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      Nutrients in the Prevention of Osteoporosis in Patients with Inflammatory Bowel Diseases

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          Abstract

          The chronic character of inflammatory bowel diseases, such as Crohn’s disease and ulcerative colitis, results in various complications. One of them is osteoporosis, manifested by low bone mineral density, which leads to an increased risk of fractures. The aetiology of low bone mineral density is multifactorial and includes both diet and nutritional status. Calcium and vitamin D are the most often discussed nutrients with regard to bone mineral density. Moreover, vitamins A, K, C, B12; folic acid; calcium; phosphorus; magnesium; sodium; zinc; copper; and selenium are also involved in the formation of bone mass. Patients suffering from inflammatory bowel diseases frequently consume inadequate amounts of the aforementioned minerals and vitamins or their absorption is disturbed, resulting innutritional deficiency and an increased risk of osteoporosis. Thus, nutritional guidelines for inflammatory bowel disease patients should comprise information concerning the prevention of osteoporosis.

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          Most cited references116

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          Effect of High-Dose Vitamin D Supplementation on Volumetric Bone Density and Bone Strength

          Few studies have assessed the effects of daily vitamin D doses at or above the tolerable upper intake level for 12 months or greater, yet 3% of US adults report vitamin D intakes of at least 4000 IU per day.
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            Prevention and management of osteoporosis.

            (2002)
            Bone is hard tissue that is in a constant state of flux, being built up by bone-forming cells called osteoblasts while also being broken down or resorbed by cells known as osteoclasts. During childhood and adolescence, bone formation is dominant; bone length and girth increase with age, ending at early adulthood when peak bone mass is attained. Males generally exhibit a longer growth period, resulting in bones of greater size and overall strength. In males after the age of 20, bone resorbtion becomes predominant, and bone mineral content declines about 4% per decade. Females tend to maintain peak mineral content until menopause, after which time it declines about 15% per decade. Osteoporosis is a disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility and an increased susceptibility to fractures, especially of the hip, spine, and wrist. Osteoporosis occurs primarily as a result of normal ageing, but can arise as a result of impaired development of peak bone mass (e.g. due to delayed puberty or undernutrition) or excessive bone loss during adulthood (e.g. due to estrogen deficiency in women, undernutrition, or corticosteroid use). Osteoporosis-induced fractures cause a great burden to society. Hip fractures are the most serious, as they nearly always result in hospitalization, are fatal about 20% of the time, and produce permanent disability about half the time. Fracture rates increase rapidly with age and the lifetime risk of fracture in 50 year-old women is about 40%, similar to that for coronary heart disease. In 1990, there were 1.7 million hip fractures alone worldwide; with changes in population demographics, this figure is expected to rise to 6 million by 2050. To help describe the nature and consequences of osteoporosis, as well as strategies for its prevention and management, a WHO Scientific Group meeting of international experts was held in Geneva, which resulted in this technical report. This monograph describes in detail normal bone development and the causes and risk factors for developing osteoporosis. The burden of osteoporosis is characterized in terms of mortality, morbidity, and economic costs. Methods for its prevention and treatment are discussed in detail for both pharmacological and non-pharmacological approaches. For each approach, the strength of the scientific evidence is presented. The report also provides cost-analysis information for potential interventions, and discusses important aspects of developing national policies to deal with osteoporosis. Recommendations are made to the general population, care providers, health administrators, and researchers. Lastly, national organizations and support groups are listed by country.
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              Glucocorticoids and bone: consequences of endogenous and exogenous excess and replacement therapy

              Osteoporosis associated with long-term glucocorticoid therapy remains a common and serious bone disease. Additionally, in recent years it has become clear that more subtle states of endogenous glucocorticoid excess may have a major impact on bone health. Adverse effects can be seen with mild systemic glucocorticoid excess, but there is also evidence of tissue-specific regulation of glucocorticoid action within bone as a mechanism of disease. This review article examines (1) the role of endogenous glucocorticoids in normal bone physiology, (2) the skeletal effects of endogenous glucocorticoid excess in the context of endocrine conditions such as Cushing disease/syndrome and autonomous cortisol secretion (subclinical Cushing syndrome), and (3) the actions of therapeutic (exogenous) glucocorticoids on bone. We review the extent to which the effect of glucocorticoids on bone is influenced by variations in tissue metabolizing enzymes and glucocorticoid receptor expression and sensitivity. We consider how the effects of therapeutic glucocorticoids on bone are complicated by the effects of the underlying inflammatory disease being treated. We also examine the impact that glucocorticoid replacement regimens have on bone in the context of primary and secondary adrenal insufficiency. We conclude that even subtle excess of endogenous or moderate doses of therapeutic glucocorticoids are detrimental to bone. However, in patients with inflammatory disorders there is a complex interplay between glucocorticoid treatment and underlying inflammation, with the underlying condition frequently representing the major component underpinning bone damage.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                06 June 2020
                June 2020
                : 12
                : 6
                : 1702
                Affiliations
                Department of Gastroenterology, Dietetics and Internal Diseases, Poznan University of Medical Sciences, 49 Przybyszewskiego Street, 60-355 Poznan, Poland; a.m.rychter@ 123456gmail.com (A.M.R.); aga.zawada@ 123456gmail.com (A.Z.); agdob@ 123456ump.edu.pl (A.D.)
                Author notes
                [* ]Correspondence: alicjaewaratajczak@ 123456gmail.com (A.E.R.); krela@ 123456op.pl (I.K.-K.); Tel.: +48-667-385-996 (A.E.R.); +48-8691-343 (I.K.-K.); Fax: +48-8691-686 (A.E.R.)
                Author information
                https://orcid.org/0000-0002-7731-6965
                https://orcid.org/0000-0002-6586-3611
                https://orcid.org/0000-0001-6995-090X
                https://orcid.org/0000-0002-3647-5070
                https://orcid.org/0000-0001-5122-8003
                Article
                nutrients-12-01702
                10.3390/nu12061702
                7352179
                32517239
                a20bc022-7864-41dd-983c-f4ee1126aa40
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 12 May 2020
                : 03 June 2020
                Categories
                Review

                Nutrition & Dietetics
                bowel diseases,diet,osteoporosis,bone density,nutrients
                Nutrition & Dietetics
                bowel diseases, diet, osteoporosis, bone density, nutrients

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