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Low Calcium and vitamin D makes osteomalacia but either makes osteoporosis – Sept 2010

Experimental Evidence for the Effects of Calcium and Vitamin D on Bone: A Review

Nutrients 2010, 2(9), 1026-1035; doi:10.3390/nu2091026; 17 September 2010
Howard A. Morris 1,2,3, Peter D. O’Loughlin 2,3 and Paul H. Anderson 2,3
1 School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia 5001, Australia; howard.morris at health.sa.gov.au
2 Endocrine Bone Research Laboratory, Hanson Institute, SA Pathology, Adelaide, South Australia 5000, Australia
3 Chemical Pathology, SA Pathology, Adelaide, South Australia 5000, Australia


Animal models fed low calcium diets demonstrate a negative calcium balance and gross bone loss while the combination of calcium deficiency and oophorectomy enhances overall bone loss. Following oophorectomy the dietary calcium intake required to remain in balance increases some 5 fold, estimated to be approximately 1.3% dietary calcium. In the context of vitamin D and dietary calcium depletion, osteomalacia occurs only when low dietary calcium levels are combined with low vitamin D levels and osteoporosis occurs with either a low level of dietary calcium with adequate vitamin D status or when vitamin D status is low in the presence of adequate dietary calcium intake. Maximum bone architecture and strength is only achieved when an adequate vitamin D status is combined with sufficient dietary calcium to achieve a positive calcium balance. This anabolic effect occurs without a change to intestinal calcium absorption, suggesting dietary calcium and vitamin D have activities in addition to promoting a positive calcium balance. Each of the major bone cell types, osteoblasts, osteoclasts and osteocytes are capable of metabolizing 25 hydroxyvitamin D (25D) to 1,25 dihydroxyvitamin D (1,25D) to elicit biological activities including reduction of bone resorption by osteoclasts and to enhance maturation and mineralization by osteoblasts and osteocytes. Each of these activities is consistent with the actions of adequate circulating levels of 25D observed in vivo.

Conclusions (extracted from the PDF)

Studies in animals have identified that feeding low levels of dietary calcium produces a negative calcium balance and gross bone loss. The calcium requirement in the estrogen deficient state is markedly increased and therefore the combination of calcium deficiency and oophorectomy enhances overall bone loss. In the context of vitamin D and dietary calcium depletion,

osteomalacia occurs only when both vitamin D and dietary calcium levels are reduced and
osteoporosis occurs with either a low calcium diet in the presence of adequate vitamin D
or when vitamin D status is low in the presence of adequate dietary calcium.

Maximum bone architecture and strength is only achieved when an adequate vitamin D status is combined with sufficient dietary calcium to achieve a positive calcium balance. Each of the major bone cells, osteoblasts, osteoclasts and osteocytes are capable of metabolizing 25D to 1,25D to elicit biological activities including reduction of bone resorption by osteoclasts and to enhance maturation and mineralization by osteoblasts and osteocytes.

Thus optimal bone health is only achieved when the vitamin D status is improved thus providing adequate levels of the circulating pro-hormone 25D for local metabolism by bone cells into the active hormone 1,25D. Each of these bone cell activities is consistent with the actions of adequate circulating levels of 25D observed in vivo and with clinical outcomes from vitamin D and calcium dietary supplementation.

Valuable data have been derived from animal experimentation on the physiological responses of bone mineral homeostasis to variations in dietary calcium intake and vitamin D status in both the context of estrogen sufficiency and deficiency. Such data provide support for clinical studies, often derived from epidemiological or case control study formats, indicating that nutritional deficiencies of calcium and vitamin D, especially in postmenopausal women, produce adverse bone health outcomes and increase the risk of osteoporotic fractures. Animal studies provide research models for investigating the mechanisms by which such adverse outcomes may arise allowing the combined investigation of bone architecture, bone cell activities and molecular changes in response to nutritional manipulation. Knowledge of the molecular and cellular basis is essential for defining the nutritional levels required for optimal health outcomes, for acceptance by the clinical community of the essential requirements for calcium and vitamin D nutrition and for the development of public health policies aimed at osteoporosis prevention.

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