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Preventive Nutrition pp 443–469Cite as

Diet, Osteoporosis, and Fracture Prevention: The Totality of the Evidence

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Part of the book series: Nutrition and Health ((NH))

Abstract

Osteoporosis is currently defined as a condition of skeletal fragility due to decreased bone mass and to microarchitectural deterioration of bone tissue, with consequent increased risk of fracture. The condition is multifactorial in pathogenesis. Nutrition affects bone health in two distinct ways. First, bone tissue deposition, maintenance, and repair are the result of cellular processes, which are as dependent on nutrition as are the corresponding processes of any other tissue. The production of bone matrix, for example, requires the synthesis and post-translational modification of collagen and an array of other proteins. Nutrients involved in these cellular activities include not only the amino acid building blocks of the protein itself, but vitamins C, D, and K, and the minerals phosphorus, copper, manganese, and zinc. Additionally, the regulation of calcium homeostasis through modulation of bone resorption requires normal magnesium nutrition. Second, the skeleton serves as a very large nutrient reserve for two elements, calcium and phosphorus.

Key Points

• Bone health requires total nutrition. This is because the integrity of bone tissue depends on the integrity of its cells, which like most other tissues, needs a broad array of macro- and micronutrients. Additionally, calcium and protein play key structural roles, since the bulk of the bony material is made up of these substances

• Bone health requires total nutrition. This is because the integrity of bone tissue depends on the integrity of its cells, which like most other tissues, needs a broad array of macro- and micronutrients. Additionally, calcium and protein play key structural roles, since the bulk of the bony material is made up of these substances.

• Bone turns over relatively slowly. Thus the effects of inadequate nutrition on bone are often delayed and the structural properties of bone tend to reflect past nutrition more than current intakes.

• Calcium is a threshold nutrient. The minimum daily requirement is the intake at which bony response plateaus. To ensure reaching this threshold, calcium intake should be 1,500 mg/day both during growth and once again after age 50. Risk of osteoporotic hip and other non-spine fractures can be reduced by 30–50% with life-long calcium intakes in this range.

• Vitamin D is produced predominantly in the skin. Recommended daily oral intakes are sufficient only to prevent the most extreme bony manifestations of vitamin D deficiency. Optimal vitamin D status is ensured by serum 25(OH)D values ≥80 nmol/L (32 ng/mL). Lower values are associated with impaired regulation of calcium absorption and increased osteoporotic fracture risk. Daily utilization of vitamin D may be as high as 4,000 IU (100 μg). For most elderly individuals a daily oral dose of 1,000–2,000 IU is necessary to sustain adequate serum 25(OH)D concentrations.

• Protein, once thought to be potentially harmful to bone when ingested in large quantities, is now best understood as complementary to calcium. Together the two nutrients provide the bulk constituents of bony material. To achieve the full benefit of either, the intake of the other must be adequate as well. Protein intakes that optimize bony response are uncertain, but appear from available data to be above 1.0 g/kg/day.

• Recovery from hip fracture can be substantially improved with aggressive attention to the nutritional status of hip fracture patients, with special emphasis on repairing the protein malnutrition common in such patients.

• Even though typical magnesium intakes are below the RDA (310 mg/day and 400 mg/day for women and men, respectively), there appear to be few skeletal consequences of the shortfall. Supplemental magnesium does not improve calcium absorption in individuals consuming typical diets and has no recognized effect on calcium balance.

• Vitamin K, zinc, manganese, and copper are involved in various aspects of bone matrix formation, but it is not known whether deficiency of any of them contributes to the development or severity of typical osteoporosis.

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  1. Department of Medicine, Creighton University, 68178, Omaha, Nebraska, USA

    Robert P. Heaney MD

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  1. Robert P. Heaney MD
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Correspondence to Robert P. Heaney MD .

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  1. New Products Research, GlaxoSmithKline Consumer Healthcare, Littleton Road 1500 , Parsippany, 07054, U.S.A.

    Adrianne Bendich

  2. Inst. Human Nutrition, Columbia University, West 168th St. 630 , New York, 10032, U.S.A.

    Richard J. Deckelbaum

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Heaney, R.P. (2010). Diet, Osteoporosis, and Fracture Prevention: The Totality of the Evidence. In: Bendich, A., Deckelbaum, R. (eds) Preventive Nutrition. Nutrition and Health. Humana Press. https://doi.org/10.1007/978-1-60327-542-2_19

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