adequate intake, it means there is less evidence to support the specified amount.

    Some recommended adequate intakes include:

    • infants aged 0–6 months: 2 mcg
    • Infants aged 7–12 months: 2.5 mcg
    • children aged 1-3 years: 30 mcg
    • children aged 4–8 years: 55 mcg
    • children aged 9–13 years: 60 mcg
    • children aged 14-18 years: 75 mcg
    • adult women: 90 mcg
    • adult men: 120 mcg


    Vitamin K is not stored in as great an amount in the body as vitamin A or D. This can lead a person to experience a vitamin K deficiency very quickly.

    If a person has a vitamin K deficiency, they have a greater risk of excess bleeding and reduced bone density that can lead to fractures.


    Naturally occurring vitamin K has no known issues with overdose. Synthetic vitamin K-3, however, may cause overdose when taken in excess.

    In general, vitamin K is considered safe to consume.


    Fat-soluble vitamins play an essential role in a person's overall health.

    It is important to manage the amount of each vitamin to avoid deficiencies and overdosing. Both can have adverse effects that may require medical attention.

    Before starting a vitamin supplement, a person should speak to a doctor, and seek medical attention if a deficiency or overdose is expected.

    One thought on “Essay On Water Soluble Vitamins

    Leave a comment

    L'indirizzo email non verrà pubblicato. I campi obbligatori sono contrassegnati *