Calcium excretion

JAHNEN A, HEYNCK H, GERTZ B, CLABEN A, HESSE A (1992) Dietary fiber the effectiveness of a high bran intake in reducing renal calcium excretion. Urol Res, 20 3-6. 

Thiazide diuretics decrease urinary calcium excretion and may decrease bone turnover. However, their effects on bone mineral density and fracture rates have not been studied in controlled trials. Thiazide diuretics are not recommended solely for potential beneficial effects in osteoporosis. 

Postmenopausal women (60-69 y) N=571 Observational Urinary mineral excretion, bone mass Self report No association between calcium excretion or bone mass in abstainers and coffee drinkers with similar smoking habits and degree of obesity. 

Premenopausal Blinded, Urinary Oral caffeine Significantly increased calcium excretion with... 

Calcium excretion increased significantly after caffeine challenges with no adaptation to caffeine-induced excretion after one week. 

Massey, L. K., Opryszek, M. S., No effects of adaptation to dietary caffeine on calcium excretion in young women, Nutrition Research, 10, 741, 1990. 

In a study with 40 healthy men and women, average age 63.7 years, who were randomized to either an alkali diet (meat plus fruits and vegetables) or an acid diet (meat plus cereal grains) (Jajoo and others 2006), altering the renal net acid excretion over a period of 60 days affected several biochemical markers of bone turnover and calcium excretion. The acidity of the diet had a significant effect on increasing NTX, a urinary marker of bone breakdown, and increasing the amount of calcium excreted in the urine. 

Jajoo R, Song L, Rasmussen H, Harris S and Dawson-Hughes B. 2006. Dietary acid-base balance, bone resorption and calcium excretion. J Nutrition 25 223—230. 

Because excessive caffeine consumption increases calcium excretion, caffeine intake should ideally be limited to two servings per day. Moderate caffeine intake (2 to 4 servings per day) should not be a concern if adequate calcium intake is achieved. 

Prescribing thiazide diuretics solely for osteoporosis is not recommended but is a reasonable choice for patients with osteoporosis who require a diuretic and for patients on glucocorticoids with a 24-hour urinary calcium excretion >300 mg. 

Glucocorticoids decrease bone formation through decreased proliferation and differentiation, and enhanced apoptosis of osteoblasts. They also increase bone resorption, decrease calcium absorption, increase renal calcium excretion, and result in secondary hyperparathyroidism. 

Many other dietary factors have been reported to affect calcium bioavailability. Phytate, fiber, cellulose, uronic acids, sodium alginate, oxalate, fat (only in the presence of steatorrhea), and alcohol have been reported to decrease calcium bioavailability (15). Lactose and medium chain triglyceride increase it (15). FTuoride also affects calcium retention primarily by stimulating bone formation thereby decreasing calcium excretion (33-38). The effects of fluoride on calcium utilization have been variable (34,38,39). 

Table VII. Calcium Excretion and Retention as Affected by Orthophosphate, Hexametaphosphate (Polyphospate), and Calcium...

Such acid and calcium excretion may be important in development of osteoporosis. To test diets of meat and vegetable protein upon urinary acid and calcium, nine human adults, aged 22 to 69 years, were fed isonitrogenous diets of chicken or soy beans in seven-day feeding periods. Diets provided daily ... 

Many animal species excrete more calcium if fed an acid or acidforming compounds. In the calf, Steenbock and coworkers (13) observed hypercalciuria and acidic urine after feeding hydrochloric acid to the calf. Stehle (14) pointed out that calcium represented the main long-term fixed base to be lost in the urine of the dog loaded with excessive amounts of hydrochloric acid. Walzer and Browder (15) demonstrated that when infused with a sulfate containing solution, the dog excreted several fold more acid and calcium than saline-infused controls the increased calcium loss returned to normal upon removal of the sulfate. Marone, et al. (16) demonstrated increased excretion of calcium in the acidotic dog. Correction of the acidosis reduced the excessive fractional calcium excretion rate, but did not alter sodium excretion. 

In six subjects, urinary calcium excretion during the soy period peaked by day 5, and began to decrease, but in three subjects, it began to decline by day 2. Two subjects did not show any rise in urinary calcium. In one subject the value on day 5 was lower than that on day 2 thereafter, it resumed its upward trend. For all subjects, the kinetics of the rise and fall to near initial values suggested that an equilibrium may have been established. 

During the meat diet period, calcium excretion of six of the nine subjects reached a maximum by day 2. Yet in three subjects calcium excretion continued to increase till day 7. From these data, one may infer that an equilibrium probably had not been established during this seven-day period. 

Statistical analyses of the calcium excretion data of the prediet, soy, and meat periods revealed significant differences. The paired differences between the calcium loss in urine during meat and soy diets was significant at the P<0.05 level. 

No marked differences in dietary influence upon acid or calcium excretion or sulfate loss was observed in males compared with the females in this study. 

The meat diet resulted in markedly greater titratable acid and calcium excretion compared with the soy diet (P<0.02). This occurred despite the fact that each diet contained the same amounts of protein, calcium, phosphorus, and sulfur. Increased urinary calcium excretion in subjects accompanied this increased output of TTA (P<0.02) ... 

Earlier animal work showed similar results in terms of urinary acid production from dietary precursors that could be converted into acid before excretion. However, most investigators used salts rather than foods containing the anion or its precursor. The addition of acid, in the form of hydrochloric, sulfuric, or ammonium chloride, acid phosphate salts, or ascorbate resulted in enhanced urinary acidity and concomitant calcium excretion. For example, in the detailed study of bone salt metabolism, Barzel and Jowsey (19) showed that the rat fed supplementary ammonium chloride subsequently lost more calcium, and developed markedly demineralized fat-free bone mass. 

Our studies show that sulfur feeding in the form of meat also induced greater acid and calcium excretion in the urine than soy. 

Since this increased calcium loss, the quality of dietary protein may be important in conserving body calcium in the bone reservoir via the kidney. Human renal studies have corroborated animal data in-so-far as calcium excretion as influenced by urinary acidity is concerned. This was emphasized by Marone et al. (15) who reported increased excretion of calcium in the acidotic dog and by Zemel, et al. (27) who studied calcium filtration by the kidney. They fed subjects low or high-protein (50 or 150 g/d) diets, then compared... 

Dietary phosphorus exerts variable influence on calcium loss depending on the nature of the dietary protein. Humans fed food containing abundant phosphorus to calcium excreted little more calcium unless the meat content of the diet changed markedly. 

Bloom (12J reported that in both older rats (63 days of age) and younger rats (33 days of age) the amount of calcium retained was less when 5% dried spinach, either raw or cooked, was included in the diet in 1-week balance studies (Figure 1). The experimental diets contained about 0.4% calcium, and one drop of cod liver oil was given each rat every day. Most of the calcium excretion on the spinach diet was in the feces. Retentions of calcium on the basal low fiber diet and on diets containing filter paper in amounts to equal the crude fiber in spinach or 12 times the crude fiber in spinach were high. There was no significant difference in calcium retentions between raw and cooked spinach. The low retention of calcium from spinach could not be attributed to the presence of crude fiber in the diet. 

The results of experiments conducted by MacKenzie and McCollum (15) indicate that the effect of dietary oxalic acid on the rat depends on the composition of the diet. There was no effect on rate of growth or calcium excretion of 50 g rats fed for 10 weeks a diet containing 0.6% calcium, 0.7% phosphorus, and optimum vitamin D, when levels of potassium oxalate up to 2.5% were fed. The percent bone ash on the 2.5% oxalate diet was somewhat lower than on the control diet. On a 0.35% calcium, 0.35% phosphorus, and vitamin D-free diet, 1.7% potassium oxalate resulted in restricted growth and bone formation of weanling rats. 

McLaughlin (25) reported that although calcium balances for seven women were somewhat lower during 6 days in which spinach replaced milk in the diet, all balances were positive. The women were fed diets containing about 500 mg of calcium/day in which 79% came from milk for 6 days and 73% came from spinach (about 276 g/day) for 6 days. The spinach diet contained 2.0 g oxalic acid/day. The calcium excretion in urine was 2-3 times greater during the milk period. 

In the studies on humans there appeared to be decreased calcium balances when 200 g or more of spinach per day was included in the diet. In two of the studies in which women were fed spinach, calcium intakes were below the Recommended Dietary Allowance of 800 mg/day (37). Some studies were conducted for short period of a week or less, which may not be sufficient time to adjust to a change in diet. From measurement of calcium excretion in urine after a test meal, it was shown that the calcium in oxalate-containing vegetables was less well-absorbed than that of milk or of vegetables not containing oxalic acid. However, this would not necessarily affect calcium balance, since the total amount of calcium in the diet would have to be considered. The effect of a combination of oxalic acid and fiber on calcium bioavailability should be further investigated. 

For more than forty years, it has been known that increasing the protein content of the diet causes an increase in urinary calcium excretion (1, 2). There is, in fact, a direct correlation between urine calcium output and dietary protein level, so that excretion is 800 percent higher if dietary protein is increased from 6 g per day to 560 g per day (3 ). This relationship between urinary calcium and protein ingestion is not affected by the level of dietary calcium, and is evident even when severely calcium-deficient diets are consumed (3). 

Since the early 1970 s, research has been directed at identifying the mechanism by which the calciuria is induced. Attention was given first to the question of whether the elevated urinary calcium excretion was caused by an increase in the intestinal absorption of calcium. Results of calcium balance studies in human subjects showed that protein ingestion either had no effect on calcium absorption (4) or that the effect was insufficient to account for the calciuria (5j. Consequently, negative calcium balance is a frequent observation in human studies when high protein diets are fed, and this situation is not improved by high calcium intakes (4 ). 

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