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Calcium And Phosphorus

J Am Coll Nutr. 2002 Jun;21(3):239-44.
Calcium effects on phosphorus absorption: implications for the prevention and co-therapy of osteoporosis.
Heaney RP, Nordin BE.
Creighton University, Omaha, Nebraska 68131, USA.

OBJECTIVE: To evaluate the effect of calcium intake on absorption of dietary phosphorus, with special reference to typical calcium intakes and to those likely to be encountered in prevention and treatment of osteoporosis. SETTING: Two academic health sciences centers; inpatient metabolic research unit. METHODS: Evaluation of calcium and phosphorus balance data obtained in two data sets, the first, 543 studies of healthy women aged 35-65, and the second, 93 men and women aged 19-78; development of multiple regression models predicting fecal phosphorus (the complement of net absorbed phosphorus); data from the two centers analyzed separately as a check on the consistency of the findings. RESULTS: Mean net absorption of phosphorus was 60.3% (+/- 18.1) for data set 1 and 53.0% (+/-9.4) for data set 2. Just two variables, fecal calcium and diet phosphorus, were positively and independently associated with fecal phosphorus. These variables explained 73% of the variance in fecal phosphorus in data set 1 and 33% in data set 2. Fecal calcium alone explained the lion’s share of the relationship. The coefficients of the fecal calcium term in the models fitted to the data were 0.332+/-0.022 and 0.155+/-0.039, for data sets I and 2, respectively. Adjusting for the relationship between fecal calcium and calcium intake and using the parameters of the larger data set, it follows that each increase in calcium intake of 0.5 g (12.5 mmol) decreases phosphorus absorption by 0.166 g (5.4 mmol). CONCLUSIONS: As calcium intake increases without a corresponding increase in phosphorus intake, phosphorus absorption falls and the risk of phosphorus insufficiency rises. Intakes with high Ca:P ratios can occur with use of supplements or food fortificants consisting of non-phosphate calcium salts. Older patients with osteoporosis treated with current generation bone active agents should receive at least some of their calcium co-therapy in the form of a calcium phosphate preparation.

J Bone Miner Metab. 2000;18(6):321-7.
Effects of phosphorus-containing calcium preparation (bone meal powder) and calcium carbonate on serum calcium and phosphorus in young and old healthy volunteers: a double-blinded crossover study.
Tsuboi M, Shiraki M, Hamada M, Shimodaira H.
New Medical Research System Clinic, Tokyo, Japan.

To evaluate the effects of bone meal powder (BEC) on calcium and phosphorus metabolism, a calcium absorption test was conducted using a preparation of calcium carbonate (CAC) as the control drug. A total of 12 healthy volunteers, consisting of 6 younger (aged 20-29 years, 3 men and 3 women) and 6 older (aged 60-69 years, 3 men and 3 women) persons, were subjected to a double-blinded crossover study. Serum calcium (s-Ca) level significantly increased to 105.3% +/- 1.9% (P < 0.01 vs the basal value; mean +/- SD) from the basal value in the BEC group and to 104.4% +/- 2.7% (P < 0.01) in the CAC group at 3h post load. Urinary excretions of calcium (u-Ca/glomerular filtration rate, u-Ca/GF) after BEC and CAC load rose to 226.6% +/- 154.5% (P < 0.05) and 211.1% +/- 148.0% (P < 0.05), respectively. Serum phosphorus (s-P) levels after BEC load increased to 110.0% +/- 15.1% (P < 0.05), whereas that after CAC load showed no significant change (99.3% +/- 7.9%). On the other hand, urinary excretion of phosphorus (u-P/GF) after CAC load decreased to 60.0% +/- 32.4% (P < 0.01) and that in the BEC group showed no significant change (92.5% +/- 49.5%). The increase in s-Ca led to decrease in serum intact parathyroid hormone (i-PTH) level [77.3% +/- 33.4% (P < 0.05) for BEC and 69.5% +/- 20.3% (P < 0.01) for CAC] although s-P was increased by the BEC load. The responses to BEC and CAC administration were compared in the younger and the older groups. The responses in the younger and the older group showed fundamentally the same trends and to the same extent. However, the changes in serum ionized calcium (i-Ca) and i-PTH levels at 1.5 h post load were significantly smaller in the older group than in the younger group (P < 0.01; P < 0.05). The increment in s-P level after BEC load in the older group was larger than that in the younger group. In conclusion, BEC can modulate not only calcium but also phosphorus metabolism in both younger and older subjects. Further investigations are required to evaluate the effects of BEC on bone density and safety for renal function in long-term observations.

Biofactors. 2004;21(1-4):39-42.
Effect of dietary calcium: Phosphorus ratio on bone mineralization and intestinal calcium absorption in ovariectomized rats.
Koshihara M, Masuyama R, Uehara M, Suzuki K.
Department of Nutritional Science, Faculty of Applied Bioscience, Tokyo University of Agriculture, 1-1-1 Sakuragaoka, Setagaya-ku, Tokyo 156-8502, Japan.

We investigated the effect of dietary calcium:phosphorus (Ca:P) ratio on bone mineralization and intestinal Ca absorption in ovariectomized (OVX) rat models of osteoporosis and sham-operated rats. Thirty 12-wk-old female Wistar rats were divided into three groups of OVX rats and three groups of sham rats. Thirty days after the adaptation period, OVX rats and sham rats were fed a diet formulated Ca:P, 1:0.5, 1:1 or 1:2 (each diet containing 0.5% Ca), respectively for 42 d. In both sham and OVX rats, serum osteocalcin, a marker of bone turnover, was increased by decreasing Ca:P ratio (1:2). In contrast, rats fed the Ca:P = 1:0.5 diet (dietary P restriction) suppressed the increased serum parathyroid hormone, osteocalcin and urinary deoxypyridinoline, and increased Ca absorption in both sham and OVX rats compared to the Ca:P = 1:1 and 1:2 diets. Especially, in OVX rats, the decreased bone mineral density of the fifth lumbar was also suppressed when rats were fed the Ca:P = 1:0.5 diet. These results indicated that the elevation of dietary Ca:P ratio may inhibit bone loss and increase intestinal Ca absorption in OVX rats.

Bone Miner. 1987 Jul;2(4):333-6.
Hypercalcemia of sarcoidosis treated with cellulose sodium phosphate.
Dwarakanathan A, Ryan WG.
Department of Medicine, Rush-Presbyterian-St Luke’s Medical Center, Chicago, IL 60612.

A patient with pulmonary sarcoidosis and symptomatic hypercalcemia had elevated serum 1,25-dihydroxyvitamin D and angiotensin-converting enzyme levels, with evidence of deterioration of renal function. Pulmonary function tests were normal and there were no other findings to warrant immediate steroid use. She was treated with cellulose sodium phosphate, in an effort to control the hypercalcemia. Serum calcium declined to normal values within 4 weeks and was associated with symptomatic improvement and normalization of BUN and creatinine, indicating perhaps a direct relationship between serum calcium and renal function in this setting. These observations suggest that the hypercalcemia of sarcoidosis may be successfully treated with cellulose sodium phosphate presumably by reducing intestinal calcium absorption, but further clinical trials will be necessary to establish its effectiveness in the long term.

Kidney Int. 1991 May;39(5):973-83.
Potassium administration reduces and potassium deprivation increases urinary calcium excretion in healthy adults [corrected]
Lemann J Jr, Pleuss JA, Gray RW, Hoffmann RG.
Department of Medicine, Medical College of Wisconsin, Milwaukee.

This study was undertaken to evaluate the effects of dietary K intake, independent of whether the accompanying anion is Cl- or HCO3-, on urinary Ca excretion in healthy adults. The effects of KCl, KHCO3, NaCl and NaHCO3 supplements, 90 mmol/day for four days, were compared in ten subjects fed normal constant diets. Using synthetic diets, the effects of dietary KCl-deprivation for five days followed by recovery were assessed in four subjects and of KHCO3-deprivation for five days followed by recovery were assessed in four subjects. On the fourth day of salt administration, daily urinary Ca excretion and fasting UCa V/GFR were lower during the administration of KCl than during NaCl supplements (delta = -1.11 +/- 0.28 SEM mmol/day; P less than 0.005 and -0.0077 +/- 0.0022 mmol/liter GFR; P less than 0.01), and lower during KHCO3 than during control (-1.26 +/- 0.29 mmol/day; P less than 0.005 and -0.0069 +/- 0.0019 mmol/liter GFR; P = 0.005). Both dietary KCl and KHCO3 deprivation (mean reduction in dietary K intake -67 +/- 8 mmol/day) were accompanied by an increase in daily urinary Ca excretion and fasting UCaV/GFR that averaged on the fifth day +1.31 +/- 0.25 mmol/day (P less than 0.005) and +0.0069 +/- 0.0012 mmol/liter GFR (P less than 0.005) above control. Both daily urinary Ca excretion and fasting UCaV/GFR returned toward or to control at the end of recovery. These observations indicate that: 1) KHCO3 decreases fasting and 24-hour urinary Ca excretion; 2) KCl nor NaHCO3, unlike NaCl, do not increase fasting or 24-hour Ca excretion and 3) K deprivation increases both fasting and 24-hour urinary Ca excretion whether the accompanying anion is Cl- or HCO3-. The mechanisms for this effect of K may be mediated by: 1) alterations in ECF volume, since transient increases in urinary Na and Cl excretion and weight loss accompanied KCl or KHCO3 administration, while persistent reductions in urinary Na and Cl excretion and a trend for weight gain accompanied K deprivation; 2) K mediated alterations in renal tubular phosphate transport and renal synthesis of 1.25-(OH)2-vitamin D, since KCl or KHCO3 administration tended to be accompanied by a rise in fasting serum PO4 and TmPO4 and a fall in fasting UPO4 V/GFR, a fall in serum 1,25-(OH)2-D and a decrease in fasting UCa V/GFR, while dietary KCl or KHCO3 deprivation were accompanied by a reverse sequence.

Clin Calcium. 2005 Sep;15(9):1501-6.
[Phosphorus intake and bone mineral density (BMD)]
Kawaura A, Nishida Y, Takeda E. [Article in Japanese] Department of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima Graduate School.

Phosphorus regulates the bone formation and inhibits the bone resorption. It is still expected as one of anti-osteoporosis nutrients. The amounts of phosphorus intake with calcium are increasing from 1960 to 1995. Because phosphorus affects the regulation of calcium metabolism, the balance of these nutrients is important. Tuero suggested that more than 1,000 mg/day of calcium intake and more than 0.74 of Ca/P were associated with better bone mineral density (BMD) values in young women. However, there are few reports of correlations between appropriate phosphorus intake, Ca/P rate and BMD.

Best Pract Res Clin Endocrinol Metab. 2003 Dec;17(4):623-51
Diagnosis and management of electrolyte emergencies.
Weiss-et EM, Takala J, Jakob SM.
Department of Intensive Care Medicine, Inselpital, University Hospital Bern, CH-3010 Bern, Switzerland.

Electrolyte and fluid imbalances are disorders frequently observed in critical care patients. In many instances patients are asymptomatic, but they may also present with neurological alterations, severe muscle weakness, nausea and vomiting or cardiovascular emergencies. Therefore, a pathophysiological understanding of these disorders is necessary for initiating an appropriate therapy. After a precise history-including drug prescriptions-has been obtained from the patient or his/her relatives, determination of the hydration status of the patient and measurement of acid-base status, plasma and urine osmolality and electrolytes are the first steps in the assessment of the disease. Once a diagnosis has been established, great attention has to be paid to the rate at which the disorder is corrected because this-if inappropriate-may cause more severe damage to the patient than the disease itself. This chapter addresses the initial diagnostic and therapeutic steps of the most common electrolyte emergencies.

Eur J Nutr. 2001 Oct;40(5):200-13.
Diet, evolution and aging–the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet.
Frassetto L, Morris RC Jr, Sellmeyer DE, Todd K, Sebastian A.
University of California, San Francisco 94143, USA.

Theoretically, we humans should be better adapted physiologically to the diet our ancestors were exposed to during millions of years of hominid evolution than to the diet we have been eating since the agricultural revolution a mere 10,000 years ago, and since industrialization only 200 years ago. Among the many health problems resulting from this mismatch between our genetically determined nutritional requirements and our current diet, some might be a consequence in part of the deficiency of potassium alkali salts (K-base), which are amply present in the plant foods that our ancestors ate in abundance, and the exchange of those salts for sodium chloride (NaCl), which has been incorporated copiously into the contemporary diet, which at the same time is meager in K-base-rich plant foods. Deficiency of K-base in the diet increases the net systemic acid load imposed by the diet. We know that clinically-recognized chronic metabolic acidosis has deleterious effects on the body, including growth retardation in children, decreased muscle and bone mass in adults, and kidney stone formation, and that correction of acidosis can ameliorate those conditions. Is it possible that a lifetime of eating diets that deliver evolutionarily superphysiologic loads of acid to the body contribute to the decrease in bone and muscle mass, and growth hormone secretion, which occur normally with age? That is, are contemporary humans suffering from the consequences of chronic, diet-induced low-grade systemic metabolic acidosis? Our group has shown that contemporary net acid-producing diets do indeed characteristically produce a low-grade systemic metabolic acidosis in otherwise healthy adult subjects, and that the degree of acidosis increases with age, in relation to the normally occurring age-related decline in renal functional capacity. We also found that neutralization of the diet net acid load with dietary supplements of potassium bicarbonate (KHCO3) improved calcium and phosphorus balances, reduced bone resorption rates, improved nitrogen balance, and mitigated the normally occurring age-related decline in growth hormone secretion–all without restricting dietary NaCl. Moreover, we found that co-administration of an alkalinizing salt of potassium (potassium citrate) with NaCl prevented NaCl from increasing urinary calcium excretion and bone resorption, as occurred with NaCl administration alone. Earlier studies estimated dietary acid load from the amount of animal protein in the diet, inasmuch as protein metabolism yields sulfuric acid as an end-product. In cross-cultural epidemiologic studies, Abelow found that hip fracture incidence in older women correlated with animal protein intake, and they suggested a causal relation to the acid load from protein. Those studies did not consider the effect of potential sources of base in the diet. We considered that estimating the net acid load of the diet (i. e., acid minus base) would require considering also the intake of plant foods, many of which are rich sources of K-base, or more precisely base precursors, substances like organic anions that the body metabolizes to bicarbonate. In following up the findings of Abelow et al., we found that plant food intake tended to be protective against hip fracture, and that hip fracture incidence among countries correlated inversely with the ratio of plant-to-animal food intake. These findings were confirmed in a more homogeneous population of white elderly women residents of the U.S. These findings support affirmative answers to the questions we asked above. Can we provide dietary guidelines for controlling dietary net acid loads to minimize or eliminate diet-induced and age-amplified chronic low-grade metabolic acidosis and its pathophysiological sequelae. We discuss the use of algorithms to predict the diet net acid and provide nutritionists and clinicians with relatively simple and reliable methods for determining and controlling the net acid load of the diet. A more difficult question is what level of acidosis is acceptable. We argue that any level of acidosis may be unacceptable from an evolutionarily perspective, and indeed, that a low-grade metabolic alkalosis may be the optimal acid-base state for humans.

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