scholarly journals Do Only Calcium and Vitamin D Matter? Micronutrients in the Diet of Inflammatory Bowel Diseases Patients and the Risk of Osteoporosis

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 525
Author(s):  
Alicja Ewa Ratajczak ◽  
Anna Maria Rychter ◽  
Agnieszka Zawada ◽  
Agnieszka Dobrowolska ◽  
Iwona Krela-Kaźmierczak

Osteoporosis is one of the most common extraintestinal complications among patients suffering from inflammatory bowel diseases. The role of vitamin D and calcium in the prevention of a decreased bone mineral density is well known, although other nutrients, including micronutrients, are also of extreme importance. Despite the fact that zinc, copper, selenium, iron, cadmium, silicon and fluorine have not been frequently discussed with regard to the prevention of osteoporosis, it is possible that a deficiency or excess of the abovementioned elements may affect bone mineralization. Additionally, the risk of malnutrition, which is common in patients with ulcerative colitis or Crohn’s disease, as well as the composition of gut microbiota, may be associated with micronutrients status.

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1702
Author(s):  
Alicja Ewa Ratajczak ◽  
Anna Maria Rychter ◽  
Agnieszka Zawada ◽  
Agnieszka Dobrowolska ◽  
Iwona Krela-Kaźmierczak

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.


2019 ◽  
Vol 28 (7) ◽  
pp. 955-960 ◽  
Author(s):  
Aleksandra Szymczak-Tomczak ◽  
Iwona Krela-Kaźmierczak ◽  
Marta Kaczmarek-Ryś ◽  
Szymon T. Hryhorowicz ◽  
Kamila Stawczyk-Eder ◽  
...  

2014 ◽  
Vol 8 (9) ◽  
pp. 1062-1071 ◽  
Author(s):  
Maria Martinesi ◽  
Stefano Ambrosini ◽  
Cristina Treves ◽  
Ulrich Zuegel ◽  
Andreas Steinmeyer ◽  
...  

2008 ◽  
Vol 22 (5) ◽  
pp. 497-504 ◽  
Author(s):  
Neeraj Narula ◽  
Richard N Fedorak

Crohn’s disease and ulcerative colitis are both idiopathic inflammatory bowel diseases (IBDs) that affect 0.5% of Canadians. As yet, there is no known cure for either disease, and symptoms are treated with an array of medicines. The objective of the present review was to present the role of exercise and its impact on all facets of IBD. Exercise has been speculated to be protective against the onset of IBD, but the literature is inconsistent and weak. Preliminary studies reveal that exercise training may be beneficial to reduce stress and symptoms of IBD. Current research also recommends exercise to help counteract some IBD-specific complications by improving bone mineral density, immunological response, psychological health, weight loss and stress management ability. However, the literature advises that some patients with IBD may have limitations to the amount and intensity of exercise that they can perform. In summary, exercise may be beneficial to IBD patients, but further research is required to make a convincing conclusion regarding its role in the management of IBD and to help establish exercise regimens that can account for each IBD patient’s unique presentation.


Author(s):  
Alicja Ewa Ratajczak ◽  
Anna Maria Rychter ◽  
Agnieszka Zawada ◽  
Agnieszka Dobrowolska ◽  
Iwona Krela-Kaźmierczak

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 is the most often discussed minerals with regard to bone mineral density. Moreover, phosphorus; magnesium and sodium are also involved in the formation of bone mass. Patients suffering from inflammatory bowel diseases frequently consume inadequate amounts of the aforementioned minerals  or their absorption is disturbed, resulting innutritional deficiency and an increased risk of osteoporosis. 


2011 ◽  
Vol 300 (2) ◽  
pp. G191-G201 ◽  
Author(s):  
Fayez K. Ghishan ◽  
Pawel R. Kiela

Chronic inflammatory disorders such as inflammatory bowel diseases (IBDs) affect bone metabolism and are frequently associated with the presence of osteopenia, osteoporosis, and increased risk of fractures. Although several mechanisms may contribute to skeletal abnormalities in IBD patients, inflammation and inflammatory mediators such as TNF, IL-1β, and IL-6 may be the most critical. It is not clear whether the changes in bone metabolism leading to decreased mineral density are the result of decreased bone formation, increased bone resorption, or both, with varying results reported in experimental models of IBD and in pediatric and adult IBD patients. New data, including our own, challenge the conventional views, and contributes to the unraveling of an increasingly complex network of interactions leading to the inflammation-associated bone loss. Since nutritional interventions (dietary calcium and vitamin D supplementation) are of limited efficacy in IBD patients, understanding the pathophysiology of osteopenia and osteoporosis in Crohn's disease and ulcerative colitis is critical for the correct choice of available treatments or the development of new targeted therapies. In this review, we discuss current concepts explaining the effects of inflammation, inflammatory mediators and their signaling effectors on calcium and phosphate homeostasis, osteoblast and osteoclast function, and the potential limitations of vitamin D used as an immunomodulator and anabolic hormone in IBD.


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