Calcium excretion dietary protein

The rat has been used rather widely to study the relation between dietary protein, or acid salt feeding, and calcium loss. Barzel and Jowsey (19) showed that the rat fed a control diet supplemented with ammonium chloride excreted excessive urinary calcium, and experienced a concomitant loss of fat-free bone tissue. Draper, et al. (20) extending this work, reported an inverse relation between dietary phosphate and loss of bone calcium and dry, fat-free tissue. In subsequent studies (21), they reported that this process was accompanied by reduced serum calcium levels the high phosphorus, low calcium diet increased urinary calcium loss. Whereas, increasing the phosphorus content of the diet stopped the excessive urinary calcium loss. To test possible zinc loss that might result from this sort of acid salt feeding, Jacob and her coworkers (22) fed rats a supplement of ammonium chloride and then measured urinary zinc and calcium. The hypercalciuria occurred exclusive of an effect upon urinary zinc loss. 

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. 

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. 

Limited data are available about the effects of individual dietary components on absorption, and consequently the requirement, of Mn. Dietary protein and phosphorus levels (33), calcium level (34) and the effect of a partial substitution of soy protein for meat (28) have been tested in balance studies without any obvious effect of Mn absorption or retention. However, since the main route of excretion is via the bile, the conventional balance technique is probably not sensitive enough to identify dietary factors that influence Mn absorption. 

The mechanism by which dietary protein induces an increase in urinary calcium is not clear. The effect has been attributed, in part, to the catabolism of sulfur-containing amino acids to yield sulfate. Elevated levels of plasma sulfate can form a complex with calcium. The complex passes into the renal tubule, where it is poorly reabsorbed, resulting in its excretion in the urine. The mechanism by which phosphate reverses the h5rpercalciuric effect of protein is also not clear. 

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. 

Excess dietary protein also leads to an increase in urinary calcium in adult rodents, but there is no attendant loss of calcium from the skeleton or negative calcium balance. This difference between species appears to be due to two factors a smaller fractional excretion of endogenous calcium in the urine of rodents (less than 5%) and a greater capacity to buffer metabolic acid. Only when acid loads are sufficient to depress... 

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... 

Itoh, R, Nishiyama, N., and Suyama, Y, Dietary protein intake and urinary excretion of calcium a cross-sectional study in a healthy Japanese population. Am J Clin Nutr, 67, 438, 1998. 

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 present communication is concerned with calcium balance studies carried out during the Intake of a variety of dietary factors including minerals and protein as well as drugs. The studies were performed In adult males under strictly controlled conditions in the Metabolic Research Unit. The diet was kept constant throughout the relatively long term studies and complete collections of urine and stool were obtained. The composition of this diet was previously described (5). The diet and the excretions in urine and stool were analyzed for calcium throughout the studies. These data formed the basis of calcium balances which were determined for several weeks. Calcium was analyzed by atomic absorption spectroscopy (6). 

A wide range of plasma phosphorus concentration has been observed by other workers in primary hyperparathyroidism (C7) and explained in terms of diet and renal excretion. Unlike the calcium concentration, which is normally very constant regardless of dietary intake and urinary excretion, the concentration of inorganic phosphate in plasma is the resultant of the rate of phosphorus absorption from the gut and protein catabolism, on the one hand, and of renal excretion, on the other. Although the parathyroid hormone promotes phosphorus excretion, this is only one of the factors governing plasma phosphate concentration. Plasma phosphate in cases of hyperparathyroidism on a relatively high phosphorus intake may therefore not be distinguishable from that in normal subjects on a lower intake. 

Human adults fed experimental diets high in purified proteins exhibit an increased loss of calcium in the urine and an increase in the amount of dietary calcium required to maintain balance. Calciuria is due mainly to increased acid production arising from the oxidation of excess sulfur amino acids. Acid excretion is associated with a decreased fractional reabsorption of calcium from the renal tubules. 

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