Alta prevalência de quantidade inadequada/baixa de vitamina D e Implicações para a Saúde – High Prevalence of Vitamin D Inadequacy and Implications for Health

High Prevalence of Vitamin D Inadequacy and Implications for Health

 

Abstract

During the past decade, major advances have been made in vitamin D research that transcend the simple concept that vitamin D is important for the prevention of rickets in children and has little physiologic relevance for adults. Inadequate vitamin D, in addition to causing rickets, prevents children from attaining their genetically programmed peak bone mass, contributes to and exacerbates osteoporosis in adults, and causes the often painful bone disease osteomalacia. Adequate vitamin D is also important for proper muscle functioning, and controversial evidence suggests it may help prevent type 1 diabetes mellitus, hypertension, and many common cancers. Vitamin D inadequacy has been reported in approximately 36% of otherwise healthy young adults and up to 57% of general medicine inpatients in the United States and in even higher percentages in Europe. Recent epidemiological data document the high prevalence of vitamin D inadequacy among elderly patients and especially among patients with osteoporosis. Factors such as low sunlight exposure, age-related decreases in cutaneous synthesis, and diets low in vitamin D contribute to the high prevalence of vitamin D inadequacy. Vitamin D production from cutaneous synthesis or intake from the few vitamin D-rich or enriched foods typically occurs only intermittently. Supplemental doses of vitamin D and sensible sun exposure could prevent deficiency in most of the general population. The purposes of this article are to examine the prevalence of vitamin D inadequacy and to review the potential implications for skeletal and extraskeletal health.

Article

High Prevalence of Vitamin D Inadequacy and Implications for Health

 

 High Prevalence of Vitamin D Inadequacy and Implications for Health Mayo Clinic Proceedings, Volume 81, Issue 3, Pages 353-373 Michael F. Holick

 

 

  • ·       Vitamin D, Skin and Bone Research Laboratory, Section of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, Boston, Mass

http://www.sciencedirect.com/science/article/pii/S0025619611614651

 

ScienceDirect

 

SOURCES OF VITAMIN D

VITAMIN D PHOTOBIOCHEMISTRY, METABOLISM, AND FUNCTIONS

1MHOLICK

ASSESSMENT OF VITAMIN D STATUS

2MHOLICK

EPIDEMIOLOGY OF VITAMIN D INADEQUACY

TABLE 1

FACTORS THAT CONTRIBUTE TO VITAMIN D INADEQUACY

SKELETAL CONSEQUENCES OF VITAMIN D INADEQUACY

3MHOLIC

TABLE 2

NEUROMUSCULAR FUNCTION

4MHOLICK

VITAMIN D AND EXTRASKELETAL HEALTH

VITAMIN D AND CANCER

VITAMIN D AND CARDIOVASCULAR DISEASE

VITAMIN D AND PSORIASIS

VITAMIN D AND MULTIPLE SCLEROSIS

VITAMIN D AND TYPE I DIABETES MELLITUS

VITAMIN D IN OTHER DISEASES

VITAMIN D DOSING, SUPPLEMENTATION, AND UV IRRADIATION AND/OR SENSIBLE SUN EXPOSURE

TREATMENT OF SEVERE VITAMIN D DEFICIENCY

CONCLUSION

Acknowledgments

REFERENCES

 

mholick

Mayo Clinic Proceedings

Volume 81, Issue 3, March 2006, Pages 353–373

REVIEW

High Prevalence of Vitamin D Inadequacy and Implications for Health

Michael F. Holick, PhD, MD,

Vitamin D, Skin and Bone Research Laboratory, Section of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, Boston, Mass

 

Individual reprints of this article are not available. Address correspondence to Michael F. Holick, PhD, MD, Vitamin D, Skin and Bone Research Laboratory, Section of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, 715 Albany St, Room M-1013, Boston, MA 02118

Available online 28 September 2011

http://dx.doi.org/10.4065/81.3.353, How to Cite or Link Using DOI

View full text

 

SOURCES OF VITAMIN D

VITAMIN D PHOTOBIOCHEMISTRY, METABOLISM, AND FUNCTIONS

ASSESSMENT OF VITAMIN D STATUS

EPIDEMIOLOGY OF VITAMIN D INADEQUACY

FACTORS THAT CONTRIBUTE TO VITAMIN D INADEQUACY

SKELETAL CONSEQUENCES OF VITAMIN D INADEQUACY

NEUROMUSCULAR FUNCTION

VITAMIN D AND EXTRASKELETAL HEALTH

VITAMIN D AND CANCER

VITAMIN D AND CARDIOVASCULAR DISEASE

VITAMIN D AND PSORIASIS

VITAMIN D AND MULTIPLE SCLEROSIS

VITAMIN D AND TYPE I DIABETES MELLITUS

VITAMIN D IN OTHER DISEASES

VITAMIN D DOSING, SUPPLEMENTATION, AND UV IRRADIATION AND/OR SENSIBLE SUN EXPOSURE

TREATMENT OF SEVERE VITAMIN D DEFICIENCY

CONCLUSION

Acknowledgments

REFERENCES

Refers to

Robert P. Heaney

Nutrition and Chronic Disease

Mayo Clinic Proceedings, Volume 81, Issue 3, March 2006, Pages 297-299

PDF (32 K)

Referred to by

Robert P. Heaney

Nutrition and Chronic Disease

Mayo Clinic Proceedings, Volume 81, Issue 3, March 2006, Pages 297-299

PDF (32 K)


 

During the past decade, major advances have been made in vitamin D research that transcend the simple concept that vitamin D is important for the prevention of rickets in children and has little physiologic relevance for adults. Inadequate vitamin D, in addition to causing rickets, prevents children from attaining their genetically programmed peak bone mass, contributes to and exacerbates osteoporosis in adults, and causes the often painful bone disease osteomalacia. Adequate vitamin D is also important for proper muscle functioning, and controversial evidence suggests it may help prevent type 1 diabetes mellitus, hypertension, and many common cancers. Vitamin D inadequacy has been reported in approximately 36% of otherwise healthy young adults and up to 57% of general medicine inpatients in the United States and in even higher percentages in Europe. Recent epidemiological data document the high prevalence of vitamin D inadequacy among elderly patients and especially among patients with osteoporosis. Factors such as low sunlight exposure, age-related decreases in cutaneous synthesis, and diets low in vitamin D contribute to the high prevalence of vitamin D inadequacy. Vitamin D production from cutaneous synthesis or intake from the few vitamin D-rich or enriched foods typically occurs only intermittently. Supplemental doses of vitamin D and sensible sun exposure could prevent deficiency in most of the general population. The purposes of this article are to examine the prevalence of vitamin D inadequacy and to review the potential implications for skeletal and extraskeletal health.

 

Keywords

1α(OH)D3, 1α-hydroxyvitamin D3;

1,25(OH)2D, 1,25-dihydroxyvitamin D;

25(OH)D, 25-hydroxyvitamin D;

BMD, bone mineral density;

PTH, parathyroid hormone;

RCT, randomized controlled trial;

RECORD, Record Evaluation of Calcium or Vitamin D;

VDR, vitamin D receptor


Figures and tables from this article:

 

FIGURE 1. Cutaneous production of vitamin D and its metabolism and regulation for calcium homeostasis and cellular growth. 7-Dehydrocholesterol or provitamin D3 (proD3) in the skin absorbs solar UV-B radiation and is converted to previtamin D3 (preD3). D3 undergoes thermally induced (δH) transformation to vitamin D3. Vitamin D from the diet or from the skin is metabolized in the liver by the vitamin D-25-hydroxylase to 25-hydroxyvitamin D3 (25[OH]D3). 25(OH)D3 is converted in the kidney by the 25(OH)D3-1α-hydroxylase to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]. A variety of factors, including serum phosphorus (PO2−4) and parathyroid hormone (PTH), regulate the renal production of 1,25(OH)2D3. 1,25(OH)2D regulates calcium metabolism through its interaction with its major target tissues, the bone and the intestine. From Osteoporos Int,21 with permission from Springer Science and Business Media.

 

FIGURE 2. Left, Relationship between serum 25-hydroxyvitamin D (25[OH]D) concentrations and mean ± SE (error bars) serum concentrations of parathyroid hormone in patients with osteoporosis receiving treatment. Right, Percentage of subjects with secondary hyperparathyroidism by 25(OH)D level. The percentage of subjects with secondary hyperparathyroidism (parathyroid hormone level >40 pg/mL) sorted by subgroups with serum 25(OH)D concentrations delineated by predefined cutoffs for analyses of 25(OH)D inadequacy. Left and right, From J Endocrinol Metab,30 with permission from The Endocrine Society, Copyright 2005.

 

 

FIGURE 3. Mean ± SD (error bars) serum 25-hydroxyvitamin D (25[OH]D) concentrations (shown as nmol/L and ng/mL) in women older than 70 years, stratified by supplement use and residential status. Adapted from J Clin Endocrinol Metab,97 with permission from The Endocrine Society, Copyright 1988.

 

 

FIGURE 4. Relative to therapy with 1200 mg/d of calcium for 12 weeks, daily therapy with 800 IU of vitamin D and 1200 mg of calcium accounted for a 49% reduction in the relative risk of falls among older women (mean age, 85.3 years) in long-term geriatric care. Ca = calcium; Ca + D = Ca plus vitamin D. Adapted from J Bone Miner Res,174 with permission from The American Society for Bone and Mineral Research.

 

 

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FIGURE 5. Endocrine and autocrine or paracrine functions of 1,25-dihydroxyvitamin D (1,25[OH]2D). The kidneys serve as the endocrine organ to convert 25-hydroxyvitamin D (25[OH]D) to 1,25(OH)2D. 1,25(OH)2D carries out its calcium-regulating functions for bone health by stimulating intestinal calcium and phosphorus absorption. The circulating levels of 1,25(OH)2D can also potentially influence the activity of other tissues and cells that have a vitamin D receptor (VDR) and have no function in regulating calcium homeostasis and bone health. These include, among others, the heart skeletal muscle, active T and B lymphocytes, breast, colon, and prostate. In addition, a multitude of in vitro studies with human and animal cells have shown that most tissues and cells not only express the VDR but also express the same 1α-hydroxylase as the kidney. Thus, it has been suggested that most cells, including lung, colon, prostate, and breast, locally produce 1,25(OH)2D3 to help regulate a variety of cellular functions including growth and differentiation. This may help explain the epidemiological evidence that sun exposure at lower altitudes and higher serum levels of 25(OH)D are related to a decreased risk of a wide variety of chronic illnesses. It has been speculated that when 25(OH)D levels are above 30 ng/mL this serves as the substrate for the external 25(OH)D3-1α-hydroxylase to produce 1,25(OH)2D in the colon, prostate, breast, and lung to modulate cell growth and reduce risk of the cells becoming malignant.

 

 

TABLE 1. Vitamin D Inadequacy in Osteoporosis: Summary of Reports Published in 2003 and 2004*

View Within Article

TABLE 2. Hierarchy of Evidence for Studies Relating Vitamin D to Pathologic Conditions*

View Within Article

This work was supported in part by National Institutes of Health grants MOIRR00533 and AR369637 and the UV Foundation.

Individual reprints of this article are not available. Address correspondence to Michael F. Holick, PhD, MD, Vitamin D, Skin and Bone Research Laboratory, Section of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, 715 Albany St, Room M-1013, Boston, MA 02118

*

Dr Holick is an Academic Associate for Nichols Institute Diagnostics.

Copyright © 2006 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved.

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