Assessment of Vitamin A Nutritional Status

An early sign of vitamin A deficiency is impaired dark adaptation - an increase in the time ttiken to adapt to seeing in dim light. The apparatus required is not suitable for use in field studies, or for use with children (the group most at risk from deficiency), tmd the dtuk adaptation test is Mgely of historictd interest. Balemce, colorvision, tmdthe senses oftaste and smell tue also tdfected in eeuly deficiency, but none of these provides a sensitive or specific test of status. 

Liver reserves of vitamin A can be estimated by isotope dilution tifter a test dose of isotopically labeled retinol, but this is not a suitable technique for assessment of status in population studies. 

Assessment of vitamin A nutritional status depends on the biochemictd criteria shown in Table 2.3. 

Interpretation of plasma concentrations of retinol is confounded by the fact that both RBP and transthyretin are negative acute phase proteins, and their synthesis falls, and hence the plasma concentration of retinol fall, in response to infection. Similarly, both protein-energy malnutrition and zinc deficiency result in a low plasma concentration, despite possibly adequate liver reserves as a result of impaired synthesis of RBP. 

Carotene inplasmais mainlyin lipoproteins thus, as with vitamin E (Section 4.5), measurements of plasma concentrations of carotene should be related to either cholesterol or total plasma lipids. Only 10% to 20% of toted plasma carotenoids is fi -carotene, with a very wide range of individual variation. There are no reliable determinations of /3 - carotene or total provitamin A carotenoids 

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HC Barnard, JJ de Kock, WJH Vermaak, GM Potgieter. A new perspective in the assessment of vitamin B nutritional status during pregnancy in humans. J Nutr... 

Hansen CM, Shultz TD, Kwak HK, Memon HS, and Leklem JE (2001) Assessment of vitamin B-6 status in young women consuming a controlled diet containing four levels ofvitamin B-6 provides an estimated average requirement and recommended dietary allowance./owma/ of Nutrition 131,1777-86. 

Underwood B (1990) Methods for assessment of vitamin A status. Journal of Nutrition 56, 1459-63. 

A number of studies have shown that between 10 and 20% of the apparently healthy population have low plasma concentrations of pyridoxal phosphate or abnormal erythrocyte transaminase activation coefficient, suggesting vitamin Bg inadequacy or deficiency. In most studies, only one of these indices of vitamin Bg nutritional status has been assessed. Where both have been assessed, while each shows some 10% of the population apparently inadequately provided with vitamin Bg, few of the subjects show inadequacy by both criteria. 

The usual method of assessing vitamin K nutritional status, or monitoring the efficacy of anticoagulant therapy, is a functional test of blood clotting, and hence the ability to synthesize the vitamin K-dependent clotting factors. 

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). 

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. 

Sokoll LJ and Sadowski JA (1996) Comparison of biochemical indexes for assessing vitamin K nutritional status in a healthy adult population. American Journal of Clinical Nutrition 63, 566-73. 

Tanumihardjo S, Barua A, and Olson J (1987) Use of 3,4-didehydroretinol to assess vitamin A status in rats. International Journal of Vitamin and Nutrition Research 57, 127-32. 

A variety of studies have shown that 10% to 20% of the population of developed countries have marginal or inadequate status, as assessed by erythrocyte trtmstiminase activation coefficient (Section 9.5.36) or plasma pyridoxtd phosphate (Section 9.5.1 Bender, 1989b). This may be sufficient to enhance the responsiveness of target tissues to steroid hormones (Section 9.3.3), emd may be important in the induction emd subsequent development of hormone-dependent cancer of the breast and prostate. Vitamin Bg supplementation may be a useful adjunct to other therapy in these common cemcers certainly, there is evidence that poor vitamin Bg nutritioned status is associated with a poor prognosis in women with breast cancer. 

The classical way of assessing vitamin K nutritional status was by determination of prothrombin time. Can you suggest a more sensitive way of detecting marginal vitamin K deficiency ... 

Kynureninase is a pyridoxal phosphate (vitamin Bg)-dependent enzyme, and its activity is extremely sensitive to vitamin depletion. Indeed, the ability to metabolize a test dose of tryptophan has been used to assess vitamin B nutritional status (section 11.9.5.1). Deficiency of vitamin B will lead to severe impairment of NAD synthesis from tryptophan. Kynureninase is also inhibited by oestrogen metabolites. 

The early method of assessing vitamin C nutritional status was by testing the extent of saturation of the body s reserves by giving a test dose of 500 mg (2.8 mmol) and measuring the amoimt excreted in the urine, fii a subject with high status, more or less all of the test dose is recovered over a period of 5 or 6h. 

When the alcoholic first presents for treatment, his/her nutritional status should be fully assessed. Vitamin supplementation should always be a component of this treatment. In the emergency room setting, the alcoholic patient usually receives intravenous fluids containing magnesium, thiamine, and multivitamin supplements. The yellow-colored fluid is commonly called a banana bag or rally pack. A daily... 

Deficiency syndromes of Zn, Cu, Cr, Se and Mo have occurred in patients on total parenteral nutrition (TPN). There is still much research to be done in assessing the nutritional status of many elements and understanding their metabolism, so that normal dietary intake may be supplemented for health benefits. Table 2 is a summary of the amounts required, the functions and the nutritional (usually dietary) imbalances in humans, where known, of the essential trace elements.31-33 (Note that this summary does not attempt to include imbalances related to environmental toxicology and occupational hazards.) Several trace elements have important functions in the immune system. Some are associated with nucleic acid. Others have structural roles, such as Si in cartilage, F and Zn in bone. They may be parts of vitamins, such as Co in vitamin B12, or hormones, such as iodine in thyroid hormones, Zn and Cr have a role in the synthesis and action of insulin.31-33... 

Some biologically active vitamin Be is excreted in the urine, and a number of studies have assessed nutritional status by microbiological measurement of this excretion it is difficult to interpret the results in terms of underlying nutritional status rather than as a reflection of recent intake, although the excretion does fall in deficiency (Sauberlich et al., 1972, 1974). A possibly important source of error here is that minor renal damage, resulting in albuminuria, will result in a considerable increase in urinary albumin-bound pyridoxal phosphate. 

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