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Summary The Women's Health Initiative (WHI) double-blind, placebo-controlled clinical trial randomly assigned 36,282 postmenopausal women in the U.S. to 1,000 mg elemental calcium carbonate plus 400 IU of vitamin D 3 daily or placebo, with average intervention period of 7.0 years. The trial was designed to test whether calcium plus vitamin D supplementation in a population in which the use of these supplements was widespread would reduce hip fracture, and secondarily, total fracture and colorectal cancer. Introduction This study further examines the health benefits and risks of calcium and vitamin D supplementation using WHI data, with emphasis on fractures, cardiovascular disease, cancer, and total mortality. Methods WHI calcium and vitamin D randomized clinical trial (CT) data through the end of the intervention period were further analyzed with emphasis on treatment effects in relation to duration of supplementation, and these data were contrasted and combined with corresponding data from the WHI prospective observational study (OS). Results Among women not taking personal calcium or vitamin D supplements at baseline, the hazard ratio [HR] for hip fracture occurrence in the CT following 5 or more years of calcium and vitamin D supplementation versus placebo was 0.62 (95 % confidence interval (CI), 0.38–1.00). In combined analyses of CT and OS data, the corresponding HR was 0.65 (95 % CI, 0.44–0.98). Supplementation effects were not apparent on the risks of myocardial infarction, coronary heart disease, total heart disease, stroke, overall cardiovascular disease, colorectal cancer, or total mortality, while evidence for a reduction in breast cancer risk and total invasive cancer risk among calcium plus vitamin D users was only suggestive. Conclusion Though based primarily on a subset analysis, long-term use of calcium and vitamin D appears to confer a reduction that may be substantial in the risk of hip fracture among postmenopausal women. Other health benefits and risks of supplementation at doses considered, including an elevation in urinary tract stone formation, appear to be modest and approximately balanced.

The efficacy of calcium with vitamin D supplementation in preventing hip and other fractures in healthy postmenopausal women remains equivocal. In this Women's Health Initiative trial, 36,282 such women received calcium with vitamin D or placebo, with an average follow-up of seven years. Calcium with vitamin D supplementation moderately but significantly improved hip bone density, did not significantly reduce hip fracture, and increased the risk of kidney stones. In healthy postmenopausal women, calcium with vitamin D supplementation moderately but significantly improved hip bone density, did not significantly reduce hip fracture, and increased the risk of kidney stones. Osteoporosis, a major cause of injury, loss of independence, and death, 1 , 2 contributes to more than 300,000 hip fractures in the United States annually. 3 Observational evidence 4 and data from randomized clinical trials 5 , 6 suggest that calcium or vitamin D supplements or both may slow bone loss 5 , 6 and reduce the risk of falls 7 , 8 in postmenopausal and elderly women. However, evidence from trials, 5 , 9 – 19 observational studies, 20 , 21 and meta-analyses 6 , 22 , 23 of calcium and vitamin D supplementation with respect to hip and other fractures is limited. In two recent randomized trials, calcium plus vitamin D supplements (1000 mg of . . .

Ca supplements are used for bone health; however, they have been associated with increased cardiovascular risk, which may relate to their acute effects on serum Ca concentrations. Microcrystalline hydroxyapatite (MCH) could affect serum Ca concentrations less than conventional Ca supplements, but its effects on bone turnover are unclear. In the present study, we compared the acute and 3-month effects of MCH with conventional Ca supplements on concentrations of serum Ca, phosphate, parathyroid hormone and bone turnover markers. We randomised 100 women (mean age 71 years) to 1 g/d of Ca as citrate or carbonate (citrate–carbonate), one of two MCH preparations, or a placebo. Blood was sampled for 8 h after the first dose, and after 3 months of daily supplementation. To determine whether the acute effects changed over time, eight participants assigned to the citrate dose repeated 8 h of blood sampling at 3 months. There were no differences between the citrate and carbonate groups, or between the two MCH groups, so their results were pooled. The citrate–carbonate dose increased ionised and total Ca concentrations for up to 8 h, and this was not diminished after 3 months. MCH increased ionised Ca concentrations less than the citrate–carbonate dose; however, it raised the concentrations of phosphate and the Ca–phosphate product. The citrate–carbonate and MCH doses produced comparable decreases in bone resorption (measured as serum C-telopeptide (CTX)) over 8 h and bone turnover (CTX and procollagen type-I N-terminal propeptide) at 3 months. These findings suggest that Ca preparations, in general, produce repeated sustained increases in serum Ca concentrations after ingestion of each dose and that Ca supplements with smaller effects on serum Ca concentrations may have equivalent efficacy in suppressing bone turnover.

Supplemental calcium and vitamin D have been associated with a reduced risk of colorectal cancer in epidemiologic and polyp-prevention studies, but evidence from randomized trials was lacking. Although the long latency involved in colorectal cancer may be relevant, this Women's Health Initiative trial involving 36,282 postmenopausal women showed that daily calcium plus vitamin D supplementation for an average of seven years had no effect on the incidence of colorectal cancer. Although the long latency involved in colorectal cancer may be relevant, this trial involving postmenopausal women showed that daily calcium plus vitamin D supplementation for an average of seven years had no effect on the incidence of colorectal cancer. As the second leading cause of death from cancer in the United States, 1 colorectal cancer is the focus of considerable preventive effort. 2 Most observational studies have associated increased calcium and vitamin D intake with a decreased risk of colorectal cancer 3 – 6 and recurrent polyps. 7 , 8 Although the results are somewhat mixed, one pooled analysis of 10 cohort studies that assessed dietary consumption and total calcium intake (diet plus supplements) reported a reduction in the incidence of colorectal cancer of 10 to 15 percent, 9 whereas an earlier pooled analysis found no effect. 10 The suggestion that increased calcium intake helped prevent colorectal . . .

Ocean warming and acidification threaten the future growth of coral reefs. This is because the calcifying coral reef taxa that construct the calcium carbonate frameworks and cement the reef together are highly sensitive to ocean warming and acidification. However, the global-scale effects of ocean warming and acidification on rates of coral reef net carbonate production remain poorly constrained despite a wealth of studies assessing their effects on the calcification of individual organisms. Here, we present global estimates of projected future changes in coral reef net carbonate production under ocean warming and acidification. We apply a meta-analysis of responses of coral reef taxa calcification and bioerosion rates to predicted changes in coral cover driven by climate change to estimate the net carbonate production rates of 183 reefs worldwide by 2050 and 2100. We forecast mean global reef net carbonate production under representative concentration pathways (RCP) 2.6, 4.5, and 8.5 will decline by 76, 149, and 156%, respectively, by 2100. While 63% of reefs are projected to continue to accrete by 2100 under RCP2.6, 94% will be eroding by 2050 under RCP8.5, and no reefs will continue to accrete at rates matching projected sea level rise under RCP4.5 or 8.5 by 2100. Projected reduced coral cover due to bleaching events predominately drives these declines rather than the direct physiological impacts of ocean warming and acidification on calcification or bioerosion. Presently degraded reefs were also more sensitive in our analysis. These findings highlight the low likelihood that the world’s coral reefs will maintain their functional roles without near-term stabilization of atmospheric CO₂ emissions.

Patients with chronic kidney disease (CKD) are given calcium carbonate to bind dietary phosphorus, reduce phosphorus retention, and prevent negative calcium balance; however, data are limited on calcium and phosphorus balance during CKD to support this. Here, we studied eight patients with stage 3 or 4 CKD (mean estimated glomerular filtration rate 36ml/min) who received a controlled diet with or without a calcium carbonate supplement (1500mg/day calcium) during two 3-week balance periods in a randomized placebo-controlled cross-over design. All feces and urine were collected during weeks 2 and 3 of each balance period and fasting blood, and urine was collected at baseline and at the end of each week. Calcium kinetics were determined using oral and intravenous 45calcium. Patients were found to be in neutral calcium and phosphorus balance while on the placebo. Calcium carbonate supplementation produced positive calcium balance, did not affect phosphorus balance, and produced only a modest reduction in urine phosphorus excretion compared with placebo. Calcium kinetics demonstrated positive net bone balance but less than overall calcium balance, suggesting soft-tissue deposition. Fasting blood and urine biochemistries of calcium and phosphate homeostasis were unaffected by calcium carbonate. Thus, the positive calcium balance produced by calcium carbonate treatment within 3 weeks cautions against its use as a phosphate binder in patients with stage 3 or 4 CKD, if these findings can be extrapolated to long-term therapy.

Amorphous calcium carbonate (ACC) is a metastable phase often observed during low temperature inorganic synthesis and biomineralization. ACC transforms with aging or heating into a less hydrated form, and with time crystallizes to calcite or aragonite. The energetics of transformation and crystallization of synthetic and biogenic (extracted from California purple sea urchin larval spicules, Strongylocentrotus purpuratus) ACC were studied using isothermal acid solution calorimetry and differential scanning calorimetry. Transformation and crystallization of ACC can follow an energetically downhill sequence: more metastable hydrated ACC → less metastable hydrated ACC ⇒ anhydrous ACC ∼ biogenic anhydrous ACC ⇒ vaterite → aragonite → calcite. In a given reaction sequence, not all these phases need to occur. The transformations involve a series of ordering, dehydration, and crystallization processes, each lowering the enthalpy (and free energy) of the system, with crystallization of the dehydrated amorphous material lowering the enthalpy the most. ACC is much more metastable with respect to calcite than the crystalline polymorphs vaterite or aragonite. The anhydrous ACC is less metastable than the hydrated, implying that the structural reorganization during dehydration is exothermic and irreversible. Dehydrated synthetic and anhydrous biogenic ACC are similar in enthalpy. The transformation sequence observed in biomineralization could be mainly energetically driven; the first phase deposited is hydrated ACC, which then converts to anhydrous ACC, and finally crystallizes to calcite. The initial formation of ACC may be a first step in the precipitation of calcite under a wide variety of conditions, including geological CO₂ sequestration.

Calcium carbonate formation is the primary pathway by which carbon is returned from the ocean–atmosphere system to the solid Earth 1 , 2 . The removal of dissolved inorganic carbon from seawater by precipitation of carbonate minerals—the marine carbonate factory—plays a critical role in shaping marine biogeochemical cycling 1 , 2 . A paucity of empirical constraints has led to widely divergent views on how the marine carbonate factory has changed over time 3 – 5 . Here we use geochemical insights from stable strontium isotopes to provide a new perspective on the evolution of the marine carbonate factory and carbonate mineral saturation states. Although the production of carbonates in the surface ocean and in shallow seafloor settings have been widely considered the predominant carbonate sinks for most of the history of the Earth 6 , we propose that alternative processes—such as porewater production of authigenic carbonates—may have represented a major carbonate sink throughout the Precambrian. Our results also suggest that the rise of the skeletal carbonate factory decreased seawater carbonate saturation states. Geochemical insights from a dataset of carbonate stable strontium isotopes suggest that porewater production of authigenic carbonates may have been an overlooked carbonate sink for much of Earth’s history.

Turning cast-off shells into nitrogen-rich chemicals would benefit economies and the environment, say Ning Yan and Xi Chen.

Elevated serum phosphorus and calcium are associated with arterial calcification and mortality in dialysis patients. Unlike calcium-based binders, sevelamer attenuates arterial calcification but it is unknown whether sevelamer affects mortality or morbidity. In a multicenter, randomized, open-label, parallel design trial we compared sevelamer and calcium-based binders on all-cause and cause-specific mortality (cardiovascular, infection, and other) in prevalent hemodialysis patients. A total of 2103 patients were initially randomized to treatment and 1068 patients completed the study. All-cause mortality rates and cause-specific mortality rates were not significantly different. There was a significant age interaction on the treatment effect. Only in patients over 65 years of age was there a significant effect of sevelamer in lowering the mortality rate. There was a suggestion that sevelamer was associated with lower overall, but not cardiovascular-linked, mortality in older patients. We suggest that further research is needed to confirm these findings.