A low blood calcium level usually implies abnormal function of the glands that produce parathyroid hormone (see Health Functions) responsible for regulating calcium levels. Calcium deficiency is rarely due to low dietary calcium intake since the skeleton (bones) provides a large reserve of calcium for maintaining normal blood levels.
Other causes include chronic kidney failure, vitamin D deficiency, and low blood magnesium levels that occur mainly in cases of severe alcoholism.
In addition, high sodium intake results in increased loss of calcium in the urine, possibly due to competition between sodium and calcium for re-uptake ('reabsorption') in the kidney. Because urinary losses account for about half of the difference in calcium retention among individuals, dietary sodium has a large potential to influence bone loss. In adult women, each extra gram of sodium consumed per day is projected to produce an additional rate of bone loss of 1% per year if all of the calcium loss comes from the skeleton (45, 46).
As dietary protein intake increases, the urinary excretion of calcium also increases. High protein intakes have been associated with poor recovery from osteoporotic fractures and an increased hip fracture risk (2).
Caffeine in large amounts can increase urinary calcium content for a short time. However, two studies found no association between caffeine intake and bone loss in postmenopausal women (47, 48). One observational study found accelerated bone loss in postmenopausal women who consumed less than 744 mg of calcium/day and reported that they drank 2–3 cups of coffee/day (49).
A long-lasting ('chronically') low calcium intake in growing individuals may prevent the attainment of optimal peak bone mass. Once peak bone mass is achieved, inadequate calcium intake may contribute to accelerated bone loss and ultimately to the development of osteoporosis.
Authored by Dr Peter Engel in 2010, reviewed and updated by Dr Igor Bendik-Falconnier on 17.10.17.
