Calcium excretion diets

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. 

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 ... 

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. 

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) ... 

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 ). 

Table IV. Postprandial Effects of Ca and P Levels in High Protein Diets on Urinary Calcium Excretion of Men...

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). 

Four children with the nephrotic syndrome developed transient hypercalciuria and intraluminal calcification in renal histopathological specimens without radiological evidence of renal calcification. These children were resistant to corticosteroids and were receiving furosemide plus albumin for the management of edema (10). This result stresses the pervasive effect of furosemide, and probably all loop diuretics, in increasing urinary calcium excretion, with resultant nephrocalcinosis. Whenever possible, steps should be taken to limit the hypercalciuric effect of loop diuretics. Such maneuvers could include limiting the sodium content of the diet and/or combining the loop diuretic with a thiazide diuretic. 

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. 

Calcium withdrawn from our bones to combat acidity is dumped into our urine along with the acid expelled by our kidneys. A 2001 study by Dr. David Bushinsky proved that chronic acidity causes an increase in calcium excretion through the urine however, no change in intestinal calcium absorption was observed (we absorb most nutrients, including calcium, through the walls of our intestines).5 Because bone contains most of the body s calcium, it is widely regarded as the source of the increased calcium excretion in urine. This net loss of calcium is rarely reversed on the Standard American Diet. Nor can it be resolved simply by popping calcium pills. Unless we address the cause of the calcium loss—acidity—it is a lost battle. 

Normal men and women excrete up to 300 mg (7.49 mmol) of calcium per day on a diet with unrestricted calcium content and up to 200 mg/day (4.99 ramol/d) on a calcium-restricted diet (500 mg [12.48 mmol] dietary calcium per day or less for several days). 

A 30-85% increase in oxygen consumption was observed in mice exposed to 110 mg/kg/day in the diet for 26 days (Pugsley 1936). Fecal excretion of calcium and urinary excretion of creatine and creatinine were increased to 200%, 45%, and 400%, respectively, of preexposure levels. The toxicological significance of these changes in excretion was not clear, but high calcium excretion would be expected to result in neuromuscular toxicity and high excretion of creatine and creatinine are often a result of muscle toxicity. 

Protein intake can increase IGF-1, low-protein diets can increase PTH, and high-protein diets can increase urinary calcium excretion. Many observational studies reported higher BMD with higher protein intakes however, most observational studies also found low protein intake to be associated with a lower fracture rate. Moderate protein intake is recommended. 

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. 

Most of the calcium that is lost from the body is excreted in the faeces, this being mainly unabsorbed dietary calcium. However, the digestive secretions all contain small amounts of calcium, and individuals on a calcium-free diet continue to excrete faecal calcium. The normal daily excretion is of the order of 0-1-0-3 g (2-5-7-5 mmol). The quantity of phosphorus excreted daily varies with the dietary intake. As with calcium an appreciable proportion of ingested phosphorus remains unabsorbed and is eliminated in the faeces. Phosphorus is also excreted in the urine, almost entirely in the form of orthophosphates (e.g. NaH2P04 and Na2HP04). Their role in the regulation of acid-base balance is discussed on page 395. Urinary excretion of phosphate is increased in hyperparathyroidism. 

---