Calcium excretion dietary

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. 

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

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. 

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). 

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. 

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. 

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. 

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. 

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). 

The effects of varying either the calcium or phosphorus level in conjunction with a high beef meal on the urinary calcium excretion of men are shown in Table IV. Urinary calcium excretion (total and ionized) was significantly elevated (P < 0.005) when the high protein beef meal contained 466 mg rather than 166 mg calcium. Increasing the phosphorus level from 308 mg to 700 mg in the high beef meal reduced both total and ionized calcium excretion in the urine, but the response was not statistically significant. Serum levels of calcium (ionized and total) and phosphorus were within normal limits and were unaffected by any of the dietary treatments. 

Increasing the dietary calcium level in the high beef meal resulted in hypercalciuria. This effect was obtained in the absence of an altered insulin response which suggests that factors other than or in addition to serum insulin were involved in the control of urinary calcium excretion. 

Most of the forementioned studies which examined the influence of various dietary fiber on the bioavailability of calcium by human subjects have depended upon the comparative measurements of calcium content of diets and calcium contents of stools and urine. As reviewed by Allen (3), calcium balance studies have distinct limitations relative to accuracy and precision. However, their ease of application and cost, laboratory equipment requirements, and real (or perceived) safety in comparison to available radioactive or stable isotope methods continue to make their use popular. In calcium balance studies, calcium absorption is assumed to be the difference between calcium excretion in the feces and calcium intake. Usually this is expressed as a percent of the calcium intake. This method assumes that all fecal calcium loss is unabsorbed dietary calcium which is, of course, untrue since appreciable amounts of calcium from the body are lost via the intestinal route through the biliary tract. Hence, calcium absorption by this method may underestimate absorption of dietary calcium but is useful for comparative purposes. It has been estimated that bile salts may contribute about 100 g calcium/day to the intestinal calcium contents. Bile salt calcium has been found to be more efficiently absorbed through the intestinal mucosa than is dietary calcium (20) but less so by other investigators (21). 

The suppression of PTH secretion from the parathyroid gland that accompanies the constitutive activation of the CASR makes the disorder difficult to recognize and treat. In some cases, it has been reported that seizures can be intractable. The abnormal set point of calcium regulation complicates treatment with calcitriol and dietary calcium supplementation because the CASR expressed in the kidney controls calcium excretion. The constitutively activated CASR mutant induces hypercalciuria, which may compound the hypocalcemia (42). 

Other methods used to decrease the recurrence of urolithiasis include dietary modifications that decrease calcium excretion and promote diuresis. Changing the diet from alfalfa to grass or oat hay decreases the calcium intake and should decrease the urinary excretion of calcium, since fecal calcium excretion is relatively constant in horses. Although this dietary change should decrease the total calcium excretion, it may also decrease the urinary excretion of nitrogen and the daily urine volume. The latter changes could enhance the supersaturation of urine. In theory, diuresis could be promoted further by the addition of loose salt (50-75 g per day) to the concentrate portion of the diet. However, in one study where ponies were fed sodium chloride (1, 3 or 5% of the total diet dry matter (1% is approximately 75 g sodium chloride for a 500 kg horse)), there were no differences in water intake, urine production or calcium excretion. 

As intestinal absorption of calcium increases, urinary calcium excretion also increases. When the latter exceeds 300 mg/d, formation of calcium phosphate or calcium oxalate stones (urolithiasis) may occur. Hypercalciuria may result from decreased reabsorption of calcium due to a renal tubular defect or from increased intestinal absorption of calcium. Hypercalciuria may be due to an intrinsic defect in the intestinal mucosa or secondary to increased synthesis of 1,25-(OH)2D in the kidney. Disordered regulation of 1,25-(0H)2D synthesis is relatively common in idiopathic hypercalciuria. Treatment usually includes reduction in dietary calcium. Increased vitamin D intake, hyperparathyroidism, and other disorders can also cause hypercalciuria and urolithiasis. 

Normally, 65-80% of filtered calcium and 85-90% of filtered phosphate are reabsorbed, mainly in the proximal tubule. The daily loss of 700-800 mg of phosphate is balanced by dietary intake. Fine-tuning of calcium excretion is accomplished by PTH in the distal convoluted tubules and collecting ducts. Phosphate excretion is regulated by PTH in the proximal tubules. Elevation of the PTH level increases reabsorption of calcium and decreases reabsorption of phosphate from the tubules. This phos-phaturic action opposes the phosphate-sparing action of 1,25-(0H)2D. 

Hypocalcemia can result from inadequate dietary intake, decreased fractional calcium absorption (as seen with increasing age), or enhanced calcium excretion. To restore calcium homeostasis after hypocalcemia, PTH concentrations rise, and vitamin D metabolism increases to enhance intestinal calcium absorption (see Fig. 88-3), renal calcium reabsorption, and bone resorption. Fracture risk is greatest with low calcium intake and low fractional calcium absorption." ... 

Garland, H.O., A.G. Porshaw, and C.P. Sibley. 1997. Dietary essential fatty acid supplementation, urinary calcium excretion and reproductive performance in the diabetic pregnant rat. J. Endocrinol. 153(3) 357-363. 

A single dose of 500 ml cranberry juice had no effect on urinary oxalate secretion but significantly increased mean urinary calcium levels (Brinkley et al. 1981). A significant increase in urinary calcium excretion was observed in a small study after consumption of 2 pints of cranberry juice (Kahn et al. 1967). Consumption of 2 pints daily of cranberry juice for 1 month reduced urinary ionized calcium by 50% (Light et al. 1973). A study on dietary intake and urinary excretion of oxalates indicated that cranberry juice had no effect on oxalate excretion (Massey et al. 1993). 

In a normal adult the kidney has to excrete nearly the same amount of calcium as is absorbed by the intestine. However, studies of the relationship between dietary calcium intake and calcium excretion have revealed that only 6% of an oral calcium load appears in the urine, i.e., other dietary factors modulate intestinal calcium absorption. Indeed, proteins and carbohydrates increase the intestinal absorption, and oxalate, phosphate, and phytic acid decrease it. 

Since excess dietary protein and excess phosphorus have opposing effects on urinary calcium, the natural association of these nutrients in the human diet tends to ameliorate the effect of both on calcium excretion and bone loss. Whether the relative amounts of protein and phosphorus in high protein diets are always compatible with calcium homeostasis is unclear. This question is not amenable to study in rodents because feeding excess protein has no effect on calcium balance. Excess phosphorus causes bone loss irrespective of the protein content of the diet. Hence, adult rodents and adult humans differ with respect to their skeletal response to both excess protein and excess phosphorus. 

The amount of calcium excreted in the urine is related to skeletal size, the acid-base regulation of the body, and the dietary protein intake. Urinary excretion of calcium rises when dietary protein is increased and falls when dietary protein is decreased, it appears that calcium losses can be substantial when protein intake is high hence, if this type of diet is continued for a prolonged period, it could result in a considerable loss of body calcium and even osteoporosis. FHow-ever, studies show that a high protein intake from a high meat diet has little effect on calcium excretion, possibly because of the high phosphate intake with the meat diet. A recent study suggests that increased phosphorus intakes reduce urinary excretion of calcium and lower serum calcium levels. 

Collectively, the possible effects of high dietary intakes of protein and phosphate on urinary calcium excretion and enhanced bone resorption, respectively, along with the possibility of reduced calcium absorption with advancing age, argue for recommending an ample intake of calcium. 

Finally, there is evidence that high intake of dietary protein, such as 100 to 150 g/day results in increased calcium excretion in the urine, thereby raising the requirement for dietary caicium to replace the extra loss from the body. Failure to provide the additional calcium in the diet may lead to the removal of calcium from bone, since the body maintains the... 

Dietary calcium has a relatively small impact on urinary calcium (e.g., only 6-8% of an increase in dietary calcium intake will appear in the urine). The major food components that affect urinary calcium are protein, phosphorus, caffeine, and sodium. For each 50-g increment in dietary protein, approximately 1.5 mmol (60 mg) of additional calcium is lost in urine. The higher amounts of phosphorus consumed concurrently with a high-protein diet can blunt, but not eliminate, this phenomenon. Dietary phosphorus (as well as intravenously administered phosphorus) increases PTH synthesis and subsequently stimulates renal calcium reabsorption and reduces the urinary excretion of calcium. Caffeine causes a reduction in renal reabsorption of calcium and a subsequently increased loss of urinary calcium soon after it is consumed. It has been shown repeatedly in animals and humans that dietary sodium, in the form of salt (NaCl), increases urinary calcium excretion. On average, for every 100 mmol (2300 mg) of sodium excreted in urine, there is an approximately 0.6-1 mmol (24-40 mg) loss of calcium in free-living healthy populations of various ages. Because most of the urinary calcium is of bone origin, it is commonly hypothesized that those nutrients or food components that are hypercalciuretic are also detrimental to the skeleton. On the other hand, thiazide medications are hypocalciuric and, as such, may have modest positive effects on bone. 

The amount of each element required in daily dietary intake varies with the individual bioavailabihty of the mineral nutrient. BioavailabiUty depends both on body need as deterrnined by absorption and excretion patterns of the element and by general solubiUty, and on the absence of substances that may cause formation of iasoluble products, eg, calcium phosphate, Ca2(P0 2- some cases, additional requirements exist either for transport of substances or for uptake or binding. For example, calcium-binding proteias are iavolved ia calcium transport an intrinsic factor is needed for vitamin cobalt,... 

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