Journal of Clinical Densitometry: Assessment & Management of Musculoskeletal Health, vol. 16, no. 4, 387e388, 2013 Ó Copyright 2013 by The International Society for Clinical Densitometry 1094-6950/13/16:387e388/$36.00 http://dx.doi.org/10.1016/j.jocd.2013.10.001
Special Section on Bone and Nutrition
Introduction From the Guest Editors Sarah L. Morgan*,1, Neil Binkley 2, and Susan E. Williams 3 1
Division of Clinical Immunology and Rheumatology, Department of Medicine, UAB Osteoporosis Prevention and Treatment Clinic, University of Alabama at Birmingham, Birmingham, AL, USA; 2University of Wisconsin School of Medicine and Public Health, Madison, WI, USA; and 3Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, and Endocrinology and Metabolism Institute, Department of Endocrinology, Diabetes and Metabolism, Cleveland Clinic, Cleveland, OH, USA
of these index diseases. Evolving concepts in nutrition sciences acknowledge that there are longer term consequences of lesser degrees of deficiency (4). The metabolic mechanisms for the index deficiency may differ from those of longer-term inadequacy (1). Osteoporosis is considered to be a long-latency disease. In this issue, the articles related to calcium, vitamin D, and vitamin K are related to this concept. The interpretation of the nutrition literature related to bone suffers from several limitations that likely explain the conflicting conclusions related to optimal vitamin D intake to prevent fractures and whether calcium causes cardiovascular toxicity (4e6). The first limitation is that the dependent variable of fragility fractures and the independent variable of calcium intake are problematic (4). Variations in hip fracture rates not only relate to nutritional factors but also are affected by hip geometry and falling patterns, among other considerations. Calcium intakes are difficult to adequately quantify in observational, epidemiological trials. Many studies also fail to take into account baseline nutrient status and dose-response relationships (5). If a study subject is already vitamin D sufficient, the effect of vitamin D on an outcome, even if given in an adequate dose, will likely be negative. It is also difficult to study single nutrients, such as calcium (6), because it is necessary to account for nutrients that interact with calcium, such as vitamin D. To summarize, current nutritional knowledge remains less than ideal related to metabolic bone disease. Nonetheless, clinicians must apply the best existing data. These reviews provide a succinct,
Nutritional interventions are an integral component of disease management for many forms of metabolic bone disease. Not only do many individuals with metabolic bone disease have coexisting malnutrition (1,2) but also nutrient sufficiency is essential for optimizing the response to pharmacological therapy (3). In this issue of the Journal of Clinical Densitometry, bone-related nutritional topics are discussed including calcium; vitamins A, D, and K; the acidash hypothesis; soy; obesity/fat mass; celiac sprue; and eating disorders. Additionally, supplements/ medical foods and nutrition-related patient education tools for osteoporosis management are discussed. Each author has taken a no-nonsense approach to their specialty area and has provided bulleted Key Points to assist the reader in ‘‘taking away’’ the most salient points. As you peruse these articles, there are several important overarching concepts to consider about nutrition and bone (4,5). The public is captivated by the notion that certain nutrients are toxic, such as sodium, saturated fat, and cholesterol. The reviews of vitamin A, calcium, and the acid-ash hypothesis discuss whether nutrients cause adverse bone effects. Early nutrition scientists documented specific nutrient deficiencies that caused index diseases (4). These classic nutritional deficiencies, including scurvy, pellagra, rickets, and beriberi, occur fairly rapidly (short latency). Many current recommendations for dietary intakes are based on prevention *Address correspondence to: Sarah L. Morgan, MD, RD, CCD, 830 Faculty Office Tower, 510 20th Street South, Birmingham, Al 35294-3408. E-mail: [email protected]
387
388 clinically relevant synthesis of current knowledge and its application to patient care.
References 1. Buehring B, Krueger D, Binkley N. 2013 Effect of including historical height and radius BMD measurement on sarcoosteoporosis prevalence. J Cachexia Sarcopenia Muscle 4:47e54. 2. Montalcini T, Romeo S, Ferro Y, et al. 2013 Osteoporosis in chronic inflammatory dIsease: the role of malnutrition. Endocrine 43:59e64.
Morgan, Binkley, and Williams 3. Peris P, Martinez-Ferrer A, Monegal A, et al. 2012 25-hydroxyvitamin D serum levels influence adequate response to bisphosphonate treatment in postmenopausal osteoporosis. Bone 51:54e58. 4. Heaney RP. 2003 Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr 78: 912e919. 5. Heaney RP. 2012 Vitamin D-Baseline status and effective dose. N Engl J Med 267:77e78. 6. Bockman RS, Zapalowski C, Kiel DC, Adler RA. 2012 Commentary on calcium supplements and cardiovascular events. J Clin Densitom 15:130e134.
Journal of Clinical Densitometry: Assessment & Management of Musculoskeletal Health
Volume 16, 2013
Special Section on Bone and Nutrition
Introduction From the Guest Editors Sarah L. Morgan*,1, Neil Binkley 2, and Susan E. Williams 3 1
Division of Clinical Immunology and Rheumatology, Department of Medicine, UAB Osteoporosis Prevention and Treatment Clinic, University of Alabama at Birmingham, Birmingham, AL, USA; 2University of Wisconsin School of Medicine and Public Health, Madison, WI, USA; and 3Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, and Endocrinology and Metabolism Institute, Department of Endocrinology, Diabetes and Metabolism, Cleveland Clinic, Cleveland, OH, USA
of these index diseases. Evolving concepts in nutrition sciences acknowledge that there are longer term consequences of lesser degrees of deficiency (4). The metabolic mechanisms for the index deficiency may differ from those of longer-term inadequacy (1). Osteoporosis is considered to be a long-latency disease. In this issue, the articles related to calcium, vitamin D, and vitamin K are related to this concept. The interpretation of the nutrition literature related to bone suffers from several limitations that likely explain the conflicting conclusions related to optimal vitamin D intake to prevent fractures and whether calcium causes cardiovascular toxicity (4e6). The first limitation is that the dependent variable of fragility fractures and the independent variable of calcium intake are problematic (4). Variations in hip fracture rates not only relate to nutritional factors but also are affected by hip geometry and falling patterns, among other considerations. Calcium intakes are difficult to adequately quantify in observational, epidemiological trials. Many studies also fail to take into account baseline nutrient status and dose-response relationships (5). If a study subject is already vitamin D sufficient, the effect of vitamin D on an outcome, even if given in an adequate dose, will likely be negative. It is also difficult to study single nutrients, such as calcium (6), because it is necessary to account for nutrients that interact with calcium, such as vitamin D. To summarize, current nutritional knowledge remains less than ideal related to metabolic bone disease. Nonetheless, clinicians must apply the best existing data. These reviews provide a succinct,
Nutritional interventions are an integral component of disease management for many forms of metabolic bone disease. Not only do many individuals with metabolic bone disease have coexisting malnutrition (1,2) but also nutrient sufficiency is essential for optimizing the response to pharmacological therapy (3). In this issue of the Journal of Clinical Densitometry, bone-related nutritional topics are discussed including calcium; vitamins A, D, and K; the acidash hypothesis; soy; obesity/fat mass; celiac sprue; and eating disorders. Additionally, supplements/ medical foods and nutrition-related patient education tools for osteoporosis management are discussed. Each author has taken a no-nonsense approach to their specialty area and has provided bulleted Key Points to assist the reader in ‘‘taking away’’ the most salient points. As you peruse these articles, there are several important overarching concepts to consider about nutrition and bone (4,5). The public is captivated by the notion that certain nutrients are toxic, such as sodium, saturated fat, and cholesterol. The reviews of vitamin A, calcium, and the acid-ash hypothesis discuss whether nutrients cause adverse bone effects. Early nutrition scientists documented specific nutrient deficiencies that caused index diseases (4). These classic nutritional deficiencies, including scurvy, pellagra, rickets, and beriberi, occur fairly rapidly (short latency). Many current recommendations for dietary intakes are based on prevention *Address correspondence to: Sarah L. Morgan, MD, RD, CCD, 830 Faculty Office Tower, 510 20th Street South, Birmingham, Al 35294-3408. E-mail: [email protected]
387
388 clinically relevant synthesis of current knowledge and its application to patient care.
References 1. Buehring B, Krueger D, Binkley N. 2013 Effect of including historical height and radius BMD measurement on sarcoosteoporosis prevalence. J Cachexia Sarcopenia Muscle 4:47e54. 2. Montalcini T, Romeo S, Ferro Y, et al. 2013 Osteoporosis in chronic inflammatory dIsease: the role of malnutrition. Endocrine 43:59e64.
Morgan, Binkley, and Williams 3. Peris P, Martinez-Ferrer A, Monegal A, et al. 2012 25-hydroxyvitamin D serum levels influence adequate response to bisphosphonate treatment in postmenopausal osteoporosis. Bone 51:54e58. 4. Heaney RP. 2003 Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr 78: 912e919. 5. Heaney RP. 2012 Vitamin D-Baseline status and effective dose. N Engl J Med 267:77e78. 6. Bockman RS, Zapalowski C, Kiel DC, Adler RA. 2012 Commentary on calcium supplements and cardiovascular events. J Clin Densitom 15:130e134.
Journal of Clinical Densitometry: Assessment & Management of Musculoskeletal Health
Volume 16, 2013
