Essential minerals are required as cofactors for a number of enzymes. Low intakes of specific minerals over time cause a reduction in tissue concentrations of that mineral and this then decreases the activity of the specific enzymes associated with that mineral. If the deficiency of the mineral is severe, serious disease and death can result. However, chronic intakes that are suboptimal but high enough to prevent outright deficiencies can impair enzyme activity and cause reduced activity of enzymes in metabolic pathways. The disorder or condition that develops from such suboptimal intakes is often much harder to diagnose than a serious deficiency, because many of the symptoms are subclinical in nature. A general feeling of malaise, poor energy levels, cloudy thinking, aches and pains and general unease may for example result. Such borderline intakes of micronutrients are now termed insufficiencies, and evidence suggests they are widespread amongst the populations of the World.
Zinc must be consumed in the diet for health, and poor quality diets such as the typical Western diet may supply adequate levels of zinc. Zinc insufficiencies have been reported to be prevalent in Western nations, and markers that are able to allow detection of such borderline intakes are therefore useful. Borderline mineral status can result despite adequate intakes, through for example medical conditions or poor absorption. Low levels of zinc in hair and erythrocytes can be used as a marker of quite severe zinc deficiency, but their sensitivity may not allow detection of mild chronic insufficiencies, characterised by the typical Western diet. One biomarker of zinc status that may be sensitive enough to allow the detection of such borderline zinc levels is alkaline phosphatase. Alkaline phosphatase is a zinc requiring enzyme that is responsible for removing phosphate groups from a variety of organic molecules, and alkaline phosphatase is found in all tissues, with high amounts in the liver and bone.
One study1 reported on the effects of zinc repletion on serum alkaline phosphatase in patients who had developed zinc deficiencies during a period of total parenteral nutrition during a hospital stay. The subjects received either oral supplements of zinc sulphate supplying 50 mg per day elemental zinc or intravenous zinc sulfate supplying 1.6 mg per day elemental zinc. The improvements in the serum alkaline phosphatase observed in the patients correlated inversely with the pretreatment levels suggesting the zinc supplementation had caused rapid and detectable changes to the alkaline phosphatase serum levels. A review of medical records available to the researchers suggested that historic cases of zinc supplemented zinc deficient individuals showed similar linear improvements in levels of serum alkaline phosphatase during repletion. Therefore biochemical assessment of serum alkaline phosphatase may be a useful biomarker for zinc status as a linear relationship in response to zinc repletion is evident.
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