Nutritional deficiencies of vitamin

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

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... 

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. 

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). 

The solubility (or insolubility) of different vitamins is of concern in nutrition. Molecules of vitamins B and C contain several —OH groups that can form hydrogen bonds with water (Figure 10.3). As a result, they are water-soluble, readily excreted by the body, and must be consumed daily. In contrast, vitamins A, D, E, and K, whose molecules are relatively nonpolar, are water-insoluble. These vitamins are not so readily excreted they tend to stay behind in fatty tissues. This means that the body can draw on its reservoir of vitamins A, D, E, and K to deal with sporadic deficiencies. Conversely, megadoses of these vitamins can lead to very high, possibly toxic, concentrations in the body. 

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. 

The nervous system is the most sensitive target for cyanide toxicity, partly because of its high metabolic demands. High doses of cyanide can result in death via central nervous system effects, which can cause respiratory arrest. In humans, chronic low-level cyanide exposure through cassava consumption (and possibly through tobacco smoke inhalation) has been associated with tropical neuropathy, tobacco amblyopia, and Leber s hereditary optic atrophy. It has been suggested that defects in the metabolic conversion of cyanide to thiocyanate, as well as nutritional deficiencies of protein and vitamin B12 and other vitamins and minerals may play a role in the development of these disorders (Wilson 1965). 

Williams RJ, Pelton RB. Individuality in nutrition effects of vitamin A-deficient and other deficient diets on experimental animals. Proceedings of the National Academy of Sciences USA 1966 55 12634. 

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

Vitamin E is required for normal growth and reproduction. The most important natural source is a-tocopherol found in plant oils and seeds. The ester form (e.g. vitamin E acetate) can be synthesized and is used for feed supplementation. One international unit is defined as being equivalent to the activity of 1 mg DL-a-tocopherol acetate. The nutritional role of vitamin E is closely interrelated with that of selenium and is involved mainly in the protection of lipid membranes such as cell walls from oxidative damage. Although these signs are similar to those of selenium deficiency, it is not possible to substitute selenium completely for vitamin E. Both nutrients are required in the diet. 

A number of methods have been developed to permit assessment of folate and vitamin B12 nutritional status and to differentiate between deficiency of the vitamins as a cause of megaloblastic anemia. Obviously, detection of antibodies to intrinsic factor or gastric parietal cells will confirm autoimmune pernicious anemia rather than nutritional deficiency of either vitamin. 

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... 

D. This patient has exhibited symptoms of beri beri heart disease, which is a result of a nutritional deficiency in vitamin Bj (thiamine). The active form of the vitamin, thiamine pyrophosphate, is a required cofactor for a-ketoglutarate dehydrogenase. 

Nutritional rickets results from inadequate exposure to sunlight or deficiency of vitamin D. 

Nelson, J.S. (1987) Effects of free radical scavengers on the neuropathology of mammalian vitamin E deficiency. In O. Hayaishi and M. Mino (Eds.), Clinical and Nutritional Aspects of Vitamin E, Elsevier, Amsterdam, pp. 157-159. 

After infancy, coagulopathy due to dietary deficiency of vitamin K is extremely rare Vitamin K is present in many foods and also is synthesized by intestinal bacteria. Occasionally, the use of a broad-spectrum antibiotic may produce a hypoprothrombinemia that responds readily to small doses of vitamin K and reestablishment of normal bowel flora. Hypoprothrombinemia can occur in patients receiving prolonged intravenous alimentation. Patients on total parenteral nutrition should receive phylloquinone (1 mg/week, the equivalent of - 150 jig/day). 

When the body does not have sufficient red cells, the patient is said to be anemic. Anemia can result from many causes. Nutritional deficiencies of iron, folate, or vitamin B12 prevent the formation of adequate numbers of red cells. Mutations in the genes that encode red cell metabolic enzymes, membrane structural proteins, and globins cause hereditary anemias. The appearance of red cells on a blood smear frequently provides clues to the cause of an anemia. Because the mutations that give rise to hereditary anemias also provide some protection against malaria, hereditary anemias are some of the most common genetic diseases known. 

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