Calcium excretion bioavailability

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). 

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. 

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). 

Apparent absorption (intake minus fecal excretion) of calcium decreased when the diet contained muffins with added sodium phytate to increase the molar ratio of phytate/calcium from 0.04 to 0.14 and 0.24. One-half of the men excreted more calcium in feces than was consumed when the high phytate diet was consumed. People consuming diets with molar ratios of phytate/calcium exceeding 0.2 may be at risk of calcium deficiency because of low bioavailability of dietary calcium unless physiological adjustments can be accomplished that maintain homeostasis. 

High levels of dietary zinc were associated with marked decreases in bone calcium deposition and in the apparent retention of calcium in male weanling albino rats. Marked increases in fecal calcium levels were also observed in the zinc-fed rats. Excessive dietary zinc was associated with a shifting of phosphorus excretion from the urine to the feces. This resulted in an increase in fecal phosphorus and provided an environmental condition which would increase the possibility of the formation of insoluble calcium phosphate salts and a subsequent decrease in calcium bioavailability. The adverse effect of high dietary zinc on calcium status in young rats could be alleviated and/or reversed with calcium supplements. 

The data presented in this paper indicate that excess levels (0.75%) of dietary zinc result in decreases in the bioavailability of calcium and phosphorus in rats and interfere with normal bone mineralization. High dietary levels of calcium or zinc appeared to cause a shift in the excretion of phosphorus from the urine to the feces, while the presence of extra phosphorus tended to keep the pathway of phosphorus excretion via the urine. The presence of large amounts of phosphorus in the Intestinal tract due to high intakes of zinc would increase the possibility of the formation of insoluble phosphate salts with various cations, including calcium, which may be present. A shift in phosphorus excretion from the feces to the urine, however, could result in an environmental condition within the system which would tend to increase the bioavailability of cations to the animal. The adverse effect of zinc toxicity on calcium and phosphorus status of young rats could be alleviated with calcium and/or phosphorus supplements. 

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