Criteria of Vitamin Adequacy and the Stages of Development of Deficiency

For any nutrient, there is a range of intakes between that which is clearly inadequate, leading to clinical deficiency disease, and that which is so much in excess of the body's metabolic capacity that there may be signs of toxicity. Between these two extremes is a level of intake that is adequate for normal health and the maintenance of metabolic integrity, and a series of more precisely definable levels of intake that are adequate to meet specific criteria and may be used to determine requirements and appropriate levels of intake. These follow.

1. Clinical deficiency disease, with clear anatomical and functional lesions, and severe metabolic disturbances, possibly proving fatal. Prevention of deficiency disease is a minimal goal in determining requirements and is the criterion of the WHO basal requirement (WHO, 1996).

2. Covert deficiency, where there are no signs of deficiency under normal conditions, but any trauma or stress reveals the precarious state of the body reserves and may precipitate clinical signs. For example, as discussed in Section 13.7.1, an intake of 10 mg of vitamin C per day is adequate to prevent clinical deficiency, but at least 20 mg per day is required for healing of wounds.

3. Metabolic abnormalities under normal conditions, such as impaired carbohydrate metabolism in thiamin deficiency (Section 6.5) or excretion of methylmalonic acid in vitamin B12 deficiency (Section 10.10.3).

4. Abnormal response to a metabolic load, such as the inability to metabolize a test dose of histidine in folate deficiency (Section 10.10.4), or tryptophan in vitamin B6 deficiency (Section 9.5.4), although at normal levels of intake there may be no metabolic impairment.

5. Inadequate saturation of enzymes with (vitamin-derived) coenzymes. This can be tested for three vitamins, using red blood cell enzymes: thiamin (Section 6.5.3), riboflavin (Section 7.5.2), and vitamin B6 (Section 9.5.3).

6. Low plasma concentration of the nutrient, indicating that there is an inadequate amount in tissue reserves to permit normal transport between tissues. For some nutrients, this may reflect failure to synthesize a transport protein rather than primary deficiency of the nutrient itself.

7. Low urinary excretion of the nutrient, reflecting low intake and changes in metabolic turnover.

8. Incomplete saturation of body reserves.

9. Adequate body reserves and normal metabolic integrity. This is the (possibly untestable) goal. Both immune function and minimization of DNA damage offer potential methods of assessing optimum micronutrient status, but both are affected by a variety of different nutrients and other factors (Fenech, 2001).

10. Possibly beneficial effects of intakes more than adequate to meet requirements: the promotion ofoptimumhealth and life expectancy. There is evidence that relatively high intakes of vitamin E and possibly other antioxidant nutrients (Section 4.6.2) may reduce the risk of developing cardiovascular disease and some forms of cancer. High intake of folate during early pregnancy reduces the risk of neural tube defects in the fetus (Section 10.9.4).

11. Pharmacological (druglike) actions at very high levels of intake. This is beyond the scope of nutrition, and involves using compounds that happen to be vitamins for the treatment of diseases other than deficiency disease.

12. Abnormal accumulation in tissues and overloading of normal metabolic pathways, leading to signs of toxicity and possibly irreversible lesions. Niacin (Section 8.7.1), and vitamins A (Section 2.5.1), D (Section 3.6.1), and B6 (Section 9.6.4) are all known to be toxic in excess (see Section for a discussion of tolerable upper levels of intake).

Problems arise in interpreting the results, and therefore defining requirements, when different markers of adequacy respond to different levels of intake. This explains the difference in the tables of reference intakes published by different national and international authorities (see Tables 1.5-1.8).

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