Dietary Calcium Intake Levels Research Articles

Dietary calcium intake in relation to metabolic syndrome in adults: A systematic review and dose-response meta-analysis of epidemiological studies with GRADE assessment.

Numerous studies have examined the relationship of calcium intake and metabolic syndrome (MetS) in adults in previous decades; but the results were inconsistent across different societies. This systematic review and dose-response meta-analysis assessed the relation between calcium consumption and MetS in adults. We did a systematic search of all articles published up to July 2023 in Scopus, PubMed/Medline, ISI Web of Science electronic databases, and Google Scholar. Observational studies investigated the association between dietary calcium (Ca) intake and MetS in adults were eligible to be included. For computing the estimates, a random effects model was applied. Combining 24 effect size from 17 investigations (15 cross-sectional and two cohort studies) with 74,720 participants and 18,200 cases showed that highest versus lowest level of dietary Ca intake was related to 23% significant decreased odds of MetS (OR = 0.77; 95% CI: 0.66, 0.89). Linear dose-response analysis of estimates from 12 investigations showed that each 100 mg/day increment in dietary Ca intake was associated with 3% marginally significant decreased odds in MetS (OR = 0.97; 95%CI: 0.93, 1.01). In nonlinear dose-response analysis of 12 studies with 67,896 participants, a significant association between dietary calcium intake and MetS was found (Pnonlinearity <0.001); such that 500 mg/day dietary calcium intake was related to maximum decrease in odds of MetS. According to this meta-analysis, the likelihood of MetS was significantly lower in adults with higher level of dietary calcium intake. Further large-scale prospective cohort investigations are needed to obtain stronger and more accurate results.

Dietary Calcium Intake and the Risk of Metabolic Syndrome: A Systematic Review and Meta-Analysis

Growing evidence has suggested a possible relationship between dietary calcium intake and metabolic syndrome (MetS) risk. However, the findings of these observational studies are inconclusive, and the dose-response association between calcium intake and risk of MetS remains to be determined. Here, we identified relevant studies by searching PubMed and Web of Science databases up to December 2018, and selected observational studies reporting relative risk (RR) with 95% confidence interval (CI) for MetS based on calcium intake and estimated the summary RRs using random-effects models. Eight cross-sectional and two prospective cohort studies totaling 63,017 participants with 14,906 MetS cases were identified. A significantly reduced risk of MetS was associated with the highest levels of dietary calcium intake (RR: 0.89; 95% CI: 0.80–0.99; I2 = 75.3%), with stronger association and less heterogeneity among women (RR: 0.74, 95% CI: 0.66–0.83; I2 = 0.0%) than among men (RR: 1.06, 95% CI: 0.82–1.37; I2 = 72.6%). Our dose-response analysis revealed that for each 300 mg/day increase in calcium intake, the risk of MetS decreased by 7% (RR: 0.93; 95% CI: 0.87–0.99; I2 = 77.7%). In conclusion, our findings suggest that dietary calcium intake may be inversely associated with the risk of MetS. These findings may have important public health implications with respect to preventing the disease. Further studies, in particular longitudinal cohort studies and randomized clinical trials, will be necessary to determine whether calcium supplementation is effective to prevent MetS.

Protective Effect of Dietary Calcium Intake on Esophageal Cancer Risk: A Meta-Analysis of Observational Studies.

Although several epidemiological studies have investigated the association between dietary calcium intake and the risk of esophageal cancer, the results are inconsistent. This study aimed to make a comprehensive evaluation regarding the association between calcium intake and risk of esophageal cancer through a meta-analysis approach. We searched for all relevant articles from the inception to April 2017, using PUBMED, EMBASE, and Web of Knowledge. The pooled odds ratio (ORs) with the 95% confidence interval (95% CI) for the highest versus the lowest categories of calcium intake was calculated using a Mantel–Haenszel fixed-effect model. In total, 15 articles reporting 17 studies including 3396 esophageal cancer cases and 346,815 controls were selected for the meta-analysis. By comparing the highest vs. the lowest levels of dietary calcium intake, we found that dietary calcium intake was inversely associated with the risk of esophageal cancer (OR = 0.80, 95% CI: 0.71–0.91, I2 = 33.6%). The subgroup analysis indicated that the protective function of dietary calcium intake were observed in esophageal squamous cell cancer, but not in esophageal adenocarcinoma in the studies conducted in Asia, but not those in Europe and America. In conclusion, our results suggest that higher dietary calcium intake is associated with a lower risk of esophageal cancer—especially esophageal squamous cell cancer—in Asian populations, though more data from prospective cohort studies are needed.

Dietary calcium intake and the risk of colorectal cancer: a case control study.

BackgroundHigh intake of dietary calcium has been thought to be a protective factor against colorectal cancer. To explore the dose-response relationship in the associations between dietary calcium intake and colorectal cancer risk by cancer location, we conducted a case-control study among Korean population, whose dietary calcium intake levels are relatively low.MethodsThe colorectal cancer cases and controls were recruited from the National Cancer Center in Korea between August 2010 and August 2013. Information on dietary calcium intake was assessed using a semi-quantitative food frequency questionnaire and locations of the colorectal cancers were classified as proximal colon cancer, distal colon cancer, and rectal cancer. Binary and polytomous logistic regression models were used to evaluate the association between dietary calcium intake and risk of colorectal cancer.ResultsA total of 922 colorectal cancer cases and 2766 controls were included in the final analysis. Compared with the lowest calcium intake quartile, the highest quartile group showed a significantly reduced risk of colorectal cancer in both men and women. (Odds ratio (OR): 0.16, 95 % confidence interval (CI): 0.11–0.24 for men; OR: 0.16, 95 % CI: 0.09–0.29 for women). Among the highest calcium intake groups, decrease in cancer risk was observed across all sub-sites of colorectum in both men and women.ConclusionIn conclusion, calcium consumption was inversely related to colorectal cancer risk in Korean population where national average calcium intake level is relatively lower than Western countries. A decreased risk of colorectal cancer by calcium intake was observed in all sub-sites in men and women.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1963-9) contains supplementary material, which is available to authorized users.

Impact of Calcium Intake Levels on Urinary and Fecal Losses of Sodium, Potassium and Magnesium

Understanding of mineral interactions remains incomplete. Minerals such as sodium, potassium, and magnesium are known to affect calcium absorption and/or excretion; however, there is little research on whether various levels of dietary calcium can impact balance of these minerals. The objective of this study was to determine how different dietary calcium intakes could potentially affect urinary and fecal excretion of potassium, sodium, and magnesium. Thirty‐seven boys aged 12‐15 y participated in 3‐wk metabolic balance studies testing a range (700‐2100 mg/d) of calcium intakes in a crossover study design with a 2‐wk washout period. All subjects were fed the same controlled diet with adjustments in calcium intake. Each boy received a high and a low calcium diet during separate trials. Calcium, potassium, sodium, and magnesium excretion in urine and feces was determined during the final two weeks of each trial period. As previously reported, significantly more calcium was excreted in the urine and feces during higher calcium intake. Fecal excretion of sodium excretion was greater (p &lt; 0.042) during lower calcium consumption. Urinary and fecal magnesium retention tended to be greater during higher calcium intake; however, the differences were significant (p &lt; 0.033) only for urinary losses. Varying levels of dietary calcium intake did not significantly affect urinary or fecal potassium losses. In summary, fecal sodium excretion was higher during lower calcium intake, and reduced urinary magnesium losses were observed with higher calcium intake.

Vitamin D Receptor and Calcium Sensing Receptor Polymorphisms and the Risk of Colorectal Cancer in European Populations

Increased levels of vitamin D and calcium may play a protective role in colorectal cancer (CRC) risk. It has been suggested that these effects may be mediated by genetic variants of the vitamin D receptor (VDR) and the calcium sensing receptor (CASR). However, current epidemiologic evidence from European populations for a role of these genes in CRC risk is scarce. In addition, it is not clear whether these genes may modulate CRC risk independently or by interaction with blood vitamin D concentration and level of dietary calcium intake. A case-control study was conducted nested within the European Prospective Investigation into Cancer and Nutrition. CRC cases (1,248) were identified and matched to 1,248 control subjects. Genotyping for the VDR (BsmI: rs1544410; Fok1: rs2228570) and CASR (rs1801725) genes was done by Taqman, and serum vitamin D (25OHD) concentrations were measured. Conditional logistic regression was used to estimate the incidence rate ratio (RR). Compared with the wild-type bb, the BB genotype of the VDR BsmI polymorphism was associated with a reduced risk of CRC [RR, 0.76; 95% confidence interval (CI), 0.59-0.98). The association was observed for colon cancer (RR, 0.69; 95% CI, 0.45-0.95) but not rectal cancer (RR, 0.97; 95% CI, 0.62-1.49). The Fok1 and CASR genotypes were not associated with CRC risk in this study. No interactions were noted for any of the polymorphisms with serum 25OHD concentration or level of dietary calcium. These results confirm a role for the BsmI polymorphism of the VDR gene in CRC risk, independent of serum 25OHD concentration and dietary calcium intake.

Studies of Gambian and UK children and adolescents: Insights into calcium requirements and adaptation to a low calcium intake

Currently there is concern about the low dietary calcium intakes common in some sub-groups of Western societies, including children and adolescents, and in many regions of the developing world. However, there is a lack of consensus about what level of dietary calcium intake will optimise bone health at different ages and in different environments. We have been conducting a series of studies in different populations to provide insights into calcium requirements and adaptation to a low calcium intake in different populations. These include calcium intervention studies among young people in Cambridge, an affluent university city in the UK and in Keneba, a poor rural village in The Gambia, West Africa. These studies have raised questions with implications for diet and nutrition policy including what aspects of bone growth and development need to be considered for the optimisation of skeletal health through diet, whether the influence of diet differs between the sexes and at different stages of childhood, and whether there are limitations to the adaptive response to a low calcium intake. Until we have a better understanding, our studies suggest that we should exercise caution before advocating higher population calcium intakes for children and adolescents than are currently recommended.

Dietary calcium intake and Renin Angiotensin System polymorphisms alter the blood pressure response to aerobic exercise: a randomized control design

BackgroundDietary calcium intake and the renin angiotensin system (RAS) regulate blood pressure (BP) by modulating calcium homeostasis. Despite similar BP regulatory effects, the influence of dietary calcium intake alone and combined with RAS polymorphisms on the BP response following acute aerobic exercise (i.e., postexercise hypotension) has not been studied. Thus, we examined the effect of dietary calcium intake and selected RAS polymorphisms on postexercise hypotension.MethodsSubjects were men (n = 50, 43.8 ± 1.3 yr) with high BP (145.3 ± 1.5/85.9 ± 1.1 mm Hg). They completed three experiments: non-exercise control and two cycle bouts at 40% and 60% of maximal oxygen consumption (VO2max). Subjects provided 3 d food records on five protocol-specific occasions. Dietary calcium intake was averaged and categorized as low (<880 mg/d = LowCa) or high (≥ 880 mg/d = HighCa). RAS polymorphisms (angiotensin converting enzyme insertion/deletion, ACE I/D; angiotensin II type 1 receptor, AT1R A/C) were analyzed with molecular methods. Genotypes were reduced from three to two: ACE II/ID and ACE DD; or AT1R AA and AT1R CC/AC. Repeated measure ANCOVA tested if BP differed among experiments, dietary calcium intake level and RAS polymorphisms.ResultsSystolic BP (SBP) decreased 6 mm Hg after 40% and 60% VO2max compared to non-exercise control for 10 h with LowCa (p < 0.01), but not with HighCa (p ≥ 0.05). Under these conditions, diastolic BP (DBP) did not differ between dietary calcium intake levels (p ≥ 0.05). With LowCa, SBP decreased after 60% VO2max versus non-exercise control for 10 h among ACE II/ID (6 mm Hg) and AT1R AA (8 mm Hg); and by 8 mm Hg after 40% VO2max among ACE DD and AT1R CC/CA (p < 0.01). With HighCa, SBP (8 mm Hg) and DBP (4 mm Hg) decreased after 60% VO2max compared to non-exercise control for 10 h (p < 0.05), but not after 40% VO2max (p ≥ 0.05).ConclusionSBP decreased after exercise compared to non-exercise control among men with low but not high dietary calcium intake. Dietary calcium intake interacted with the ACE I/D and AT1R A/C polymorphisms to further modulate postexercise hypotension. Interactions among dietary calcium intake, exercise intensity and RAS polymorphisms account for some of the variability in the BP response to exercise.

Sex steroids and the construction and conservation of the adult skeleton.

Here we review and extend a new unitary model for the pathophysiology of involutional osteoporosis that identifies estrogen (E) as the key hormone for maintaining bone mass and E deficiency as the major cause of age-related bone loss in both sexes. Also, both E and testosterone (T) are key regulators of skeletal growth and maturation, and E, together with GH and IGF-I, initiate a 3- to 4-yr pubertal growth spurt that doubles skeletal mass. Although E is required for the attainment of maximal peak bone mass in both sexes, the additional action of T on stimulating periosteal apposition accounts for the larger size and thicker cortices of the adult male skeleton. Aging women undergo two phases of bone loss, whereas aging men undergo only one. In women, the menopause initiates an accelerated phase of predominantly cancellous bone loss that declines rapidly over 4-8 yr to become asymptotic with a subsequent slow phase that continues indefinitely. The accelerated phase results from the loss of the direct restraining effects of E on bone turnover, an action mediated by E receptors in both osteoblasts and osteoclasts. In the ensuing slow phase, the rate of cancellous bone loss is reduced, but the rate of cortical bone loss is unchanged or increased. This phase is mediated largely by secondary hyperparathyroidism that results from the loss of E actions on extraskeletal calcium metabolism. The resultant external calcium losses increase the level of dietary calcium intake that is required to maintain bone balance. Impaired osteoblast function due to E deficiency, aging, or both also contributes to the slow phase of bone loss. Although both serum bioavailable (Bio) E and Bio T decline in aging men, Bio E is the major predictor of their bone loss. Thus, both sex steroids are important for developing peak bone mass, but E deficiency is the major determinant of age-related bone loss in both sexes.

Calcium and the risk for periodontal disease.

Dietary calcium has long been a candidate to modulate periodontal disease. Animal as well as human studies of calcium intake, bone mineral density, and tooth loss provide a rationale for hypothesizing that low dietary intake of calcium is a risk factor for periodontal disease. We evaluated the role of dietary calcium intake as a contributing risk factor for periodontal disease utilizing the Third National Health and Nutrition Examination Survey (NHANES III), which is representative of the U.S. civilian non-institutionalized population. Dietary calcium intake was determined from a 24-hour dietary recall. The U.S. Department of Agriculture Nutrient Database was used as a source of nutrient composition data. Periodontal disease was measured by attachment loss. In addition, serum calcium was assessed using venous blood samples. Logistic regression analysis was used to examine the association between periodontal disease and dietary calcium intake or serum calcium levels after adjusting for covariants including age, gender, tobacco consumption, and gingival bleeding. The association of lower dietary calcium intake with periodontal disease was found for young males and females (20 to 39 years of age), and for older males (40 to 59 years of age). The relationship between low dietary calcium intake and increased levels of periodontal disease showed an estimated odds ratio (OR) of 1.84 (95% CI: 1.36 to 2.48) for young males, 1.99 (95% CI: 1.34 to 2.97) for young females, and 1.90 (95% CI: 1.41 to 2.55) for the older group of males. These odds ratios were adjusted for gingival bleeding and tobacco consumption. The dose response was also seen in females, where there was 54% greater risk of periodontal disease for the lowest level of dietary calcium intake (2 to 499 mg) and 27% greater risk in females who took moderate levels of dietary calcium (500 to 799 mg) as compared to those who took 800 mg or more dietary calcium per day. A statistically significant association between low total serum calcium and periodontal disease was found in younger females aged 20 to 39 with OR = 6.11 (95% CI: 2.36 to 15.84) but not for males or older females, after adjusting for tobacco use, gingival bleeding, and dietary calcium intake. These results suggest that low dietary intake of calcium results in more severe periodontal disease. Further studies will be needed to better define the role of calcium in periodontal disease and to determine the extent to which calcium supplementation will modulate periodontal disease and tooth loss.

A unitary model for involutional osteoporosis: estrogen deficiency causes both type I and type II osteoporosis in postmenopausal women and contributes to bone loss in aging men.

We propose here a new unitary model for the pathophysiology of involutional osteoporosis that identifies estrogen (E) deficiency as the cause of both the early, accelerated and the late, slow phases of bone loss in postmenopausal women and as a contributing cause of the continuous phase of bone loss in aging men. The accelerated phase in women is most apparent during the first decade after menopause, involves disproportionate loss of cancellous bone, and is mediated mainly by loss of the direct restraining effects of E on bone cell function. The ensuing slow phase continues throughout life in women, involves proportionate losses of cancellous and cortical bone, and is associated with progressive secondary hyperparathyroidism. This phase is mediated mainly by loss of E action on extraskeletal calcium homeostasis which results in net calcium wasting and increases in the level of dietary calcium intake required to maintain bone balance. Because elderly men have low circulating levels of both bioavailable E and bioavailable testosterone (T) and because recent data suggest that E is at least as important as T in determining bone mass in aging men, E deficiency may also contribute substantially to the continuous bone loss of aging men. In both genders, E deficiency increases bone resorption and may also impair a compensatory increase in bone formation. For the most part, this unitary model is well supported by observational and experimental data and provides plausible explanations to traditional objections to a unitary hypothesis.

Effect of dietary electrolytes upon calcium excretion

To investigate the relations of dietary sodium, potassium, calcium and magnesium with urinary calcium excretion. Cross-sectional epidemiologic study of 417 Chinese men with a wide variation of electrolyte intakes. Three consecutive 24-h dietary recall data and three 24-h urinary samples were obtained on the same days. Urinary analyses included calcium, sodium, potassium, magnesium and creatinine. A fasting blood sample was obtained on the first morning, and serum analyses included electrolytes, creatinine and urea nitrogen. Correlation and regression analyses were used to examine the relation between electrolyte intake and calcium excretion. Whilst urinary calcium was not related to dietary calcium, it was significantly correlated with dietary sodium and potassium. A linear relationship was seen between dietary sodium, potassium and urinary calcium. After adjustment for age, body mass index, serum creatinine, dietary calcium intake and other electrolytes, urinary calcium was positively related to dietary sodium and negatively related to dietary potassium. This relation was seen at different levels of dietary calcium intake. The relation between magnesium intake and calcium excretion was inconsistent. These results suggest that sodium and potassium intake influence urinary calcium excretion in normotensive men.

Dietary Calcium Intake and Other Risk Factors

Osteoporosis has become a major health problem among the elderly in Hong Kong. This study compares the level of dietary calcium intake and the differences in various risk factors among elderly fracture patients and elderly without fractures. Furthermore, this study identifies the relationship between the risk factors and the amount of calcium intake; and classifies the fracture patients and the low calcium intake group. Although the design of the present study precludes testing causal hypotheses, the findings are suggestive of factors that are likely to be important in a program to reduce fractures among elderly populations.

Dietary calcium and chronic diseases

The Agricultural Revolution was almost certainly associated with a substantial decrease in human calcium intake. Calcium intakes typical of contemporary humans may well be inadequate for many individuals. Various slowly developing chronic disorders such as osteoporosis, hypertension, hyperlipidemia, and colon cancer may be induced or exaggerated by the current low level of dietary calcium intake in Western societies. We propose two hypotheses relating calcium intake to diverse diseases: first, the adaptation required to adjust to low intakes is inadequate to maintain critical components of cellular calcium regulation; second, the constant, forced adaptive response to low intake itself produces untoward consequences.

Calcium metabolism and hypertension

Returning to the patient presented today, perhaps we can now understand some of his findings. As I noted, men are more likely to demonstrate alterations in calcium metabolism associated with elevations in blood pressure. Furthermore, blacks are more likely than whites to develop hyperparathyroidism, particularly in the third and fourth decades of life. It is unlikely, however, that parathyroid hormone was responsible for the increase in this patient's arterial pressure because PTH has a vasodilating action. Moreover, the long-term response to parathyroidectomy is more likely to be an increase rather than a decrease in blood pressure. It is also unlikely that the mild elevations in the serum total calcium observed in this patient were responsible for his hypertension. Correction of hypercalcemia by surgical intervention failed to improve the blood pressure. There is little evidence that mild, protracted hypercalcemia can account for increases in arterial pressure. Finally, the patient's alcohol abuse might have contributed to his elevated blood pressure; it is possible that his hypertension was in part a reflection of the abnormal calcium metabolism he developed as a consequence of the alcohol abuse. Answers to some questions we faced when we first studied this patient more than a decade ago can be provided by the wealth of basic research and clinical investigation that has occurred since. We now know that calcium metabolism is a factor in blood pressure regulation in some humans and in some experimental models. Epidemiologic studies document a consistent association between lower dietary calcium intake and higher blood pressures in humans. An additional non-pharmacologic approach has been identified that can produce a modest but important lowering of blood pressure in a subset of hypertensive individuals. Much data show that calcium-regulating hormones have important cardiovascular actions that might account for some of the mechanisms by which increased dietary calcium lowers blood pressure. Research in this area also has set the stage for exploring another theoretical mechanism for sodium-chloride-sensitive hypertension. Finally, a theoretical mechanism(s) has emerged that could provide a pathophysiologic link between hypertension and certain high-risk populations such as blacks, the elderly, type-II diabetics, and pregnant women. The principal clinical implication derived from this work to date is the following: In patients with mild to moderate hypertension, the level of dietary calcium intake should be assessed. Patients whose intake is deficient should be encouraged simply to maintain calcium intake at 800 to 1000 mg/day.(ABSTRACT TRUNCATED AT 400 WORDS)

Calcium intake and the relationship of dietary sodium and potassium to blood pressure.

Using First National Health and Nutrition Examination Survey (NHANES I) data, we studied the relationships of dietary sodium, potassium, and alcohol to blood pressure in relation to levels of dietary calcium intake. At low Ca intakes (less than 400 mg/d for men and less than 800 mg/d for women) the ratio of Na to K (Na:K) was significantly related to blood pressure (p less than 0.01) after controlling for age, body mass index (BMI), race, and gender. At higher Ca intakes neither Na:K nor any other nutrient (with the exception of alcohol) was related to either systolic or diastolic blood pressures. Na:K was more strongly related to blood pressure than either nutrient alone and low Ca intakes were necessary for the Na:K-blood pressure relationship to be evident. Interaction of these three dietary factors in relation to blood pressure was evident in all race and gender groups. Associations of age, BMI, gender, and alcohol with blood pressure were not affected by Ca levels.

The effect of age and level of dietary calcium intake on calcium metabolism in sheep.

1. A combination of balance and isotope techniques has been used to study the effects of age and dietary calcium content on Ca metabolism in forty-two wether sheep.2. The amount of Ca absorbed by young growing animals varied significantly with intake. The percentage of the dietary Ca absorbed, however, remained unchanged. In older animals the amount of Ca absorbed was not altered by changes in intake, but decreased slightly with age.3. Retention of Ca was directly related to the amount of Ca absorbed and was independent of age or breed. Furthermore, nearly all the Ca absorbed above the minimum mean amount required for maintenance was retained.4. Faecal endogenous loss of Ca also was related to the amount of Ca absorbed. Values for faecal endogenous Ca were much lower than those used in the calculation of dietary require-ments by the Agricultural Research Council (1965).5. Urinary Ca excretion was variable, and was not related to age or changes in dietary Ca intake.6. Increased absorption of Ca in young growing animals was accompanied by a decreased rate of bone resorption, but the rate of bone accretion remained unchanged. Changes in dietary Ca in older animals had no effect on either of these two processes. Results indicate that bone resorption is the main pathway governing Ca homoeostasis. Both the rates of Ca accretion into bone and resorption from bone decreased with age.7. Neither the rapidly exchangeable Ca pool (P) nor the slowly exchangeable bone pool (E) was altered by changes in dietary intake in young or mature animals. Both, however, decreased in size with age.8. The size of the slowly exchangeable pool (E) was directly related to the rate of Ca accretion into bone. 9. The results were used to calculate dietary Ca requirements of sheep gaining weight at different rates, and these values have been compared with values recommended by the Agricultural Research Council (1965).