Dietary deprivation

Nickel is an essential micronutrient for maintaining health in certain species of plants and animals. Its deficiency effects from dietary deprivation have been induced experimentally in many species of birds and mammals. To prevent nickel deficiency in rats and chickens, diets should contain at least 50 pg Ni/kg ration, while cows and goats require more than 100 pg Ni/kg rations, perhaps reflecting the increased use by rumen bacteria. Nickel deficiency is not a public health concern for humans because daily oral intake is sufficient to prevent deficiency effects. 

Matsuzawa, T., Nakata, M., Goto, I. and Tsushima, M. (1981). Dietary deprivation induces fetal loss and abortions in rabbits. Toxicology 22 255-259. 

Tissue reserves of retinoids in the healthy adult are sufficiently large to require long-term dietary deprivation to induce deficiency. Vitamin A deficiency occurs more commonly in chronic diseases affecting fat absorption, such as biliary tract or pancreatic insufficiency, sprue, Crohn s disease involving the terminal ileum, and portal cirrhosis deficiency may also occur following partial gastrectomy or during extreme, chronic dietary inadequacy. 

Menaquinones are synthesized by intestinal bacteria, but it is unclear how much they contribute to vitamin K nutrition, because they are extremely hydrophobic, and win only be absorbed from regions of the gastrointestinal tract where bUe salts are present - mainly the terminal Ueum. However, prolonged use of antibiotics can lead to vitamin K deficiency and the development of vitamin K-responsive hypoprothrombinemia (Section 5.4), as can dietary deprivation of phylloquinone. In vitro, menaquinones 2 to 6 have the same activity as phylloquinone as coenzyme for the solubilized liver microsomal vitamin K-dependent carboxylase (Section 5.3.1), whereas menaquinones with a side chain longer than seven have lower activity (Suttie, 1995). In extrahepatic tissues, the principal active vitamer is menaquinone-4 (Thijssen and Drittij-Reijnders, 1996 Thijssen et al., 1996). 

In many animals, dietary deprivation of choline leads to liver dysfunction and growth retardation, and some patients maintained on choline-free total parenteral nutrition develop liver damage that resolves when choline is provided, suggesting that endogenous synthesis may be inadequate to meet requirements (Zeisel, 2000). There is inadequate information to permit the setting of reference intakes, but the Acceptable Intake for adults is 550 mg (for men) or 425 mg (for women) per day (Institute of Medicine, 1998). In experimental animals choline deficiency is exacerbated by deficiency of methionine, folic acid, or vitamin B12, which impairs the capacity for de novo synthesis. 

The developmental toxicity of a 20% lipid emulsion containing a 3 1 ratio of medium-chain to long-chain triglycerides has been examined in animals. Administration was once-daily intravenously to rats and rabbits during organogenesis. Maternal and embryo/fetal toxicity were also assessed. There were no adverse effects on fetal parameters for rats even in the presence of maternal toxicity. However, embryo and fetal toxicity (resorptions) and skeletal abnormahties were noted in rabbits (135). The adverse fetal effects were probably the result of dietary deprivation, maternal toxicity, or both rather than representing a direct teratogenic effect. 

For iron, iodine, cobalt (as cobalamins), selenium, copper, and zinc there are clinical examples of reversible deficiency disease. For these elements there is enough known about their biochemical functions to explain their importance in human nutrition. For others, such as manganese, chromium, molybdenum, and vanadium, their importance remains to be fuUy accepted in clinical practice. Stfll other elements such as bromine, fluorine, cadmium, lead, strontium, lithium, and tin have been claimed by at least one investigator to be essential for one or more animal species as demonstrated by dietary deprivation studies. 

Several well-controlled dietary deprivation studies have demonstrated the utility of the clinical laboratory in providing measures of copper status. For example, plasma copper and ceruloplasmin assays are convenient and widely used to confirm severe copper deficiency. However, they are not sensitive indicators in marginal copper depletion. 

Urine copper decreases during dietary deprivation, but the change from an already low basal value is small, and difficulties in reliable collection and with sample contamination make this of limited use. 

Hypophosphatemia and phosphate depletion may result from inadequate intestinal phosphate absorption. Patients taking aluminum- or magnesium-containing antacids may develop hypophosphatemia, because these antacids bind phosphate in the intestine, rendering it nonabsorbable. The hypophosphatemia observed in patients with malabsorption maybe more closely related to their secondary hyperparathyroidism than to malabsorption of phosphate. Because phosphate is abundant in most foods, dietary deprivation is not usually a cause of phosphate depletion in patients with normal intestinal function and an adequate diet. 

Connor WE, Neuringer M, Barstad L. Lin DS. Dietary deprivation of linolenic acid in rhesus monkeys effects on plasma and tissue fatty acid composition and on visual function. Trans Assoc Am Physicians 1984 97 1-9. 

Another indirect measure of physiological function relating to PUFA metabolism comes from studies of the electroretinogram (ERG). It is known that adequate n-3 PUFA levels are essential for normal retinal function. Our group has shown that schizophrenic patients show ERG changes similar to those that occur in states of experimental dietary deprivation of n-3 in primates (Warner et al., 1999). 

Burr and Burr (1929) highlighted the importance of certain fats in the human diet and demonstrated that dietary deprivation of the essential fatty acids was deleterious to health. They concluded that the n-6 PUFAs were most important to function in mammals because their omission resulted in overt systemic dysfunction. Conversely, it has been shown that deprivation of n-3 PUFAs results in subtle dysfunction across a range of behavioral and physiological modalities. 

Increased sensitivity to painful stimuli has been reported in animals subjected to dietary deprivation of tryptophan.26 28 Rats maintained on a tryptophan-deficient diet showed increased sensitivity to painful electric foot shock.27 Also, some studies have revealed that in humans tryptophan causes decreased pain perception.25... 

The importance of red cell folate determinations in certain diagnoses of folate deficiency has been clearly established. Erythrocyte folate levels are good indicators of tissue folate stores, whereas serum folate levels are poor indicators since they reflect recent dietary intake and often provide little useful clinical information 37-34). For example, serum folate levels fall promptly after transient periods of dietary deprivation and remain abnormally low for weeks or months before red cell folate levels fall. In contrast, the fall in red cell folate immediately precedes the clinical and hematologic manifestation of folate deficiency (42). 

Nickel is an essential micronutrient for maintaining health in certain species of plants and animals. Nickel deficiency effects from dietary deprivation of nickel has been induced experimentally in many species of birds... 

Connor, W.E., Neuringer, M., Barstad, L.. and Lin. D.S. (1984) Dietary Deprivation of Linolenic Acid in Rhesus Monkeys Effects on Plasma and Tissue Fatty Acid Composition and on Visual Function, Trans. Assoc. Am. Physicians 97.1-9. 

Because it is the precursor for the retinaldehyde prosthetic group of rhodopsin (Wald, 1968), retinol is needed to maintain the visual process. Additionally, retinal neurones may require retinoids for their normal functioning. Therefore, retinoids must be supplied to the eye from the circulation, transported between its layers, and stored in its tissues as a reserve against dietary deprivation. 

METABOLISM OF PHOSPHORUS. Phosphorus absorbed from the intestine is circulated through the body and is readily withdrawn from the blood for use by the bones and teeth during periods of growth. Some incorporation into the bones occurs at all ages. It may be withdrawn from bones to maintain normal blood plasma levels during periods of dietary deprivation. 

The quality of the experimental evidence for nutritional essentiality varies widely for the ultratrace elements. The evidence for the essentiality of three elements, iodine, molybdenum and selenium, is substantial and noncontroversial specific biochemical functions have been defined for these elements. The nutritional importance of iodine and selenium are such that they have separate entries in this encyclopedia. Molybdenum, however, is given very little nutritional attention, apparently because a deficiency of this element has not been unequivocally identified in humans other than individuals nourished by total parenteral nutrition or with genetic defects causing disturbances in metabolic pathways involving this element. Specific biochemical functions have not been defined for the other 15 ultratrace elements listed above. Thus, their essentiality is based on circumstantial evidence, which most often is that a dietary deprivation in an animal model results in a suboptimal biological function that is preventable or reversible by an intake of physiological amounts of the element in question. Often the circumstantial evidence includes an identified essential function in a lower form of life, and biochemical actions consistent with a biological role or beneficial action in humans. The circumstantial evidence for essentiality is substantial for arsenic, boron, chromium, nickel, silicon, and vanadium. The evidence for essentiality for the... 

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