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Abstract
It is now generally accepted that an adequate calcium intake is important for building and maintaining a skeleton that expresses quantitatively the full genetic program and reduces lifetime fracture risk. In this brief review we focus mainly on a new and growing body of evidence indicating a benefit of adequate calcium intake on qualitative features of the skeleton that, independent of the quantity of bone, themselves influence skeletal strength and fragility.
Change in bone mass and size during growth are dependent on both calcium intake and exercise, with the largest differences being observed in prepubertal children who have both high exercise levels and high calcium intakes. Much of this benefit is expressed as increased bone diameter (and hence stiffness). Fracture risk peaks at about the time of puberty and is inversely related to bone mass. However, even prepubertally, children with low calcium intakes have been reported to have a fracture rate 2.7× that of their birth cohort.
Bone remodeling triples from age 50 to 65 in typical women and is now recognized to have primarily a homeostatic basis. While remodeling improves bone strength by repairing acquired defects, homeostatic remodeling, while necessary to maintain blood calcium levels, contributes only structural weakness to bone. High calcium intakes in postmenopausal and older women reduce this homeostatic remodeling to approximately pre-menopausal values and improve bone strength immediately, well prior to any appreciable change in bone mass.
Key teaching points:
• Low bone mass is associated with increased fracture risk in children, just as in adults.
• Low dairy intake is one of the causes of reduced bone mass during growth.
• Physical activity and calcium intake interact during growth, with the largest accumulation of bone being concentrated in children with high physical activity and high calcium intakes.
• Bone remodeling, necessary to repair or reshape bone, also serves calcium homeostasis; on prevailing diets, homeostatic remodeling is larger than structural remodeling, tripling in magnitude from the premenopausal years to age 65.
• Homeostatic remodeling, while it provides needed calcium ions to the extracellular fluid, weakens bone locally, wherever in the skeleton it occurs. Available evidence suggests that excessive remodeling is a major cause of osteoporotic bony fragility.
• Reduction in bone remodeling by high calcium intakes produces an immediate reduction in fracture risk, well before perceptible change in bone mass can occur.
Key teaching points:
• Low bone mass is associated with increased fracture risk in children, just as in adults.
• Low dairy intake is one of the causes of reduced bone mass during growth.
• Physical activity and calcium intake interact during growth, with the largest accumulation of bone being concentrated in children with high physical activity and high calcium intakes.
• Bone remodeling, necessary to repair or reshape bone, also serves calcium homeostasis; on prevailing diets, homeostatic remodeling is larger than structural remodeling, tripling in magnitude from the premenopausal years to age 65.
• Homeostatic remodeling, while it provides needed calcium ions to the extracellular fluid, weakens bone locally, wherever in the skeleton it occurs. Available evidence suggests that excessive remodeling is a major cause of osteoporotic bony fragility.
• Reduction in bone remodeling by high calcium intakes produces an immediate reduction in fracture risk, well before perceptible change in bone mass can occur.
