Dietary phosphorus, effect

Phosphorus Rat Lead retention Low dietary phosphorus enhances lead retention no effect on lead resorption in bone Quarterman and Morrison 1975... 

We have conducted two human metabolic studies (5,6) to compare the effects of increasing phosphorus intake on calcium utilization in healthy young adults maintained at low (ca. 400 mg/day) and high (ca. 1200 mg/day) levels of calcium intake. Increasing dietary phosphorus, as orthophosphate, caused a slight reduction in fecal calcium and a substantial reduction in urinary calcium losses (Table III). 

In this study, the protein-induced calciuric effect was rather modest. Such could be the response early in life or it may be due to the natural protein sources, which are reported (13, 14) to be less calciuric than purified protein sources. Proteins differ in their calciuric effect and combining them can render them less calciuric. The relative (to calcium) excess of dietary phosphorus, a hypocal-ciuric agent (14) may have also mitigated pronounced hypercalciuria due to excessive protein. 

Mechanism of Action An antihyperphosphatemia agent that binds with dietary phosphorus in the GI tract, thus allowing phosphorus to be eliminated through the normal digestive process and decreasing the serum phosphorus level. Therapeutic Effect Decreases incidence of hypercalcemic episodes in patients receiving calcium acetate treatment. 

Miller, E. R., Ullrey, D. E., Zutaut, C. L., ] loefer, j- A., and Luecke, R. W. (1964). Mineral balance studies with the baby pig Effects of dietary phosphorus level upon calcium and phosphorus balance. ]. Ntiir. 82,111-114. 

A number of investigators have studied the effects of dietary phosphorus on the bioavailability of zinc and iron to animals and human subjects. The results of these studies have not been consistent. Possible reasons for discrepancies among studies include differences in the types of phosphorus... 

Other factors in the diet have also been found to modify the effect of phosphorus on iron and zinc metabolism. One such factor is ascorbic acid. Peters, et al. (35) observed that when human subjects were fed a solution of iron chloride, they absorbed very little iron if ascorbic acid was not present in the solution (Table IV). In fact, if ascorbic acid was not present, absorption of iron was so low it was difficult to tell whether dietary factors, such as phosphorus, affected the absorption of iron. However, ascorbic acid may also counteract the effect of dietary phosphorus on the absorption of nonheme iron. Investigators have demonstrated that the addition of ascorbic acid to a diet counteracted the effect of the phosphoprotein in egg yolk on iron absorption (17. 18). 

Dietary protein may also be able to moderate the effect of dietary phosphorus on zinc utilization. Greger Snedeker (54) observed that human subjects absorbed more zinc when fed a high protein diet with a moderate level of phosphorus than when fed a high protein diet with a high level of phosphorus. This effect of phosphorus was not seen when low levels of protein were fed. 

The relative effects of various forms of dietary phosphorus (i.e. orthophosphates versus polyphosphates) on iron and zinc utilization is not clear and deserves further study. 

Antacids neutralize gastric acid, inactivate pepsin, and bind bile salts. Aluminum-containing antacids also suppress HP and enhance mucosal defense. ° G1 adverse effects are most common with antacids and are dose dependent. Magnesium salts cause an osmotic diarrhea, whereas aluminum salts cause constipation. Diarrhea usually predominates with magnesium/aluminum preparations. Aluminum-containing antacids (except aluminum phosphate) form insoluble salts with dietary phosphorus and interfere with phosphorus absorption. Hypophosphatemia occurs most often in patients with low dietary phosphate intake (e.g., malnutrition or alcoholism). Combined treatment with sucralfate may amplify the hypophosphatemia and the potential for aluminum toxicity (see section on sucralfate). 

Harrison GE, Howells GR, Pollard J, et al. 1966b. Effect of dietary phosphorus supplementation on the uptake of radioactive strontium in rats. Br J Nutr 21 561-569. 

Hyperphosphatemia is common in patients with end-stage renal disease (ESRD), since a large fraction (60-70%) of dietary phosphorus is absorbed and normally excreted by the kidneys, and as kidney function deteriorates, less phosphorus is exereted by the kidneys (Emmett 2004). Dietary restrictions have insuffieient effect. The condition may have serious consequences. Hyperphosphatemia stimulates parathyroid hormone and suppresses vitamin D3 production, and thus induces hyperparathyroid bone disease. In addition, it leads to myocardial and vascular calcification and cardiac microcirculatory abnormalities, which results in cardiac causes of death. Phosphate levels henee should be eontrolled early in 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. 

Phosphate balance in adults is almost always zero, in contrast to calcium balance, which is usually negative, because of the effective action of PTH on renal tubules to block Pi reabsorption. In late life, however, intestinal phosphate absorption decreases and the serum phosphate concentration declines. These physiological decrements may contribute to disease, especially to increased bone loss and osteopenia or more severe osteoporosis. Typically, these changes in Pi balance are also accompanied by similar changes in calcium balance. Too little dietary phosphorus and too little dietary calcium may be determinants of low bone mass and density and, hence, increased bone fragility. The usual scenario invoked to explain osteoporosis in old age, however, is that too little dietary calcium in the presence of adequate dietary phosphorus stimulates PTH release and bone loss (Figure 1). 

A wide variety of animal species are subjected to the administration of drugs during their lifetime.The various animal species can encounter drugs and other dietary additives by different routes and this is dependent on the environment in which they are kept. Intensively reared animals tend to have considerable consistency in the components of their diets and thus are much less likely to encounter the range of naturally produced compounds that extensively produced animals encounter. The desire for less expensive dietary constituents and increased efficiency of use has induced feed manufacturers and producers to add enzyme supplements to diets of most farmed animals to reduce the negative effects of indigestible dietary carbohydrates, refactory proteins and unavailable minerals such as phosphorus. This use of dietary additives to improve nutrient utilization and environmental consequences of feeding animals intensively has been the subject of intense research activity in the last five years. " The... 

However, results obtained by Koo et al. (1991) indicate that low to moderate lead exposure (average lifetime PbB level range of 4.9-23.6 pg/dL, geometric mean of 9.8 pg/dL, n=105) in young children with adequate nutritional status, particularly with respect to calcium, phosphorus, and vitamin D, has no effect on vitamin D metabolism, calcium and phosphorus homeostasis, or bone mineral content. The authors attribute the difference in results from those other studies to the fact that the children in their study had lower PbB levels (only 5 children had PbB levels >60 pg/dL and all 105 children had average lifetime PbB levels <45 pg/dL at the time of assessment) and had adequate dietary intakes of calcium, phosphorus, and vitamin D. They concluded that the effects of lead on vitamin D metabolism observed in previous studies may, therefore, only be apparent in children with chronic nutritional deficiency and chronically elevated PbB levels. Similar conclusions were reached by IPCS (1995) after review of the epidemiological data. 

Reports of lead-nutrient interactions in experimental animals have generally described such relationships in terms of a single nutrient, using relative absorption or tissue retention in the animal to index the effect. Most of the data are concerned with the impact of dietary levels of calcium, iron, phosphorus, and vitamin D. These interaction studies are summarized in Table 2-12. 

It has also been demonstrated in animals that lead blocks the intestinal responses to vitamin D and its metabolites (Smith et al. 1981). Dietary concentrations of lead in combination with a low phosphorus or a low calcium diet administered to rats suppressed plasma levels of the vitamin D metabolite, 1,25-dihydroxycholecaliferol, while dietary intakes rich in calcium and phosphorus protected against this effect (Smith et al. 1981). Thus, animals fed a diet high in calcium or phosphorus appear to be less susceptible to the effects of lead, because of hindered tissue accumulation of lead. 

Quarterman J, Morrison JN. 1975. The effects of dietary calcium and phosphorus on the retention and excretion of lead in rats. Br J Nutr 34 351-362. 

Cymbaluk, N.F. and G.I. Christison. 1989. Effects of dietary energy and phosphorus content on blood chemistry and development of growing horses. Jour. Anim. Sci. 67 951-958. 

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. 

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