In spite of extensive investigation of calcium metabolism, the most satisfactory level of calcium intake for growth or for maintenance in adult life is unknown and there are no methods available for accurate appraisal of the status of calcium nutrition.

Calcium serves as a structural component of bones and teeth which contain 99 per cent of the calcium in the body. The small portion of calcium in serum and soft tissues exists partly in ionized form and is concerned in neuromuscular excitability, the blood clotting mechanism, and membrane permeability. It is known that certain enzymes are activated by calcium. At least part of the calcium in the skeleton is available to maintain the level in blood and other tissues when dietary supply is limited. The recommended dietary allowances for calcium are based largely on balance studies with their inherent defects and difficulties in interpretation. Such studies do not indicate the distribution of calcium in the body or the extent of storage. Calcium balance tends to reflect previous dietary intake and there is evidence of adaptation to low levels of intake.

It is known that the ability to utilize calcium from ingested food varies greatly among individuals and that numerous exogenous and endogenous factors influence absorption and excretion. Utilization is usually in the neighborhood of 20 to 30 per cent but may be greater in children who are deficient in calcium. Absorption is influenced by the relative and absolute levels of calcium and phosphorus in the diet, ratios between 1:1 and 2:1 being optimal during growth. Absorption is facilitated by normal gastric acidity, enhanced by vitamin D and in-creased by protein, lactose and citrates in the diet. Absorption is decreased by the presence of phytates, oxalates and fatty acids in foods due to the formation of insoluble calcium salts.

The normal concentration of calcium in the blood is 9 to 11.5 mg per 100 ml. (4.5-6.0 mEq/1) of which 50-60 per cent is in ionized form, the remainder being bound to protein and varying with the concentration of serum proteins. The ionized fraction is responsible for the prevention of tetany. Mechanisms for the maintenance of serum calcium are complicated and are dependent upon calcification and decalcification of bone as well as on dietary calcium (63). The parathyroid hormone and vitamin D have dominant roles but the sex hormones, the kidney and the acid base balance of the body are also concerned. Relationships between calcium, phosphorus and vitamin D and changes which are observed in rickets are discussed under vitamin D nutrition.

Calcium excretion varies widely in normal subjects at any given level of intake. Excretion is influenced by the calcium intake, skeletal size, acid base balance and “endogenous factors” which include several of the body hormones.

Calcium Deficiency

There is a real need for the development of procedures for evaluating calcium nutrition and detecting deficiency at any early stage. Diagnosis at present is dependent upon the appearance of the characteristic clinical picture of tetany which is manifested by carpopedal spasm and, at times, convulsive seizures. Laryngospasm may occur particularly in children. Paresthesias of the hands, feet and lips are common. Trousseau’s and Chvostek’s signs are positive. The concentration of calcium in serum decreases to low levels, usually to less than 4 m Eq/1.

Tetany is observed frequently in association with rickets and osteomalacia and is encountered occasionally in sprue and other steatorrheas. “Hunger osteomalacia” which is observed in some subiects during starvation, may be due in part to deficiency of calcium as well as of protein.

The osteoporosis of aging is considered to represent a failure of bone matrix formation rather than calcium deficiency. Therapy with calcium is not efficacious although administration of sex hormones may be beneficial.

Hypercalcemia and metastatic calcification of tissue does not occur as a result of excessive dietary intake alone but is dependent on excessive administration of vitamin D or some metabolic abnormality such as hyperparathyroidism.