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At least 19 recordsLinked to original sources
PubMed1997

Dietary calcium, dietary protein, and kidney stone formation.

Kidney stone disease is common and is a major cause of morbidity involving the urinary tract. Rising incidence rates of calcium oxalate stone disease, the most common type of kidney stone, have focused attention on dietary habits and their potential role in the development of nephrolithiasis. Traditionally, calcium restriction had been recommended to reduce the likelihood of calcium stone formation, but recent evidence suggests that dietary calcium restriction may actually increase the risk. Observational and experimental data suggest that restriction of animal protein may lower the risk of stone formation, but a randomized trial did not confirm this finding. Dietary modification may play an important role in reducing the likelihood of stone recurrence. Notably, dietary calcium restriction should be avoided in patients who have had a calcium oxalate kidney stone.

Calcium, Dietary↗
PubMed2006

[Bioavailability of dietary calcium].

Dietary calcium (Ca) is fundamental to the bone's health. Both the purport and the element bioavailability in the food need to be considered. The purpose of this work was to summarize the factors involved in Ca absorption and point out the sources with higher bioavailability. Ca is mostly absorbed in the jejunum and low pH seems to favor its absorption, which is higher during growth, gestation/lactation and Ca and phosphorus (P) deficiency, and lower with aging. The richest and best-absorbed Ca source is cow's milk and its derivatives. Other foods show high Ca concentrations but variable bioavailability: foods rich in phytates and oxalates show a smaller absorption and carbohydrate-rich foods show higher absorption. Since Ca bioavailability in other animal's milk, soymilk and some vegetables is closer to that in cow's milk, adequate amounts of these foods could be used as an alternative.

Animals↗
PubMed1994

Carbonated beverages, dietary calcium, the dietary calcium/phosphorus ratio, and bone fractures in girls and boys.

PURPOSE: The aim of this study was to explore the association between carbonated beverage consumption, as well as other nutritional intake, and the occurrence of bone fractures in girls (mean +/- SD) 14.3 yr +/- 1.8 and boys 14.6 yr +/- 1.6. METHODS: Food-frequency questionnaires and medical histories were obtained from 76 girls and 51 boys. Subjects were recruited from a swimming club and physicians' offices; their physical characteristics are representative of the normal adolescent population. RESULTS: The data show a strong association between cola beverage consumption and bone fractures in girls [the adjusted odds ratio (OR) = 3.59; 95% confidence interval (CI) 1.21, 10.75; p = 0.022]. High intake of dietary calcium was protective (adjusted OR = 0.284; 95% CI 0.087, 0.920; p = 0.036). No association between the non-cola drinks and bone fractures was found. In boys, only total caloric intake was associated with the risk of bone fractures; the association was inverse. CONCLUSION: The high consumption of carbonated beverages and the declining consumption of milk are of great public health significance for girls and women because of their proneness to osteoporosis in later life.

Adolescent↗
PubMed2000

Parathyroid hormone is elevated but bone markers and density are normal in young female subjects who consume inadequate dietary calcium.

Dietary Ca and osteocalcin (OC), parathyroid hormone (PTH), 25-hydroxyvitamin D (25-OH-D), insulin-like growth factor (IGF)-I and sex hormone binding globulin (SHBG) were assessed simultaneously to bone mineral density (BMD) in 200 adolescent girls (aged 11-15 years) and 100 young women (aged 20-23 years), selected from the lowest and highest end of the Ca intake distribution of a larger population sample. Ca intake was evaluated by food frequency questionnaires, BMD was measured by dual energy x-ray absorptiometry at ultradistal and proximal radius of non-dominant arm, bone age was estimated from x-rays of left hand and wrist according to Tanner et al. (1983). Surprisingly, mean Ca intakes were below the dietary reference intakes in the subgroups of girls and women with the highest measured Ca consumption. Postmenarcheal, but not premenarcheal girls showed radial densities as high as the women and in no group was BMD associated with Ca intake. In all adolescents serum PTH was negatively related to dietary Ca. In girls before menarche IGF-I was positively associated with bone age, while in the same subjects the negative relationship between SHBG and BMD pointed to the crucial role of bioavailable sex steroids on bone mass apposition in early puberty. OC levels decreased progressively with age, while serum 25-OH-D significantly increased after menarche. In conclusion, although in adolescents low Ca intake has not been shown to induce any immediate deleterious effect on radial density, the compensatory hypersecretion of PTH supports the need for an adequate Ca intake to achieve peak bone mass.

25-Hydroxyvitamin D 2↗
PubMedDate not supplied

Reduced intestinal calcium and dietary calcium intake, increased aluminum absorption, and tissue concentration in the rat.

To test the influence of calcium (Ca) on aluminum (Al) absorption, Ca was withheld from or added (1mM) to the perfusate of the in situ rat gut. The rats had been maintained on Purina Rat Chow. Ca addition significantly decreased (to 70%) the rate of Al disappearance from the gut and decreased (to 55%) the area under the curve of Al appearance in portal blood. To test the influence of Ca deficiency on Al absorption, rats were maintained on a low-Ca (0.008%) or a Ca-replete (0.5%) diet for 1-4 wk. The in situ gut was prepared, and a perfusate containing approximately 1 microM Ca was used. The rate of Al disappearance from the gut of low-Ca diet rats was significantly faster than from the gut of rats maintained on the Ca-replete diet, averaging 156% of the latter. Al appearance in portal blood was significantly greater (averaging 38%) in rats maintained on the low-Ca diet than in controls. To determine if Ca deficiency influences Al tissue distribution independent of gastrointestinal Al absorption, rats maintained on a low-Ca or a Ca-replete diet received 20 ip Al injections over 1 mo. Rats eating the low-Ca diet demonstrated enhanced tissue Al accumulation in all tissues studied, except for muscle and cerebral cortex. These results demonstrate enhanced Al absorption and tissue retention in the presence of reduced intestinal Ca concentration and reduced Ca intake.

Aluminum↗
PubMed1993

Effect of calcium source, dietary calcium concentration, and gestation phase on various bone characteristics in gestating gilts.

Sixty gravid crossbred gilts were allotted to a 2 x 3 x 2 factorial arrangement of treatments: two Ca sources (sun-cured alfalfa meal and CaCO3), three dietary concentrations of Ca (50, 75, and 100% of NRC requirements), and two phases of gestation (55 and 105 d). The objectives were to determine the effect of Ca source, dietary Ca concentration, and gestation phase on bone characteristics (bone breaking strength, bone ash percentage, bone density, and bone ash density in the rib, thoracic, and coccygeal bones), to correlate bone responses to determine relative bone activity, and to determine reliability of the coccygeal bones as indicators of Ca status in the body. At 55 d, rib strength and coccygeal ash content were lower (P < .01) than at 105 d of gestation. A gestation phase x Ca concentration (P < .05) interaction occurred. As Ca concentration increased, thoracic strength and rib ash responded quadratically during each gestation phase, for which at 55 d a minima and at 105 d a maxima was produced at 75% of NRC. A Ca source x Ca concentration (P < .05) interaction occurred. Gilts fed alfalfa had the lowest rib bone and ash density when fed 75% of NRC for Ca, whereas gilts fed CaCO3 were highest at this level of Ca compared with the other concentrations. Generally, all bones were positively correlated with respect to their response to dietary Ca concentration. Few negative correlations were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1987

Genetic variability in response to dietary calcium.

Supplemental dietary calcium has been shown to reduce blood pressure in spontaneously hypertensive rats while restricted calcium diets cause an elevation in blood pressure. This latter nutrient effect has been enhanced by modest sodium restriction and is associated with a reduction in serum ionized calcium concentration. To determine whether alterations of dietary calcium and sodium have a similar influence on blood pressure in genetically normotensive rats, Fisher 344, Wistar Furth, and ACI rats were fed either a low (0.1%) calcium, low (0.25%) sodium diet or normal (1.0%) calcium, normal sodium (0.45%) diet from 4 weeks of age through 29 weeks of age. Indirect measurements of systolic blood pressure showed that only the Fisher 344 rats consistently responded to the low calcium/low sodium diets with an elevation of blood pressure. There was considerable variation in serum electrolytes across strains in the normal diets but all three strains experienced a reduction in ionized calcium and an elevation in phosphorus and magnesium on the restricted diets. In the Fisher 344 rats there were significant (p less than .05) inverse correlations among systolic blood pressure and serum ionized and total calcium concentrations and positive correlations among systolic blood pressure, phosphorus, and magnesium. There was no significant correlation between serum electrolytes and blood pressure in the other two strains. The data indicate that there is genetic variability in the blood pressure response to alterations in dietary calcium and sodium. The pattern of change in serum electrolytes across strains suggests that diet-induced alterations of serum electrolytes, specifically calcium, are not necessarily predictive of a pressor response. It would appear that some other calcium-sensitive physiological process involved in blood pressure regulation must respond differentially to calcium availability across strains.

Animals↗
PubMed1991

Calcium metabolism and dietary calcium in salt sensitive hypertension.

Evidence has accumulated over the past decade that suggests a relationship between low calcium intake, abnormalities in cation metabolism and hypertension in certain segments of the essential hypertension population. This evidence has been developed from epidemiological data, calcium intervention trials and observations related to biochemical alterations suggestive of a calcium deficiency in certain patients with hypertension and in animal models of essential hypertension. It is becoming increasingly evident that salt sensitive individuals are especially likely to be characterized by abnormalities of calcium metabolism and blood pressure responses to dietary calcium. In this review the role of calcium in the regulation of blood pressure is examined with an emphasis on epidemiological, biochemical, hemodynamic and dietary intervention data in the salt sensitive hypertensive patient.

Blood Pressure↗
PubMed1981

Incidence of normocalcemic hyperparathyroidism in idiopathic hypercalciuria: evaluation by dietary calcium deprivation test.

Calcium metabolism was studied in 37 patients with "idiopathic hypercalciuria" on a home diet and after 10 days of low calcium dietary intake (less than 400 mg/24h). After low calcium intake, urinary calcium excretion returned to within normal limits in 70% of the cases. In the group of patients which failed to respond to calcium restriction, TmPO4/GFR values were reduced and, furthermore, in 20% of them plasma iPTH and urinary cAMP levels were increased. These data seem to indicate that: the incidence of absorptive hypercalciuria is higher than hypercalciuria of renal origin; normocalcemic hyperparathyroidism due to primary calcium leak is present only in a limited number of cases, consequently, hypercalciuria secondary to renal phosphate leak is a rather frequent occurrence.

Calcium↗
PubMed1995

Morphological analysis of dentine formation in young rat molars during the recovery phase with calcium alone or combined with xylitol following a low-calcium dietary regimen.

The effects of dietary calcium deficiency and subsequent replenishment of the diet with calcium alone or with xylitol were studied. Thirty 3-week-old Wistar rats were labelled with an i.p. tetracycline injection. Twenty rats were fed a diet with 0.026% calcium (Ca-deficient); 10 received a 0.5% Ca diet (controls). After 3 weeks the tetracycline labelling was repeated. Replenishment of the diet was introduced for Ca-deficient rats, and 10 received additional 5% xylitol in the diet. After 4 weeks the labelling was repeated and the animals were decapitated. Dentine formation was measured by the tetracycline stripes in the lower first and second molars. Calcium deficiency during the first 3 weeks reduced dentine formation. In the control and xylitol groups, a much smaller amount of dentine was formed during the recovery period. With Ca alone, dentine formation was faster than in the controls or Ca-xylitol group and did not differ from the Ca-deficient period. These results indicate that in rat molars the odontoblasts can accelerate the rate of dentine formation when calcium is restored to the diet, at least during primary dentinogenesis. This effect was not seen when 5% xylitol was added to the replenishment diet.

Animals↗
PubMed1989

Colonic epithelial cell proliferation in responders and nonresponders to supplemental dietary calcium.

Supplemental dietary calcium decreased and normalized hyperproliferation of colonic epithelial cells in individuals in familial colon cancer kindreds, measured by rates and patterns of [3H]thymidine labeling of epithelial cells in colonic crypts. In whole colonic crypts hyperproliferation was decreased to lower levels in over one-half of the subjects individually studied during the course of the calcium supplementation regimen. The remaining familial colon cancer subjects did not show reductions in cell proliferation measured over the whole crypt. However, when their cell-labeling data were analyzed in regions of the colonic crypt, the size of the proliferative compartment decreased and contracted towards the crypt base after calcium, a pattern typical of individuals at decreased risk for colonic cancer. This contraction of the proliferative region of the crypts occurred through decreased cell labeling in the two crypt compartments closest to the luminal surface and increased cell labeling in the second crypt compartment nearest to the base of the crypt. Following in vitro exposure of colonic epithelial cells to increasing physiological amounts of calcium, cell proliferation in familial colon cancer subjects decreased uniformly and greater heterogeneity in responsiveness was observed in cells from individuals with familial polyposis.

Adenomatous Polyposis Coli↗
PubMed2005

Is 24-hour urinary calcium a surrogate marker for dietary calcium intake?

OBJECTIVES: To determine whether the 24-hour urinary excretion of calcium was a reliable surrogate marker for dietary calcium intake. Although dietary calcium intake has been negatively correlated with the risk of recurrent calcium-based stones, detailed dietary histories are not routinely evaluated in most patients with recurrent stone formation. METHODS: The dietary records and corresponding 24-hour urine collections of 68 randomly selected women with a history of calcium-based renal stones and two or more outpatient clinic visits were studied. Subjects were excluded if they had conditions or took medications affecting calcium absorption or excretion. Multivariate regression analysis was performed on the most recent set of data per patient with 24-hour urinary calcium as the dependent variable. Independent variables included age, weight, and dietary calcium, sodium, potassium, magnesium, fiber, and animal protein. Regression analysis was performed on the differences between the first and last visits for dietary and urinary data. Using tertiles, the positive predictive value of 24-hour urinary calcium for the respective dietary intake tertiles was calculated. RESULTS: The regression model on absolute values showed all dietary parameters to have squared partial correlation coefficients of less than 0.3 (P = 0.015, R2 = 0.264). In the second regression analysis, the model did not significantly explain the variance (P = 0.656). The positive predictive value of a mean 24-hour urinary calcium level less than 3.75 mmol/L for calcium intake less than 585 mg/day was 45%. CONCLUSIONS: The results of the present study revealed that the 24-hour urinary calcium cannot be used as a surrogate marker for dietary intake of calcium. A detailed dietary history is needed for all women with recurrent stone formation for proper assessment and potential modification of calcium intake to reduce recurrences.

Biomarkers↗
PubMed1990

Effect of dietary calcium and lead status on intestinal calcium absorption.

Dietary lead intake was demonstrated to result in two very different effects on intestinal calcium absorption and associated parameters, depending on dietary calcium status. Normal growing 14-day-old chicks were fed diets either low (0.05%) or adequate (1.2%) in calcium and containing varying levels of lead (0%-0.8%) for an additional 10 days. In chicks fed the low calcium diet, ingested lead inhibited intestinal 47Ca absorption, and intestinal calbindin D and alkaline phosphatase synthesis in a dose-dependent fashion. Even at the highest levels of lead, however, this inhibition was limited to the stimulation of these parameters by low dietary calcium. In chicks fed the normal calcium diet, lead exposure did not diminish intestinal 47Ca absorption, or calbindin D or alkaline phosphatase synthesis, but actually elevated the values of these parameters at the higher lead exposure levels. The results indicate that the primary effect of lead, in both cases, occurs at or prior to intestinal protein synthesis and most likely involves the cholecalciferol endocrine system rather than any direct interactions between lead and calcium at the intestinal level.

Alkaline Phosphatase↗
PubMed1995

Gastrointestinal calcium absorption and dietary calcium load: relationships with bone remodelling in vertebral osteoporosis.

Patients with vertebral osteoporosis have a wide range of bone loss rates, bone remodelling rates and capacities for gastrointestinal (GI) calcium absorption. To test the hypothesis that variations in GI absorptive capacity determine rates of bone loss or remodelling, we have sought relationships between calcium absorption or vitamin D metabolite levels on the one hand and rates of cancellous and cortical bone loss (measured by serial quantitative computed tomography in the radius; n = 25) or indices of bone remodelling in tetracycline-prelabelled transiliac biopsies (n = 41) on the other, in a sequential untreated group. Calcium absorption (net and true) was measured in 18-day balances and by a two-isotope deconvolution method (fractional absorption and maximum absorption rate, MAR). There was no significant seasonal effect on any of these four measures of calcium absorption (variance ratio, F = 0.52-1.61, p > 0.1) or on 1,25-dihydroxyvitamin D levels (F = 0.13, p > 0.1; range 11-69 pg/ml), notwithstanding the expected seasonal effect on 25-hydroxyvitamin D levels (mean 18.7 ng/ml, zenith mid July, semi-amplitude 7.5 ng/ml; F = 6.82, p < 0.01). Neither this metabolite nor 1,25-dihydroxyvitamin D correlated with any index of calcium absorption (p > 0.1). No measure of calcium absorption (or intake) had a significant relationship with radial cortical or cancellous bone loss (p all > 0.1) but cancellous bone loss was associated with the rate of endogenous calcium excretion (r = 0.50, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1986

Dietary calcium intake in rural black South African children. The relationship between calcium intake and calcium nutritional status.

Dietary calcium intake in relation to calcium status in rural black South African children was investigated. Fifteen subjects in each age group, 3-5 years, 8-10 years, 13-16 years with lowered serum calcium (less than 2.25 mmol/l) and raised serum alkaline phosphatase (greater than 300 i.u./l) were matched with controls having normal serum biochemistry. A dietary interview and 24-h recall was conducted with each subject; nutrient value of the diet was calculated from standard food tables. At 3-5 years, although the study group had significantly lower calcium intakes, there was no significant relationship between dietary calcium intake and calcium status. Study children in the age groups 8-10 years and 13-16 years had significantly lower dietary calcium intakes than controls and dietary calcium intake showed significant correlation with serum calcium levels, serum alkaline phosphatase levels, bone mineral density, metacarpal cortical thickness and calcium excretion. Thus it appears that low dietary calcium intakes may be reflected by hypocalcaemia, elevated alkaline phosphatase and decreased bone mineral content in pre-adolescent children.

Adolescent↗
PubMed1990

Bone mineral density in spontaneous hypertension: differential effects of dietary calcium and sodium.

Dietary calcium and sodium have been postulated to modify both bone mineral status and blood pressure regulation in humans and animals. The spontaneously hypertensive rat (SHR) manifests several defects in calcium metabolism that may contribute to its hypertension. Blood pressure and bone mineral status were measured in SHR and normotensive Wistar-Kyoto rats (WKY) as a marker of whole animal calcium metabolism. In addition, the effect of alterations in dietary calcium and sodium on bone status were examined. At 6 weeks of age, seven male SHR and seven male WKY were placed on a control diet. At the same age, 28 SHR and 28 WKY were randomized to four diets containing either 2.0% or 0.1% calcium and 1.0% or 0.25% sodium. Four markers of bone mineral status were analyzed: bone density measured by direct photon absorptiometry, and total bone calcium, phosphorus, and magnesium content measured by atomic absorption spectrophotometry. The SHR exhibited significantly lower levels (p less than 0.001) of bone density and bone magnesium content than the WKY, whereas bone phosphorus and calcium did not differ between the two strains. The 2.0% calcium diets resulted in increased bone density and bone calcium content, and lower bone magnesium in both strains. The 1.0% sodium diets were associated with decreased bone density in the SHR, but not in the WKY. These findings identify another indicator of disturbed calcium metabolism in the SHR that may be related to impaired renal calcium handling. They are consistent with previously reported reductions in renal calcium reabsorption and decreased intestinal calcium transport in older SHR.

Animals↗