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The effects and causes of calcium deficiency

A low blood calcium level usually implies abnormal parathyroid function, and is rarely due to low dietary calcium intake since the skeleton provides a large reserve of calcium for maintaining normal blood levels. Other causes of abnormally low blood calcium levels include chronic kidney failure, vitamin D deficiency, and low blood magnesium levels that occur mainly in cases of severe alcoholism. Magnesium deficiency results in a decrease in the responsiveness of osteoclasts to PTH. A 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 the development of osteoporosis (see Disease Prevention) (1). 

The Adequate Intake (AI)

Updated recommendations for calcium intake based on the optimization of bone health were released by the Food and Nutrition Board (FNB) of the Institute of Medicine in 1997. The setting of an Adequate Intake level (AI) rather than a Recommended Dietary Allowance (RDA) for calcium reflects the difficulty of estimating the intake of dietary calcium that will result in optimal accumulation and retention of calcium in the skeleton when other factors such as genetics, hormones, and physical activity, also interact to affect bone health (3).

Nutrient interactions

Vitamin D: Vitamin D is required for optimal calcium absorption (See Function). Several other nutrients (and non-nutrients) influence the retention of calcium by the body and may affect calcium nutritional status.

Sodium: Increased sodium intake results in increased loss of calcium in the urine, possibly due to competition between sodium and calcium for reabsorption in the kidney or by an effect of sodium on parathyroid hormone (PTH) secretion. Each 2.3-gram increment of sodium (6 grams of salt; NaCl) excreted by the kidney has been found to draw about 24-40 milligrams (mg) of calcium into the urine. 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. Although animal studies have shown bone loss to be greater with high salt intakes, no controlled clinical trials have been conducted to confirm the relationship between salt intake and bone loss in humans (1, 6). However, a 2-year study of postmenopausal women found increased urinary sodium excretion (an indicator of increased sodium intake) to be associated with decreased bone mineral density (BMD) at the hip (7).

Protein: As dietary protein intake increases, the urinary excretion of calcium also increases. Recommended calcium intakes for the U.S. population are higher than those for populations of less industrialized nations because protein intake in the U.S. is generally higher. The RDA for protein is 46 grams/day for adult women and 56 grams/day for adult men. However, the average intake of protein in the U.S. tends to be higher (65-70 grams/day in adult women and 90-110 grams per day in adult men) (3). Weaver and colleagues have calculated that each additional gram of protein results in an additional loss of 1.75 mg of calcium/day. Because only 30% of dietary calcium is generally absorbed, each one-gram increase in protein intake/day would require an additional 5.8 mg of calcium/day to offset the calcium loss (8). At the other end of the spectrum of protein intake, the effect of dietary protein insufficiency on bone health has received much less attention. Inadequate protein intakes have been associated with poor recovery from osteoporotic fractures and serum albumin values (an indicator of protein nutritional status) have been found to be inversely related to hip fracture risk (3).

Phosphorus: Phosphorus, which is typically found in protein-rich foods, tends to decrease the excretion of calcium in the urine. However, phosphorus-rich foods also tend to increase the calcium content of digestive secretions, resulting in increased calcium loss in the feces. Thus, phosphorus does not offset the net loss of calcium associated with increased protein intake (1). Increasing intakes of phosphates from soft drinks and food additives have caused concern among some researchers regarding the implications for bone health. Diets high in phosphorus and low in calcium have been found to increase parathyroid hormone (PTH) secretion, as have diets low in calcium.(3, 6) While the effect of high phosphorus intakes on calcium balance and bone health are presently unclear, the substitution of large quantities of soft drinks for milk or other sources of dietary calcium is cause for concern with respect to bone health in adolescents and adults.

Caffeine: Caffeine in large amounts increases urinary calcium content for a short time. However, caffeine intakes of 400 mg/day did not significantly change urinary calcium excretion over 24 hours in premenopausal women when compared to a placebo (9). Although 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 (10), a more recent study that measured caffeine intake found no association between caffeine intake and bone loss in postmenopausal women (11). On average, one 8-ounce cup of coffee decreases calcium retention by only 2-3 mg (1).

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