Supplemental Calcium Intake Research Articles

Calcium intake and mortality from all causes, cancer, and cardiovascular disease: the Cancer Prevention Study II Nutrition Cohort

AbstractBackground: Calcium intake may be important for bone health, but its effects on other outcomes, including cardiovascular disease (CVD) and cancer, remain unclear. Recent reports of adverse cardiovascular effects of supplemental calcium have raised concerns.Objective: We investigated associations of supplemental, dietary, and total calcium intakes with all-cause, CVD-specific, and cancer-specific mortality in a large, prospective cohort.Design: A total of 132,823 participants in the Cancer Prevention Study II Nutrition Cohort, who were followed from baseline (1992 or 1993) through 2012 for mortality outcomes, were included in the analysis. Dietary and supplemental calcium information was first collected at baseline and updated in 1999 and 2003. Multivariable-adjusted Cox proportional hazards models with cumulative updating of exposures were used to calculate RRs and 95% CIs for associations between calcium intake and mortality.Results: During a mean follow-up of 17.5 y, 43,186 deaths occurred. For men, supplemental calcium intake was overall not associated with mortality outcomes (P-trend > 0.05 for all), but men who were taking ≥1000 mg supplemental calcium/d had a higher risk of all-cause mortality (RR: 1.17; 95% CI: 1.03, 1.33), which was primarily attributed to borderline statistically significant higher risk of CVD-specific mortality (RR: 1.22; 95% CI: 0.99, 1.51). For women, supplemental calcium was inversely associated with mortality from all causes [RR (95% CI): 0.90 (0.87, 0.94), 0.84 (0.80, 0.88), and 0.93 (0.87, 0.99) for intakes of 0.1 to <500, 500 to <1000, and ≥1000 mg/d, respectively; P-trend < 0.01]. Total calcium intake was inversely associated with mortality in women (P-trend < 0.01) but not in men; dietary calcium was not associated with all-cause mortality in either sex.Conclusions: In this cohort, associations of calcium intake and mortality varied by sex. For women, total and supplemental calcium intakes are associated with lower mortality, whereas for men, supplemental calcium intake ≥1000 mg/d may be associated with higher all-cause and CVD-specific mortality.

Milk-alkali syndrome secondary to the intake of calcium supplements

Milk-alkali syndrome secondary to the intake of calcium supplements

Calcium supplementation for the prevention of colorectal adenomas: A systematic review and meta-analysis of randomized controlled trials.

To determine the efficacy of calcium supplementation in reducing the recurrence of colorectal adenomas. We conducted a systematic review and meta-analysis of published studies. We searched PubMed, Scopus, the Cochrane Library, the WHO International Clinical Trials Registry Platform, and the ClinicalTrials.gov website, through December 2015. Randomized, placebo-controlled trials assessing supplemental calcium intake for the prevention of recurrence of adenomas were eligible for inclusion. Two reviewers independently selected studies based on predefined criteria, extracted data and outcomes (recurrence of colorectal adenomas, and advanced or "high-risk" adenomas), and rated each trial's risk-of-bias. Between-study heterogeneity was assessed, and pooled risk ratio (RR) estimates with their 95% confidence intervals (95%CI) were calculated using fixed- and random-effects models. To express the treatment effect in clinical terms, we calculated the number needed to treat (NNT) to prevent one adenoma recurrence. We also assessed the quality of evidence using GRADE. Four randomized, placebo-controlled trials met the eligibility criteria and were included. Daily doses of elemental calcium ranged from 1200 to 2000 mg, while the duration of treatment and follow-up of participants ranged from 36 to 60 mo. Synthesis of intention-to-treat data, for participants who had undergone follow-up colonoscopies, indicated a modest protective effect of calcium in prevention of adenomas (fixed-effects, RR = 0.89, 95%CI: 0.82-0.96; random-effects, RR = 0.87, 95%CI: 0.77-0.98; high quality of evidence). The NNT was 20 (95%CI: 12-61) to prevent one colorectal adenoma recurrence within a period of 3 to 5 years. On the other hand, the association between calcium treatment and advanced adenomas did not reach statistical significance (fixed-effects, RR = 0.92, 95%CI: 0.75-1.13; random-effects, RR = 0.92, 95%CI: 0.71-1.18; moderate quality of evidence). Our results suggest a modest chemopreventive effect of calcium supplements against recurrent colorectal adenomas over a period of 36 to 60 mo. Further research is warranted.

Nephrolithiasis and Risk of Incident Bone Fracture

Higher urine calcium is a common feature of calcium nephrolithiasis and may be associated with lower bone mineral density in individuals with kidney stones. However previous population based studies of kidney stones and the risk of bone fracture demonstrate conflicting results. We examined independent associations between a history of kidney stones and incident fracture. We performed prospective studies using data from the Nurses' Health Study of 107,001 women with 32 years of followup and the Health Professionals Follow-up Study of 50,982 men with 26 years of followup. We excluded premenopausal women, men younger than 45 years and individuals who reported osteoporosis at baseline. Study outcomes were incident wrist (distal radius) or incident hip (proximal femur) fracture due to low or moderate trauma. Cox proportional hazards regression was used to adjust for multiple factors, including age, race, body mass index, thiazide use, supplemental calcium and dietary intakes. There were 4,940 wrist and 2,391 hip fractures in women, and 862 wrist and 747 hip fractures in men. All fractures were incident. The multivariable adjusted relative risk of incident wrist fracture in participants with a history ofkidney stones compared to participants without kidney stones was 1.18 (95%CI1.04-1.34) in women and 1.21 (95% CI 1.00-1.47) in men. The pooled multivariable adjusted relative risk of wrist fracture was 1.20 (95% CI1.08-1.33). The multivariable adjusted relative risk of incident hip fracture in participants with kidney stones was 0.96 (95% CI 0.80-1.14) in women and 0.92(95% CI 0.74-1.14) in men. The pooled multivariable adjusted relative risk of hip fracture was 0.94 (95% CI 0.82-1.08). Nephrolithiasis is associated with a significantly higher risk of incident wrist but not hip fracture in women and men.

Abstract 1887: Calcium intake and milk product consumption in association with risk for colorectal adenomas

Abstract Calcium intake has been consistently, albeit modestly associated with lower risk of colorectal cancer and adenomas, and supplemental calcium reduced adenoma recurrence in large randomized controlled trials. Milk-based dairy products are the major source of dietary calcium in the US, but the association between milk product consumption and colorectal cancer is unclear. Conventionally produced milk contains significant levels of insulin-like growth factor 1 (IGF-1) from the use of bovine somatotropin hormone. Calcium intake has been positively associated with IGF-1 and IGF-1 binding protein 3 (IGFBP-3) levels. Higher circulating levels of IGF-1 and the IGF-1:IGFBP-3 ratio have been associated with higher risk of certain cancers, including breast, prostate, and colorectal, as well as with adenomatous polyps. To investigate associations of calcium and milk product intakes with risk for colorectal neoplasms, we pooled data from three colonoscopy-based case-control studies of incident, sporadic colorectal adenoma (n = 786 cases, 2,020 controls) conducted between 1991 and 2002, and analyzed the data using multivariable unconditional logistic regression. Dietary and supplemental intakes in all three studies were assessed using Willett food frequency questionnaires. For indirect indicators of IGF-1 intake from milk products, dietary calcium-adjusted residuals were calculated for total milk products and non-fat milk. For total, dietary, and supplemental calcium intakes, the multivariable-adjusted odds ratios (ORs) comparing the highest to the lowest quintiles of intake were 0.87 (95% confidence interval [CI] 0.63-1.20), 0.91 (95% CI 0.65-1.28), and 0.96 (95% CI 0.70-1.31), respectively. The corresponding ORs for consumption of total milk products, total milk, non-fat milk, total milk product residuals, and non-fat milk residuals were, 1.01 (95% CI 0.74-1.36), 0.97 (95% CI 0.73-1.29), 0.95 (95% CI 0.71-1.25), 0.92 (95% CI 0.70-1.22), and 0.97 (95% CI 0.70-1.34), respectively. For those who consumed any whole milk relative to those who consumed none, the OR was 1.15 (95% CI 0.89-1.50). These results are consistent with previous findings of modestly lower risk with higher total (dietary plus supplemental) calcium intakes, but suggest that neither the consumption of specific milk products nor all milk products combined, nor the non-calcium components of milk products are associated with risk for sporadic colorectal adenoma. Citation Format: Caroline Um, Veronika Fedirko, W Dana Flanders, Roberd M. Bostick. Calcium intake and milk product consumption in association with risk for colorectal adenomas. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1887. doi:10.1158/1538-7445.AM2015-1887

Intakes of magnesium, potassium, and calcium and the risk of stroke among men.

Intakes of magnesium, potassium, and calcium have been inversely associated with the incidence of hypertension, a known risk factor for stroke. However, only a few studies have examined intakes of these cations in relation to risk of stroke. The aim of this study was to investigate whether high intake of magnesium, potassium, and calcium is associated with reduced stroke risk among men. We prospectively examined the associations between intakes of magnesium, potassium, and calcium from diet and supplements, and the risk of incident stroke among 42 669 men in the Health Professionals Follow-up Study, aged 40 to 75 years and free of diagnosed cardiovascular disease and cancer at baseline in 1986. We calculated the hazard ratio of total, ischemic, and haemorrhagic strokes by quintiles of each cation intake, and of a combined dietary score of all three cations, using multivariate Cox proportional hazard models. During 24 years of follow-up, 1547 total stroke events were documented. In multivariate analyses, the relative risks and 95% confidence intervals of total stroke for men in the highest vs. lowest quintile were 0·87 (95% confidence interval, 0·74-1·02; P, trend = 0·04) for dietary magnesium, 0·89 (95% confidence interval, 0·76-1·05; P, trend = 0·10) for dietary potassium, and 0·89 (95% confidence interval, 0·75-1·04; P, trend = 0·25) for dietary calcium intake. The relative risk of total stroke for men in the highest vs. lowest quintile was 0·74 (95% confidence interval, 0·59-0·93; P, trend = 0·003) for supplemental magnesium, 0·66 (95% confidence interval, 0·50-0·86; P, trend = 0·002) for supplemental potassium, and 1·01 (95% confidence interval, 0·84-1·20; P, trend = 0·83) for supplemental calcium intake. For total intake (dietary and supplemental), the relative risk of total stroke for men in the highest vs. lowest quintile was 0·83 (95% confidence interval, 0·70-0·99; P, trend = 0·04) for magnesium, 0·88 (95% confidence interval, 0·75-4; P, trend = 6) for potassium, and 3 (95% confidence interval, 79-09; P, trend = 84) for calcium. Men in the highest quintile for a combined dietary score of all three cations had a multivariate relative risk of 0·79 (95% confidence interval, 0·67-0·92; P, trend = 0·008) for total stroke, compared with those in the lowest. A diet rich in magnesium, potassium, and calcium may contribute to reduced risk of stroke among men. Because of significant collinearity, the independent contribution of each cation is difficult to define.

Total, dietary, and supplemental calcium intake and mortality from all-causes, cardiovascular disease, and cancer: A meta-analysis of observational studies

AimsThis systematic review and meta-analysis of observational studies was conducted to summarize the evidence on the association between calcium intake and mortality. Methods and resultsPubMed, Institute for Scientific Information (ISI) (Web of Science), SCOPUS, SciRUS, Google Scholar, and Excerpta Medica dataBASE (EMBASE) were searched to identify related articles published through May 2014. We found 22 articles that assessed the association between total, dietary, and supplementary intake with mortality from all-causes, cardiovascular disease (CVD), and cancer. Findings from this meta-analysis revealed no significant association between total and dietary calcium intake and mortality from all-causes, CVD, and cancer. Subgroup analysis by the duration of follow-up revealed a significant positive association between total calcium intake and CVD mortality for cohort studies with a mean follow-up duration of >10 years (relative risk (RR): 1.35; 95% confidence interval (CI): 1.09–1.68). A significant inverse association was seen between dietary calcium intake and all-cause (RR: 0.84; 95% CI: 0.70–1.00) and CVD mortality (RR: 0.88; 95% CI: 0.78–0.99) for studies with a mean follow-up duration of ≤10 years. Although supplemental calcium intake was not associated with CVD (RR: 0.95; 95% CI: 0.82–1.10) and cancer mortality (RR: 1.22; 95% CI: 0.81–1.84), it was inversely associated with the risk of all-cause mortality (RR: 0.91; 95% CI: 0.88–0.94). ConclusionsWe found a significant relationship between the total calcium intake and an increased risk of CVD mortality for studies with a long follow-up time and a significant protective association between dietary calcium intake and all-cause and CVD mortality for studies with a mean follow-up of ≤10 years. Supplemental calcium intake was associated with a decreased risk of all-cause mortality.

Vitamin D and parathyroid hormone status in a representative population living in Macau, China

Associations between documented sun-exposure, exercise patterns and fish and supplement intake and 25-hydroxyvitamin D (25OHD) and parathyroid hormone (PTH) were investigated in a random household survey of Macau residents (aged 18–93). Blood samples (566) taken in summer were analyzed for 25OHD and PTH.In this Chinese population, 55% were deficient (25OHD <50nmol/L: median (interquartile range)=47.7 (24.2) nmol/L). Vitamin D deficiency was greatest in those aged <50 years: median (interquartile range)=43.3 (18.2) nmol/L, females: median (interquartile range)=45.5 (19.4) nmol/L and those with higher educational qualifications: median (interquartile range)=43.1 (18.7) nmol/L.In the total Macau population, statistically significant (p<0.01) modifiable associations with lower 25OHD levels were sunlight exposure (β=0.06), physical activity (PA) (measured as hours(hrs)/day: β=0.08), sitting (measured as hrs/day β=−0.20), intake of fish (β=0.08) and calcium (Ca) supplement intake (β=0.06) [linear regression analysis adjusting for demographic risk factors]. On similar analysis, and after adjustment for 25OHD, the only significant modifiable associations in the total population with PTH were sitting (β=−0.17), Body Mass Index (β=0.07) and Ca supplement intake (β=−0.06).In this Macau population less documented sun exposure, fish and Ca supplement intake and exercise were associated with lower 25OHD levels, especially in the younger population, along with the interesting finding that more sitting was associated with both lower 25OHD and high PTH blood levels.In conclusion, unlike findings from Caucasian populations, younger participants were significantly more vitamin D deficient, in particular highly educated single females. This may indicate the desire of young females to be pale and avoid the sun. There are also big differences in lifestyle between the older generation and the younger, in particular with respect to sun exposure and PA.This article is part of a Special Issue entitled '17th Vitamin D Workshop'.

Determinants of aortic bioprosthetic valve calcification assessed by multidetector CT

BackgroundCusp calcification is the main mechanism leading to bioprosthetic heart valve (BPV) failure. Recent studies suggest that BPV calcification is an active rather than passive process probably modulated by several...

Dairy products, calcium, and prostate cancer risk: a systematic review and meta-analysis of cohort studies

Dairy product and calcium intakes have been associated with increased prostate cancer risk, but whether specific dairy products or calcium sources are associated with risk is unclear. In the Continuous Update Project, we conducted a meta-analysis of prospective studies on intakes of dairy products and calcium and prostate cancer risk. PubMed and several other databases were searched up to April 2013. Summary RRs were estimated by using a random-effects model. Thirty-two studies were included. Intakes of total dairy products [summary RR: 1.07 (95% CI: 1.02, 1.12; n = 15) per 400 g/d], total milk [summary RR: 1.03 (95% CI: 1.00, 1.07; n = 14) per 200 g/d], low-fat milk [summary RR: 1.06 (95% CI: 1.01, 1.11; n = 6) per 200 g/d], cheese [summary RR: 1.09 (95% CI: 1.02, 1.18; n = 11) per 50 g/d], and dietary calcium [summary RR: 1.05 (95% CI: 1.02, 1.09; n = 15) per 400 mg/d] were associated with increased total prostate cancer risk. Total calcium and dairy calcium intakes, but not nondairy calcium or supplemental calcium intakes, were also positively associated with total prostate cancer risk. Supplemental calcium was associated with increased risk of fatal prostate cancer. High intakes of dairy products, milk, low-fat milk, cheese, and total, dietary, and dairy calcium, but not supplemental or nondairy calcium, may increase total prostate cancer risk. The diverging results for types of dairy products and sources of calcium suggest that other components of dairy rather than fat and calcium may increase prostate cancer risk. Any additional studies should report detailed results for subtypes of prostate cancer.

No evidence of gene-calcium interactions from genome-wide analysis of colorectal cancer risk.

Calcium intake may reduce risk of colorectal cancer, but the mechanisms remain unclear. Studies of interaction between calcium intake and SNPs in calcium-related pathways have yielded inconsistent results. To identify gene-calcium interactions, we tested interactions between approximately 2.7 million SNPs across the genome with self-reported calcium intake (from dietary or supplemental sources) in 9,006 colorectal cancer cases and 9,503 controls of European ancestry. To test for multiplicative interactions, we used multivariable logistic regression and defined statistical significance using the conventional genome-wide α = 5E-08. After accounting for multiple comparisons, there were no statistically significant SNP interactions with total, dietary, or supplemental calcium intake. We found no evidence of SNP interactions with calcium intake for colorectal cancer risk in a large population of 18,509 individuals. These results suggest that in genome-wide analysis common genetic variants do not strongly modify the association between calcium intake and colorectal cancer in European populations.

Calcium intake and colorectal adenoma risk: Dose‐response meta‐analysis of prospective observational studies

Evidence from randomized controlled trials suggests that calcium may protect against recurrence of colorectal adenomas, which could lead to the subsequent prevention of cancer. Yet the trials used only a large single dose and were of small sizes, and thus, knowledge of the dose-response relationship and influence on high-risk adenomas is limited. To address these issues, we conducted linear and nonlinear dose-response meta-analyses primarily based on prospective observational studies published up to July 2014 identified from PubMed and Embase. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated for total and supplemental calcium intake, respectively, using a random-effects model. For total calcium intake, summary RR for each 300 mg/day increase was 0.95 (95% CI = 0.92-0.98; I(2) = 45%; eight studies with 11,005 cases; range of intake = 333-2,229 mg/day). Evidence of nonlinearity was indicated: approximately, compared to 550 mg/day of total calcium intake, the summary RR was 0.92 (95% CI = 0.89-0.94) at 1,000 mg/day and 0.87 (95% CI = 0.84-0.90) at 1,450 mg/day (pnonlinearity < 0.01). Associations were stronger for high-risk adenomas (≥1 cm in diameter, (tubulo)villous histology, dysplasia, or multiplicity): approximately, compared to 550 mg/day of total calcium intake, the summary RR was 0.77 (95% CI = 0.74-0.81) at 1,000 mg/day and reduced to 0.69 (95% CI = 0.66-0.73) at 1,450 mg/da (pnonlinearity < 0.01). For supplemental calcium intake, summary RR of total adenoma risk for each 300 mg/day increase was 0.96 (95% CI = 0.93-0.99; I(2) = 0%; three studies with 4,548 cases; range of supplementation = 0-1,366 mg/day). In conclusion, calcium intake may continue to decrease the risk of adenomas, particularly high-risk adenomas, over a wide range of calcium intake.

Making sense of dietary calcium and urinary stone disease.

The regulation of dietary and supplemental calcium intake in relation to urinary stone disease is not well understood (1). For instance, why do most patients with primary hyperparathyroidism with markedly increased serum and urinary calcium not have a history of urinary stone disease?

Calcium supplement intake and risk of cardiovascular disease in women.

Some recent reports suggest that calcium supplement use may increase risk of cardiovascular disease. In a prospective cohort study of 74,245 women in the Nurses' Health Study with 24 years of follow-up, we found no independent associations between supplemental calcium intake and risk of incident coronary heart disease (CHD) and stroke. Some recent reports suggest that calcium supplements may increase cardiovascular disease (CVD) risk. The objective was to examine the independent associations between calcium supplement use and risk of CVD. We conducted a prospective cohort study of supplemental calcium use and incident CVD in 74,245 women in the Nurses' Health Study (1984-2008) free of CVD and cancer at baseline. Calcium supplement intake was assessed every 4 years. Outcomes were incident CHD (nonfatal or fatal MI) and stroke (ischemic or hemorrhagic), confirmed by medical record review. During 24 years of follow-up, 4,565 cardiovascular events occurred (2,709 CHD and 1,856 strokes). At baseline, women who took calcium supplements had higher levels of physical activity, smoked less, and had lower trans fat intake compared with those who did not take calcium supplements. After multivariable adjustment for age, body mass index, dietary calcium, vitamin D intake, and other CVD risk factors, the relative risk of CVD for women taking >1,000 mg/day of calcium supplements compared with none was 0.82 (95% confidence interval [CI] 0.74 to 0.92; p for trend <0.001). For women taking >1,000 mg/day of calcium supplements compared with none, the multivariable-adjusted relative risk for CHD was 0.71 (0.61 to 0.83; p for trend < 0.001) and for stroke was 1.03 (0.87 to 1.21; p for trend = 0.61). The relative risks were similar in analyses limited to non-smokers, women without hypertension, and women who had regular physical exams. Our findings do not support the hypothesis that calcium supplement intake increases CVD risk in women.

Calcium intake and colorectal cancer risk: Dose-response meta-analysis of prospective observational studies

Mechanistic and epidemiologic studies provide considerable evidence for a protective association between calcium intake and incident colorectal cancer (CRC). While the relationship has not been substantiated by short-duration randomized controlled trials (RCTs) of CRC, trials do show a benefit on adenomas, a precursor to CRC. To address some of this inconsistency, we conducted dose-response meta-analyses by sources of calcium intake, based on prospective observational studies published up to December 2013 identified from PubMed, Embase, and BIOSIS. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using a random-effects model. For total calcium intake, each 300 mg/day increase was associated with an approximately 8% reduced risk of CRC (summary RR = 0.92, 95% CI = 0.89-0.95, I(2) = 47%, 15 studies with 12,305 cases, intake = 250-1,900 mg/day, follow-up = 3.3-16 years). While the risk decreased less steeply in higher range of total calcium intake (P(non-linearity) = 0.04), the degree of curvature was mild and statistical significance of non-linearity was sensitive to one study. For supplementary calcium, each 300 mg/day increase was associated with an approximately 9% reduced risk of CRC (summary RR = 0.91, 95% CI = 0.86-0.98, I(2) = 67%, six studies with 8,839 cases, intake = 0-1,150 mg/day, follow-up = 5-10 years). The test for non-linearity was not statistically significant (P(non-linearity) = 0.11). In conclusion, both dietary and supplementary calcium intake may continue to decrease CRC risk beyond 1,000 mg/day. Calcium supplements and non-dairy products fortified with calcium may serve as additional targets in the prevention of CRC. RCTs of calcium supplements with at least 10 years of follow-up are warranted to confirm a benefit of calcium supplements on CRC risk.

Calcium Supplements and Cardiovascular Disease: A Review.

Dietary or supplemental calcium intake has long been encouraged for optimal bone health. However, more recently, the safety of calcium supplementation has been questioned because of a possible association between supplemental calcium and cardiovascular risk. Whereas calcium may have a beneficial or neutral effect on cardiovascular risk factors such as blood pressure, cholesterol, weight, and diabetes, available evidence does not provide a definitive answer for an association with cardiovascular disease (CVD). To date, no calcium trials have studied cardiovascular disease as a primary end point, and larger trials with longer follow-up are needed. In this review, we present results from observational studies and randomized controlled trials (RCTs) that have evaluated calcium intake (dietary or supplemental) in relation to cardiovascular risk factors and cardiovascular disease as a secondary outcome. Results from RCTs are mixed regarding CVD risk in those using supplemental calcium with or without vitamin D, and more large-scale randomized trials designed specifically with CVD as the primary end point are needed. Evidence suggests that it is reasonable to encourage adequate dietary calcium intake, especially for postmenopausal women who are at greatest risk for osteoporotic fracture.

Vitamin D supplementation, body weight and human serum 25-hydroxyvitamin D response: a systematic review

There is considerable variation in incremental circulating 25-hydroxyvitamin D (25OHD) levels on vitamin D supplements, even when similar age groups and identical vitamin D doses are compared. We therefore aimed to investigate the importance of body weight for the dose-response relation in circulating 25OHD. We performed a systematic review of randomized placebo-controlled vitamin D supplementation trials in all age groups ≥10 years to clarify the influence of body weight and other parameters on incremental circulating 25OHD levels (difference between baseline and in-study values) in vitamin D-deficient and non-deficient individuals. We included 144 cohorts from 94 independent studies, published from 1990 to November 2012, in our systematic review. There was a logarithmic association between vitamin D dose per kg body weight per day and increment in circulating 25OHD. In multivariable regression analysis, vitamin D dose per kg body weight per day could explain 34.5% of variation in circulating 25OHD. Additional significant predictors were type of supplement (vitamin D2 or vitamin D3), age, concomitant intake of calcium supplements and baseline 25OHD, explaining 9.8, 3.7, 2.4 and 1.9%, respectively, of the variation in circulating 25OHD. This systematic review demonstrates that body weight is an important predictor of variation in circulating 25OHD in cohorts on vitamin D supplements. Our model provides an estimate of the daily vitamin D dose that is necessary for achieving adequate circulating 25OHD levels in vitamin D-insufficient or vitamin D-deficient individuals/cohorts with different body weights and ages.

Dietary and Supplemental Calcium Intake and Mortality

Dietary and Supplemental Calcium Intake and Mortality

Dietary and Supplemental Calcium Intake and Mortality—Reply

Dietary and Supplemental Calcium Intake and Mortality—Reply

Dietary and Supplemental Calcium Intake and Mortality

Dietary and Supplemental Calcium Intake and Mortality