Define the Calcium Toxicity?
Elevated blood calcium can occur in association with high parathyroid hormone, hyper- or hypothyroid conditions, bone metastasis, vitamin D toxicity, excess intake or absorption of calcium, Addison's disease and with thiazide diuretics. High blood calcium may be asymptomatic or can cause constipation, nausea and vomiting, increased urination, thirst, muscle weakness, kidney failure, irritability, confusion, psychosis and coma. The role of calcium supplements in eliciting hypercalcemia has always been under scrutiny. Since the efficiency of absorption from large doses is poor, no adverse effects have been found with calcium supplements providing up to 2400 mg/day. However, at such high levels, iron absorption is reduced and risk of iron deficiency increases.
A practical suggestion would be not to consume high dose of calcium with meals that provide most of the iron. Supplements of calcium do not carry the risk for renal stones in normal individuals but can increase the risk in patients with renal hypercaliuria. In fact, it has been suggested that dietary calcium may protect against renal calculi because it binds dietary oxalate and redu.ces oxalate excretion. In 1997, the Tolerable Upper Intake Level (UL) for Ca for adults was set at 2.5 g daily as a part of Dietary Reference Intakes. Toxic effects of a high calcium intake have only been described when the calcium is given as the carbonate form in very high doses; this toxicity is caused as much by the alkali as by the calcium and is due to precipitation of calcium salts in renal tissue (milk-alkali syndrome). However, in practice, an upper limit on calcium intake of 3 g (75 mmol) is recommended by the FAO/WHO 2004. So far we have read about the properties, food sources, metabolism, requirements and the effects of deficient/excess intake for calcium in this section. We also read that the requirements and absorption of calcium and phosphorus are interlinked with each other.