Introduction
A healthy diet provides not only adequate fat, carbohydrate and protein but also small amounts of so-called micronutrients such as trace elements and vitamins. Trace elements can be categorised into those which are essential for human life such as chromium (Cr), cobalt (Co), copper (Cu), iodine (I), iron (Fe), manganese (Mn), molybdenum (Mo), selenium (Se) and zinc (Zn), and those which are potentially toxic such as aluminium (Al), arsenic (As), cadmium (Cd), lead (Pb), mercury (Hg) and nickel (Ni). Some essential trace elements (eg. Co, Cr, Fe, Mn, and Se) may also be toxic when concentrations are raised.
Vitamins A (retinol), B1 (thiamin), B2 (riboflavin), B6 (pyridoxine), B12 (cyanocobalamin), C (ascorbic acid), D (cholecalciferol), E (tocopherol), and K (phylloquinone) are required for adequate nutrition. In the case of vitamins A and B6 toxicity may also occur. Vitamins can be divided into two groups – fat soluble (vitamins A, D, E, and K) and water soluble (vitamins B1, B2, B6 and C). In general, water soluble vitamins function as coenzymes and the body’s reserves are low, while fat soluble vitamins do not function as coenzymes and the body’s reserves are high.
Nutritional Deficiency
Nutritional deficiency of vitamins and trace elements is relatively uncommon in developed countries. When it occurs it is usually due to poor diet (eg. alcohol-related), malabsorption, inadequate supplementation in total parenteral nutrition (TPN), inborn errors of metabolism, and food fads. Nutritional deficiency may be sub-clinical or masked by co-existing disease so making the measurement of blood levels of vitamins and trace elements potentially useful. However, assessing the adequacy of dietary intake of nutrients is complex and the bioavailability of trace elements may be reduced by the species present and intraluminal interactions with dietary substances such as phytic acid, fibre and other trace elements. Disorders involving Fe, I, and Co can be investigated by established methods – haemoglobin, thyroid hormones and vitamin B12, and so their measurement is infrequently required.
Clinical interest in essential trace elements increased when reversible symptomatic deficiencies of Cr, Cu, Zn, Se, and Mo were described in patients receiving long-term TPN. Similarly, diets formulated for the management of inborn errors of metabolism such as phenylketonuria have been associated with deficiencies of Se, Zn and other elements. In both cases, the use of highly purified nutrients has led to deficiency diseases never before clearly observed.
Young children, especially those in malnourished populations, are also at risk. Diets used in rehabilitation may not always supply sufficient vitamins and trace elements, and growth and recovery may therefore be compromised. The premature baby has a special requirement for micronutrients which is far from understood. Oral provision is complicated by immature gut function and can result in varying degrees of malabsorption.
Acute Phase Response
The acute phase response is the term used when referring to the series of metabolic changes that occurs in the body in response to infection, surgical or accidental trauma or any noxious event causing tissue damage or necrosis. The acute phase response can result in significant changes to plasma levels of several micronutrients that are independent of nutritional status. The change varies directly with the degree of the acute phase response which can be gauged by the concentration of C-reactive protein. In the cases of zinc, selenium, and vitamins A, B2, B6 and C there are reductions in concentration of up to 50%, 50%, 50%, 60%, 50%, and 70% respectively. Plasma copper shows a positive acute phase response with levels rising by up to 30%.