Deficiencies, nutritional vitamin

The Sugars Task Force s Select Committee on Nutrition and Human Needs recommended a daily consumption of sugars at 10% of total calories, which approximates current (11%) daily intake levels in the United States. At this level, sucrose does contribute to the development of dental caries however, no firm evidence exists that it causes dietary imbalances or deficiencies of vitamins (qv), minerals, or trace nutrients (62). 

Nutritional deficiency of vitamin B12—Eat a balanced diet diat includes seafood, eggs, meals, and dairy products. 

Peptidyl hydroxyprohne and hydroxylysine are formed by hydroxylation of peptidyl proline or lysine in reactions catalyzed by mixed-function oxidases that require vitamin C as cofactor. The nutritional disease scurvy reflects impaired hydroxylation due to a deficiency of vitamin C. 

There is evidence that nutrition affects animal response to ozone. Increased susceptibility has been reported in animals deficient in vitamin E—or the converse (protection conferred by administration of vitamin E). 

The possibility of interactions of ozone with other environmental stresses has received relatively little recent attention. Two exceptions are noteworthy, however reports of increased susceptibility to some of the actions of ozone in animals that are deficient in vitamin E or the converse (protection conferred by administration of vitamin E) and observations that exposure to ozone at less than 1.0 ppm reduces activity of the ( tochrome P-450 mixed-function oxidase activity of lungs. Although the implications of these observations are not yet clear, they remind us that nutritional variations or exposure to foreign chemicals that are metabolized by lung mixed-function oxidases may provide bases for unanticipated qualitative or quantitative effects associated with oxidant exposures. 

Less activity in the open air and poor nutrition can result in a deficiency of vitamin D and be responsible, in part, for osteoporosis. 

Elevated Hey levels can also occur in nutritional deficiencies of vitamin B12 (cobalamin) and folate. Folate or vitamin B12 deficiency can even lead to tHcy levels as high as those seen in the genetic homocystinurias [13]. In addition, a reciprocal relationship between blood levels or intake of these vitamins and tHcy concentrations... 

Bowed legs of middle-aged man with osteomalacia, a nutritional vitamin D deficiency which results in malformation of the skeleton. 

The nutritional need for accessory food factors was first stated explicitly in 1905-1906, although the influence of diet in preventing or curing some diseases such as scurvy had long been known. The name vitamine was proposed in 1912, but the terminal e was dropped when it was realized that not all these compounds are nitrogenous bases. The vitamins serve as coenzymes in various metabolic processes, and the necessary quantities are usually supplied by an adequate diet or by synthesis by the intestinal flora. Vitamin deficiency can arise from a failure to absorb the compound from the gut. The symptoms of deficiency vary in different animal species, and not all the substances found necessary in other species have been shown to be essential for human nutrition. Vitamins are used for the prevention or cure of deficiency diseases and for some other pathological conditions,... 

Folic acid - [FOOD TOXICANTS, NATURALLY OCCURRING] (Volll) - [FINECHEMICALS - PRODUCTION] (Vol 10) -m animal nutrition [VITAMINS - FOLIC ACID] (Vol 25) -biosynthesis [VITAMINS - FOLIC ACID] (Vol 25) -m dairy substitutes [DAIRY SUBSTITUTES] (Vol 7) -deficiency [VITAMINS - FOLIC ACID] (Vol 25) -metabolism of [VITAMINS - FOLIC ACID] (Vol 25) -metabolites [VITAMINS - FOLIC ACID] (Vol 25) -mmilk [MILKANDMILKPRODUCTS] (Vol 16) -one-pot synthesis [VITAMINS - FOLIC ACID] (Vol 25) -properties [VITAMINS - FOLIC ACID] (Vol 25) -role m veterinary medicine [VETERINARY DRUGS] (Vol 24)... 

Vitamin D is the collective name for vitamins D1 D2, and D3. It is used as prophylaxis for nutritional vitamin D deficiency. It also is used to treat rickets,... 

The fourth section deals with various aspects Digestion, Absorption, and Nutritional Biochemistry. The chapter Obesity considers current problems with respect to the ever-increasing incidence of imbalance between energy intake and utilization. Key problems of undemutrition are discussed in the chapters Protein-Energy Malnutrition and Vitamin A Deficiency in Children. The chapters Lactose Intolerance, Pancreatic Insufficiency, and Abetalipoproteinemia focus on the biochemical processes underlying food digestion and absorption. Calcium Deficiency Rickets, Vitamin B12 Deficiency, and Hemochromatosis provide discussions of absorption and utilization of vitamin D, vitamin B12, and iron, respectively. 

There may also he an effect of selenium deficiency on vitamin E nutrition. Selenium deficiency causes a specific pancreatic atrophy, which is unresponsive to vitamin E supplements. In turn, this leads to impaired secretion of lipase, and hence impaired absorption of dietary lipids in general that will affect the absorption of vitamin E (Thompson and Scott, 1970). 

As a result of the reduced activity of the mutase in vitamin B12 deficiency, there is an accumulation of methyhnalonyl CoA, some of which is hydrolyzed to yield methylmalonic acid, which is excreted in the urine. As discussed in Section 10.10.3, this can be exploited as a means of assessing vitamin B12 nutritional status. There may also be some general metabolic acidosis, which has been attributed to depletion of CoA because of the accumulation of methyl-malonyl CoA. However, vitamin B12 deficiency seems to result in increased synthesis of CoA to maintain normal pools of metabolically useable coenzyme. Unlike coenzyme A and acetyl CoA, neither methylmalonyl CoA nor propionyl CoA (which also accumulates in vitamin B12 deficiency) inhibits pantothenate kinase (Section 12.2.1). Thus, as CoA is sequestered in these metabolic intermediates, there is relief of feedback inhibition of its de novo synthesis. At the same time, CoA may be spared by the formation of short-chain fatty acyl carnitine derivatives (Section 14.1.1), which are excreted in increased amounts in vitamin B12 deficiency. In vitamin Bi2-deficient rats, the urinary excretion of acyl carnitine increases from 10 to 11 nmol per day to 120nmolper day (Brass etal., 1990). 

The reaction catalyzed by delta-6-desaturase enzyme is the slowest reaction in the metabolic pathway of LA and is considered as a rate-limiting step (4, 5). Activity of this enzyme further decreases with age and in people suffering from various diseases, including arthritis, diabetes, hypertension, eczema, psoriasis, and so on. Lifestyle factors like stress, smoking, excessive consumption of alcohol, linoleic acid (6), saturated and trans-fatty acids and nutritional deficiencies of Vitamin B6, zinc (7), and magnesium inhibit this desaturase. As a result of limitations in in vivo production of GLA, supplementation with preformed GLA is becoming important. This has led to interest in development and commercialization of the sources of GLA. 

Nutritional scientists are attuned to the concept that some nutrients occur in the body as a "storage form," that can be mobilized during times of need. This concept applies to energy stores, vitamin A, calcium, and protein (muscle protein is readily mobilized), but probably not to vitamin Most of the body s vitamin (70 80%) occurs in muscle, where much of it resides as a cofactor in glycogen phosphoiy-lase. Evidence suggests that during dietary vitamin deficiency the vitamin is not selectively released from this enzyme and used by more vital B -requiring enzymes in the body (Cobum ft al, 1991). 

This severe CNS di.sorder results from the combination of extreme nutritional deficiency, specifically Vitamin B, or thiamine, and chronic heavy drinking. Basically there are two diseases. 

Eijkman was director of the Geneeskundig Labora-torium (medical laboratory) in Batavia from 1888 to 1896, and during that time he made a number of important discoveries in nutritional science. In 1893 he discovered that the cause of beriberi was the deficiency of vitamins, not of bacterial origin as thought by the scientific community. He discovered vitamin B, and this discovery led to the whole concept of vitamins. For this discovery he was given the Nobel Prize in physiology or medicine for 1929. 

Among the many possible consequences of a dietary deficiency of vitamin E, there is observed in many species a profound atrophy of the skeletal muscles with corresponding weakness. This nutritional muscular... 

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