The Effects of 3 Years of Calcium Supplementation on Common Carotid Artery Intimal Medial Thickness and Carotid Atherosclerosis in Older Women: An Ancillary Study of the CAIFOS Randomized Controlled Trial

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Abstract

Calcium is an essential nutrient for skeletal health; however, it has been suggested that supplemental calcium may be associated with adverse cardiovascular effects, raising widespread concern about their use. One suggested mechanism is via increasing carotid atherosclerosis, however few randomized controlled trials (RCT) of calcium supplements have assessed these mechanisms. The calcium intake fracture outcome study (CAIFOS) was a 5-year RCT (1998 to 2003) of 1.2 g of elemental calcium in the form of calcium carbonate in 1460 elderly women. An ancillary study of 1103 women assessed common carotid artery intimal medial thickness (CCA-IMT) and carotid atherosclerosis at year 3 (2001). The effects of supplementation were studied in intention-to-treat (ITT) and per-protocol (PP) analyses before and after adjustment for baseline cardiovascular risk factors. The mean age of participants at baseline was 75.2 ± 2.7 years. In ITT analyses, women randomized to calcium supplementation had no difference in multivariable-adjusted mean CCA-IMT (calcium 0.778 ± 0.006 mm, placebo 0.783 ± 0.006 mm, p = 0.491) and maximum CCA-IMT (calcium 0.921 ± 0.007 mm, placebo 0.929 ± 0.006 mm, p = 0.404). Women randomized to calcium did not have increased carotid atherosclerosis (calcium 47.2%, placebo 52.7%, p = 0.066). However, in women taking at least 80% of the supplements, a significant reduction in carotid atherosclerosis was observed in unadjusted but not in multivariate-adjusted models (p = 0.033 and p = 0.064, respectively). Participants in the highest tertile of total calcium (diet and supplements) had reduced carotid atherosclerosis in unadjusted and multivariable-adjusted analyses compared with participants in the lowest tertile (odds ratio [OR] = 0.67 [95% confidence interval (CI) 0.50–0.90], p = 0.008, and OR = 0.70 [95% CI 0.51–0.96], p = 0.028, respectively). In conclusion, these findings do not support the hypothesis that calcium supplementation increases carotid artery intimal medial thickness or carotid atherosclerosis, and high calcium intake may reduce this surrogate cardiovascular risk factor. © 2014 American Society for Bone and Mineral Research.
Original languageEnglish
Pages (from-to)534-541
JournalJournal of Bone and Mineral Research
Volume29
Issue number3
Early online date19 Feb 2014
DOIs
Publication statusPublished - Mar 2014

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Tunica Intima
Carotid Artery Diseases
Common Carotid Artery
Randomized Controlled Trials
Outcome Assessment (Health Care)
Calcium
Placebos
Odds Ratio
Confidence Intervals
Intention to Treat Analysis
Calcium Carbonate
Carotid Arteries

Cite this

@article{b3f110bcdda743a995af6413b122d4fe,
title = "The Effects of 3 Years of Calcium Supplementation on Common Carotid Artery Intimal Medial Thickness and Carotid Atherosclerosis in Older Women: An Ancillary Study of the CAIFOS Randomized Controlled Trial",
abstract = "Calcium is an essential nutrient for skeletal health; however, it has been suggested that supplemental calcium may be associated with adverse cardiovascular effects, raising widespread concern about their use. One suggested mechanism is via increasing carotid atherosclerosis, however few randomized controlled trials (RCT) of calcium supplements have assessed these mechanisms. The calcium intake fracture outcome study (CAIFOS) was a 5-year RCT (1998 to 2003) of 1.2 g of elemental calcium in the form of calcium carbonate in 1460 elderly women. An ancillary study of 1103 women assessed common carotid artery intimal medial thickness (CCA-IMT) and carotid atherosclerosis at year 3 (2001). The effects of supplementation were studied in intention-to-treat (ITT) and per-protocol (PP) analyses before and after adjustment for baseline cardiovascular risk factors. The mean age of participants at baseline was 75.2 ± 2.7 years. In ITT analyses, women randomized to calcium supplementation had no difference in multivariable-adjusted mean CCA-IMT (calcium 0.778 ± 0.006 mm, placebo 0.783 ± 0.006 mm, p = 0.491) and maximum CCA-IMT (calcium 0.921 ± 0.007 mm, placebo 0.929 ± 0.006 mm, p = 0.404). Women randomized to calcium did not have increased carotid atherosclerosis (calcium 47.2{\%}, placebo 52.7{\%}, p = 0.066). However, in women taking at least 80{\%} of the supplements, a significant reduction in carotid atherosclerosis was observed in unadjusted but not in multivariate-adjusted models (p = 0.033 and p = 0.064, respectively). Participants in the highest tertile of total calcium (diet and supplements) had reduced carotid atherosclerosis in unadjusted and multivariable-adjusted analyses compared with participants in the lowest tertile (odds ratio [OR] = 0.67 [95{\%} confidence interval (CI) 0.50–0.90], p = 0.008, and OR = 0.70 [95{\%} CI 0.51–0.96], p = 0.028, respectively). In conclusion, these findings do not support the hypothesis that calcium supplementation increases carotid artery intimal medial thickness or carotid atherosclerosis, and high calcium intake may reduce this surrogate cardiovascular risk factor. {\circledC} 2014 American Society for Bone and Mineral Research.",
author = "Joshua Lewis and Kun Zhu and Peter Thompson and Richard Prince",
year = "2014",
month = "3",
doi = "10.1002/jbmr.2117.",
language = "English",
volume = "29",
pages = "534--541",
journal = "Journal of Bone & Mineral Research",
issn = "0884-0431",
publisher = "John Wiley & Sons",
number = "3",

}

TY - JOUR

T1 - The Effects of 3 Years of Calcium Supplementation on Common Carotid Artery Intimal Medial Thickness and Carotid Atherosclerosis in Older Women: An Ancillary Study of the CAIFOS Randomized Controlled Trial

AU - Lewis, Joshua

AU - Zhu, Kun

AU - Thompson, Peter

AU - Prince, Richard

PY - 2014/3

Y1 - 2014/3

N2 - Calcium is an essential nutrient for skeletal health; however, it has been suggested that supplemental calcium may be associated with adverse cardiovascular effects, raising widespread concern about their use. One suggested mechanism is via increasing carotid atherosclerosis, however few randomized controlled trials (RCT) of calcium supplements have assessed these mechanisms. The calcium intake fracture outcome study (CAIFOS) was a 5-year RCT (1998 to 2003) of 1.2 g of elemental calcium in the form of calcium carbonate in 1460 elderly women. An ancillary study of 1103 women assessed common carotid artery intimal medial thickness (CCA-IMT) and carotid atherosclerosis at year 3 (2001). The effects of supplementation were studied in intention-to-treat (ITT) and per-protocol (PP) analyses before and after adjustment for baseline cardiovascular risk factors. The mean age of participants at baseline was 75.2 ± 2.7 years. In ITT analyses, women randomized to calcium supplementation had no difference in multivariable-adjusted mean CCA-IMT (calcium 0.778 ± 0.006 mm, placebo 0.783 ± 0.006 mm, p = 0.491) and maximum CCA-IMT (calcium 0.921 ± 0.007 mm, placebo 0.929 ± 0.006 mm, p = 0.404). Women randomized to calcium did not have increased carotid atherosclerosis (calcium 47.2%, placebo 52.7%, p = 0.066). However, in women taking at least 80% of the supplements, a significant reduction in carotid atherosclerosis was observed in unadjusted but not in multivariate-adjusted models (p = 0.033 and p = 0.064, respectively). Participants in the highest tertile of total calcium (diet and supplements) had reduced carotid atherosclerosis in unadjusted and multivariable-adjusted analyses compared with participants in the lowest tertile (odds ratio [OR] = 0.67 [95% confidence interval (CI) 0.50–0.90], p = 0.008, and OR = 0.70 [95% CI 0.51–0.96], p = 0.028, respectively). In conclusion, these findings do not support the hypothesis that calcium supplementation increases carotid artery intimal medial thickness or carotid atherosclerosis, and high calcium intake may reduce this surrogate cardiovascular risk factor. © 2014 American Society for Bone and Mineral Research.

AB - Calcium is an essential nutrient for skeletal health; however, it has been suggested that supplemental calcium may be associated with adverse cardiovascular effects, raising widespread concern about their use. One suggested mechanism is via increasing carotid atherosclerosis, however few randomized controlled trials (RCT) of calcium supplements have assessed these mechanisms. The calcium intake fracture outcome study (CAIFOS) was a 5-year RCT (1998 to 2003) of 1.2 g of elemental calcium in the form of calcium carbonate in 1460 elderly women. An ancillary study of 1103 women assessed common carotid artery intimal medial thickness (CCA-IMT) and carotid atherosclerosis at year 3 (2001). The effects of supplementation were studied in intention-to-treat (ITT) and per-protocol (PP) analyses before and after adjustment for baseline cardiovascular risk factors. The mean age of participants at baseline was 75.2 ± 2.7 years. In ITT analyses, women randomized to calcium supplementation had no difference in multivariable-adjusted mean CCA-IMT (calcium 0.778 ± 0.006 mm, placebo 0.783 ± 0.006 mm, p = 0.491) and maximum CCA-IMT (calcium 0.921 ± 0.007 mm, placebo 0.929 ± 0.006 mm, p = 0.404). Women randomized to calcium did not have increased carotid atherosclerosis (calcium 47.2%, placebo 52.7%, p = 0.066). However, in women taking at least 80% of the supplements, a significant reduction in carotid atherosclerosis was observed in unadjusted but not in multivariate-adjusted models (p = 0.033 and p = 0.064, respectively). Participants in the highest tertile of total calcium (diet and supplements) had reduced carotid atherosclerosis in unadjusted and multivariable-adjusted analyses compared with participants in the lowest tertile (odds ratio [OR] = 0.67 [95% confidence interval (CI) 0.50–0.90], p = 0.008, and OR = 0.70 [95% CI 0.51–0.96], p = 0.028, respectively). In conclusion, these findings do not support the hypothesis that calcium supplementation increases carotid artery intimal medial thickness or carotid atherosclerosis, and high calcium intake may reduce this surrogate cardiovascular risk factor. © 2014 American Society for Bone and Mineral Research.

U2 - 10.1002/jbmr.2117.

DO - 10.1002/jbmr.2117.

M3 - Article

VL - 29

SP - 534

EP - 541

JO - Journal of Bone & Mineral Research

JF - Journal of Bone & Mineral Research

SN - 0884-0431

IS - 3

ER -