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Vitamin adults

Most studies of vitamin B requirements have followed the development of abnormalities of tryptophan and methionine metabolism during depletion and normalization during repletion with graded intakes of the vitamin. Adults maintained on vitamin B -deficient diets develop abnormalities of tryptophan and methionine metabolism faster, and their blood vitamin B falls more rapidly, when their protein... [Pg.376]

Infants maybe sensitive to doses of vitamin A [11103-57-4] in the range of 75,000—200,000 lU (22.5—60 mg), although the toxic dose in adults is probably 2—5 million lU (90.6—1.5 g). Intakes in this range from normal food suppHes without oral supplements are simply beyond imagination (79). Vitamin D [1406-16-2] toxicity is much more difficult to substantiate clinically. Humans can synthesize active forms of the vitamin in the skin upon irradiation of 7-dehydrocholesterol. Toxic symptoms are relatively nonspecific, and dangerous doses seem to He in the range of 1000—3000 lU/kg body wt (25—75 flg/kg body wt) (80). Cases of toxicity of both vitamins E and K have been reported, but under ordinary circumstances these vitamins are considered relatively innocuous (81). [Pg.479]

Of the water-soluble vitamins, intakes of nicotinic acid [59-67-6] on the order of 10 to 30 times the recommended daily allowance (RE)A) have been shown to cause flushing, headache, nausea, and moderate lowering of semm cholesterol with concurrent increases in semm glucose. Toxic levels of foHc acid [59-30-3] are ca 20 mg/d in infants, and probably approach 400 mg/d in adults. The body seems able to tolerate very large intakes of ascorbic acid [50-81-7] (vitamin C) without iH effect, but levels in excess of 9 g/d have been reported to cause increases in urinary oxaHc acid excretion. Urinary and blood uric acid also rise as a result of high intakes of ascorbic acid, and these factors may increase the tendency for formation of kidney or bladder stones. AH other water-soluble vitamins possess an even wider margin of safety and present no practical problem (82). [Pg.479]

Mobilization and Metabolism. The total ascorbic acid body pool in healthy adults has been estimated to be approximately 1.5 g, which increases to 2.3—2.8 g with intakes of 200 mg/d (151—158). Depletion of the body pool to 600 mg initiates physiological changes, and signs of clinical scurvy are reported when the body pool falls below 300 mg (149). Approximately 3—4% of the body pool turns over daily, representing 40—60 mg/d of metabolized, or consumed, vitamin C. Smokers have a higher metaboHc turnover rate of vitamin C (approximately 100 mg/d) and a lower body pool than nonsmokers, unless compensated through increased daily intakes of vitamin C (159). The metaboHsm of ascorbic acid varies among different species. [Pg.22]

In humans, vitamin B in phosphorylated forms is mostly unavaHable until hydrolyzed, then passively absorbed in the smaH intestine. The free vitamins are interconverted and suppHed to the ckculation by the Hver, then enter ceHs by simple diffusion and are phosphorylated. A typical adult pool of... [Pg.68]

In humans, vitamin A deficiency manifests itself in the following ways night blindness, xerophthalmia, Bitot s spots, and corneal involvement and ulceration. Changes in the skin have also been observed. Although vitamin A deficiency is seen in adults, the condition is particularly harmful in the very young. Often, this results from malnutrition (56). [Pg.104]

Clinical manifestation of vitamin B 2 deficiency is usually a result of absence of the gastric absorptive (intrinsic) factor. Dietary deficiency of vitamin B 2 is uncommon and may take 20 to 30 years to develop, even in healthy adults who foUow a strict vegetarian regimen. An effective enterohepatic recycling of the vitamin plus small amounts from bacterial sources and other contaminants greatly minimizes the risk of a complete dietary deficiency. Individuals who have a defect in vitamin B 2 absorption, however, may develop a deficiency within three to seven years. [Pg.112]

Vitamin Deficiency. Vitamin deficiency is uncommon in normal adults. However, when it does occur, it can be serious, particularly in pregnant women. Some vitamin deficiency can occur because of a large reduction of fat intake, which decreases absorption. Strict vegetarians also risk reduced vitamin intake. Premature infants and elderly people who are exposed to minimal sunlight and consume Htde vitamin also have a reduced capacity to metabolize and can develop vitamin deficiency. [Pg.137]

The symptoms of vitamin E deficiency in animals are numerous and vary from species to species (13). Although the deficiency of the vitamin can affect different tissue types such as reproductive, gastrointestinal, vascular, neural, hepatic, and optic in a variety of species such as pigs, rats, mice, dogs, cats, chickens, turkeys, monkeys, and sheep, it is generally found that necrotizing myopathy is relatively common to most species. In humans, vitamin E deficiency can result from poor fat absorption in adults and children. Infants, especially those with low birth weights, typically have a vitamin E deficiency which can easily be corrected by supplements. This deficiency can lead to symptoms such as hemolytic anemia, reduction in red blood cell lifetimes, retinopathy, and neuromuscular disorders. [Pg.147]

The recommended daily allowance for vitamin E ranges from 10 international units (1 lU = 1 mg all-rac-prevent vitamin E deficiency in humans. High levels enhance immune responses in both animals and humans. Requirements for animals vary from 3 USP units /kg diet for hamsters to 70 lU /kg diet for cats (13). The complete metaboHsm of vitamin E in animals or humans is not known. The primary excreted breakdown products of a-tocopherol in the body are gluconurides of tocopheronic acid (27) (Eig. 6). These are derived from the primary metaboUte a-tocopheryl quinone (9) (see Eig. 2) (44,45). [Pg.147]

The nutritional requirement for vitamin Bjg is low. Adult humans require only about 3 micrograms per day, an amount easily acquired with normal eating habits. However, because plants do not synthesize vitamin Bjg, pernicious anemia symptoms are sometimes observed in strict vegetarians. [Pg.599]

Due to bleeding risk, individuals on anticoagulant therapy or individuals who are vitamin K-deficient should not take vitamin E supplementation without close medical supervision. Absent of that, vitamin E is a well-tolerated relatively non-toxic nutrient. A tolerable upper intake level of 1,000 mg daily of a-tocopherol of any form (equivalent to 1,500 IU of RRR a-tocopherol or 1,100 IU of all-rac-a-tocopherol) would be, according to the Food and Nutrition Board of the Institute of Medicine, the highest dose unlikely to result in haemorrhage in almost all adults. [Pg.1298]

Vitamin D is not strictly a vitamin since it can be synthesized in the skin, and under most conditions that is its major source. Only when sunlight is inadequate is a dietary source required. The main function of vitamin D is in the regulation of calcium absorption and homeostasis most of its actions are mediated by way of nuclear receptors that regulate gene expression. Deficiency—leading to rickets in children and osteomalacia in adults—continues to be a problem in northern latitudes, where sunlight exposure is poor. [Pg.484]

In the vitamin D deficiency disease rickets, the bones of children are undermineralized as a result of poor absorption of calcium. Similar problems occur in adolescents who are deficient during their growth spurt. Osteomalacia in adults results from demineralization of bone in women who have little exposure to sunlight, often after several pregnancies. Although vitamin D is essential for prevention and treatment of osteomalacia in the elderly, there is little evidence that it is beneficial in treating osteoporosis. [Pg.485]

Vitamin C occurs as L-ascorbic acid and dihydroascorbic acid in fruits, vegetables and potatoes, as well as in processed foods to which it has been added as an antioxidant. The only wholly undisputed function of vitamin C is the prevention of scurvy. Although this is the physiological rationale for the currently recommended intake levels, there is growing evidence that vitamin C may provide additional protective effects against other diseases including cancer, and the recommended dietary allowance (RDA) may be increased in the near future. Scurvy develops in adults whose habitual intake of vitamin C falls below 1 mg/d, and under experimental conditions 10 mg/d is sufficient to prevent or alleviate symptoms (Bartley et al., 1953). The RDA is 60 mg per day in the USA, but plasma levels of ascorbate do not achieve saturation until daily intakes reach around 100 mg (Bates et al., 1979). Most of the ascorbate in human diets is derived from natural sources, and consumers who eat five portions, or about 400-500 g, of fruits and vegetables per day could obtain as much as 200 mg of ascorbate. [Pg.28]

One other study deserves a mention. The Cancer Prevention Study 11 was a prospective investigation using a very large cohort of over one million adult Americans, in which the effects of commercial multivitamin supplements and vitamins A, C or E on mortality were studied, during a follow-up period of seven years. The results were complex in that the use of multivitamins plus vitamins A, C and/or E significantly reduced the risk of lung cancer in both former smokers and life-long non-smokers, but vitamins A, C and E apparently increased the risk in current smokers. [Pg.34]

BARTLEY w, KREBS H A and o brien J p (1953) Vitamin C Requirements of Human Adults, London, HMSO. [Pg.40]

Jeffrey, G.P., Muller, D.P.R., Burroughs, A.K., Matthews, S., Kemp, C., Epstein, O., Metcalfe, T.A., Southam, E., Tazir-Melbourcy, M., Thomas, P.K. and McIntyre, N. (1987). Vitamin E deficiency and its clinical significance in adults with primary biliary cirrhosis and other forms of chronic liver disease. J. Hepatol. 4, 307-317. [Pg.165]

Fat-soluble vitamin supplementation is usually required in pancreatic insufficiency. Specially-formulated products for CF patients (ADEKs and Vitamax ) are usually sufficient to attain normal serum vitamin levels at a dose of 1 tablet daily for younger children and 2 tablets daily for teenagers and adults. Additional supplementation may be needed in uncontrolled malabsorption or for replacement of severe vitamin deficiency.5,15 Appetite stimulants such as cyproheptadine may be an option for promoting nutrition and weight gain, but efficacy has not been established. [Pg.253]

Calcium is essential for bones, teeth, metabolic signaling and regulation, and other bodily functions. Adults require an intake of around lg per day only about 10% of the calcium ingested is absorbed into the body - less from a low-protein diet, more from a high-protein diet. Vitamin D facilitates absorption, as does... [Pg.334]

The answer is c. (Hardman, p 15.33.) Enthusiastic over medication with vitamin D may lead to a toxic syndrome called hy/jervitamijmsis D. The initial symptoms can include weakness, nausea, weight loss, anemia, and mild acidosis. As the excessive doses are continued, signs of nephrotoxicity are manifested, such as polyuria, polydipsia, azotemia, and eventually nephrocalcinosis. In adults, osteoporosis can occur. Also, there is CNS impairment, which can result in mental retardation and convulsions. [Pg.258]

Calcitonin is a polypeptide hormone that (along with PTH and the vitamin D derivative, 1,25-dihydroxycholecalciferol) plays a central role in regulating serum ionized calcium (Ca2+) and inorganic phosphate (Pi) levels. The adult human body contains up to 2 kg of calcium, of which 98 per cent is present in the skeleton (i.e. bone). Up to 85 per cent of the 1 kg of phosphorus present in the body is also found in the skeleton (the so-called mineral fraction of bone is largely composed of Ca3(P04)2, which acts as a body reservoir for both calcium and phosphorus). Calcium concentrations in human serum approximate to 0.1 mg ml-1 and are regulated very tightly (serum phosphate levels are more variable). [Pg.324]


See other pages where Vitamin adults is mentioned: [Pg.902]    [Pg.902]    [Pg.351]    [Pg.88]    [Pg.104]    [Pg.125]    [Pg.70]    [Pg.71]    [Pg.605]    [Pg.1294]    [Pg.1300]    [Pg.159]    [Pg.481]    [Pg.485]    [Pg.137]    [Pg.864]    [Pg.323]    [Pg.494]    [Pg.15]    [Pg.558]    [Pg.30]    [Pg.28]    [Pg.34]    [Pg.331]    [Pg.125]    [Pg.200]    [Pg.709]    [Pg.965]    [Pg.1054]    [Pg.1311]   
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