Summary Calorie restriction (CR) reduces bone quantity but not bone quality in rodents. Nothing is known regarding the long‐term effects of CR with adequate intake of vitamin and minerals on bone quantity and quality in middle‐aged lean individuals. In this study, we evaluated body composition, bone mineral density (BMD), and serum markers of bone turnover and inflammation in 32 volunteers who had been eating a CR diet (∼35% less calories than controls) for an average of 6.8 ± 5.2 years (mean age 52.7 ± 10.3 years) and 32 age‐ and sex‐matched sedentary controls eating Western diets (WD). In a subgroup of 10 CR and 10 WD volunteers, we also measured trabecular bone (TB) microarchitecture of the distal radius using high‐resolution magnetic resonance imaging. We found that the CR volunteers had significantly lower body mass index than the WD volunteers (18.9 ± 1.2 vs. 26.5 ± 2.2 kg m −2 ; P = 0.0001). BMD of the lumbar spine (0.870 ± 0.11 vs. 1.138 ± 0.12 g cm −2 , P = 0.0001) and hip (0.806 ± 0.12 vs. 1.047 ± 0.12 g cm −2 , P = 0.0001) was also lower in the CR than in the WD group. Serum C‐terminal telopeptide and bone‐specific alkaline phosphatase concentration were similar between groups, while serum C‐reactive protein (0.19 ± 0.26 vs. 1.46 ± 1.56 mg L −1 , P = 0.0001) was lower in the CR group. Trabecular bone microarchitecture parameters such as the erosion index (0.916 ± 0.087 vs. 0.877 ± 0.088; P = 0.739) and surface‐to‐curve ratio (10.3 ± 1.4 vs. 12.1 ± 2.1, P = 0.440) were not significantly different between groups. These findings suggest that markedly reduced BMD is not associated with significantly reduced bone quality in middle‐aged men and women practicing long‐term calorie restriction with adequate nutrition.

The new definition of osteoporosis as a disease of fracture risk and the increased availability of bone mineral density (BMD) measurement devices has changed the approach to the patient with or who is considered at risk for osteoporosis. The disease or disease risk should be detected in the asymptomatic state by BMD measurement just as heart attack risk is assessed by serum lipid measurements or stroke risk assessed by blood pressure measurement in asymptomatic patients. BMD predicts fracture risk as well as blood pressure predicts risk of stroke and better than total serum cholesterol predicts risk of acute myocardial infarction. All patients who sustain an unexplained fragility fracture should be considered to have osteoporosis and have BMD measured. This chapter describes the clinical situations where a BMD study is and is not appropriate on the basis of the history and physical examination and where it is not clearly indicated but might be beneficial. Once a low BMD has been documented, a number of laboratory studies should be performed to make certain that a correctable secondary cause for osteoporosis does not exist. The potential roles of biochemical markers of bone remodeling in the evaluation of the patient with low BMD are also discussed in this chapter.

1,25-Dihydroxyvitamin D(3) levels begin to drop early in the course of kidney disease, leading to elevated parathyroid hormone levels and disrupted mineral metabolism. Impaired mineral metabolism seems to be associated not only with bone disease but also with vascular calcification. Animal models have identified molecular mechanisms by which high mineral levels and other uremic substances induce vascular smooth muscle cells to undergo phenotypic changes that initiate the calcification process. Moreover, several epidemiologic and clinical studies showed strong associations between bone loss, arterial calcification, and cardiovascular disease in populations with and without kidney disease. This review discusses evidence that two early complications of chronic kidney disease--vitamin D deficiency and secondary hyperparathyroidism--contribute to bone and cardiovascular disease. New treatment strategies aimed at the prevention of bone loss and parathyroid hyperplasia, such as vitamin D receptor ligand therapy, calcimimetic agents, and noncalcifying phosphate binders, are being investigated for their impact on improving overall outcome in dialysis patients.

Osteoporosis is a prevalent condition that may exist in a silent form, in which increased fracture risk can be detected by measurement of bone mineral density (BMD), or as a symptomatic condition after a fragility fracture has occurred. In October 2004, the Surgeon General of the United States published a lengthy report on osteoporosis (1), which is a must-read for healthcare professionals interested in this disease. The chapter “Assessing the Risk of Bone Disease and Fracture” discusses many aspects of bone mass measurement, but relegates biochemical markers of bone turnover to the subsection “Looking to the Future: Potential Complements to BMD” (1). In a sense, this designation is appropriate because these markers currently have no “diagnostic” value, whereas the WHO has designated a BMD >2.5 SD below the mean for healthy adults younger than 50 years as diagnostic for osteoporosis even in the absence of a bone fracture. Considerable evidence exists, however, that biochemical marker data alone can be used to assess fracture risk in older persons and are additive to BMD data with respect to fracture risk prediction. In reality, neither clinical tool is optimal for this purpose. Two recent studies in older populations have pointed out that among individuals who have sustained a fragility fracture, before the fracture only 40%–45% would have been diagnosed with …

Beyond the obvious clinical signs of damage, fracture in older persons invariably is a sign of osteoporosis onset. This prevalent disease of older age, however, is preventable and treatable. Because no agent or exercise regimen can reverse osteoporosis, proactive physicians can help patients prolong osteoporosis onset and lower the risk of fracture incidence by creating a preventive regimen that employs exercise diet, vitamin D and calcium supplementation, and when, necessary, administration of pharmacologies including estrogen, bisphosphonates, calcitonin-salmon, and the new selective estrogen receptor modulator.