Micronutrients
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), & 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 (e.g. Co, Cr, Fe, Mn, Se and Zn) may also be toxic when concentrations are raised.
Vitamins A (retinol), B 1 (thiamin), B2 (riboflavin), B6 (pyrid oxine), B12 (cyanocobalamin), C (ascorbic acid), D (calciferol), E (tocopherol), and K (phylloquinone) are required for adequate nutrition. In the case of vitamins A & B6, toxicity may also occur. Vitamins can be divided into two groups – fat soluble (vitamins A, D, E, & K) and water soluble (B & C vitamins). 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, food fads), malabsorption, inadequate supplementation in total parenteral nutrition (TPN) and inborn errors of metabolism. 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 chemical form of the micronutrient and/or intraluminal interactions with dietary substances such as phytic acid, fibre and other trace elements. Disorders involving iron, iodine, and cobalt 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 chromium, copper, molybdenum, manganese, selenium and zinc 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 zinc, selenium 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.
Systemic Inflammatory Response
The systemic inflammatory (or acute phase) response is the term used when referring to the series of metabolic changes that occur in the body in response to infection, surgery, trauma or any noxious event causing tissue damage or necrosis. The systemic inflammatory response can result in significant changes to plasma levels of several micronutrients that are independent of nutritional status. This is mainly due to redistribution of their binding proteins and increased uptake by tissues. The magnitude of the change varies with the degree of the systemic inflammatory response which can be gauged by the concentration of C-reactive protein (CRP). The magnitude of this response is greatest for selenium and vitamins A and C for which the median reductions in concentration are over 40%. Plasma copper, selenium and vitamin C are unreliable when the CRP is >10 mg/L and plasma zinc, vitamin A and vitamin D are unreliable when the CRP is >20 mg/L (see table below). Further information is available on the individual micronutrient pages which can be accessed by clicking on the name of the analyte.
Analyte |
Sample matrix |
Effect of Acute phase response |
CRP concentration causing clinically** significant effect (mg/L) |
Plasma |
Increased* concentration28 |
>10 |
|
Plasma |
Decreased concentration28 |
>20 |
|
Plasma |
Decreased concentration28 |
>10 |
|
Red cells |
No effect27 |
|
|
Whole blood |
No effect |
|
|
Plasma |
Decreased concentration28 |
>20 |
|
Plasma |
No effect68 |
|
|
Whole blood |
No clinically significant effect76 |
|
|
Red cells |
No effect76 |
|
|
Red cells |
No effect76 |
|
|
Plasma |
Decreased concentration28 |
>10 |
|
Plasma |
Decreased concentration28 |
>20 |
|
Plasma |
No effect85 |
|
*In severe systemic inflammation, plasma copper may be low.
** N.B. The CRP concentration when a statistically significant effect is observed may be lower than the CRP concentration when the effect becomes clinically significant.
References