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Dietary sources of inorganic microparticles and their intake in healthy subjects and patients with Crohn's disease

Published online by Cambridge University Press:  09 March 2007

Miranda C. E. Lomer ,
Carol Hutchinson ,
Sara Volkert ,
Simon M. Greenfield ,
Adrian Catterall ,
Richard P. H. Thompson  and
Jonathan J. Powell
Miranda C. E. Lomer*
Affiliation:
Gastrointestinal Laboratory, The Rayne Institute, St Thomas' Hospital, Lambeth Palace Road, London, SE1 7EH, UK
Carol Hutchinson
Affiliation:
Department of Nutrition and Dietetics, Franklin-Wilkins Building, King's College London, 150 Stamford Street, London, SE1 9NN, UK
Sara Volkert
Affiliation:
Department of Nutrition and Dietetics, Franklin-Wilkins Building, King's College London, 150 Stamford Street, London, SE1 9NN, UK
Simon M. Greenfield
Affiliation:
Department of Gastroenterology, Queen Elizabeth II Hospital, Howlands, Welwyn, Garden City, Hertfordshire AL7 4HQ, UK
Adrian Catterall
Affiliation:
Department of Gastroenterology, Lister Hospital, Coreys Mill Lane, Stevenage, Hertfordshire SG1 4AB, UK
Richard P. H. Thompson
Affiliation:
Gastrointestinal Laboratory, The Rayne Institute, St Thomas' Hospital, Lambeth Palace Road, London, SE1 7EH, UK
Jonathan J. Powell
Affiliation:
Gastrointestinal Laboratory, The Rayne Institute, St Thomas' Hospital, Lambeth Palace Road, London, SE1 7EH, UK MRC Human Nutrition Research, Elsie Widdowson Laboratory, Fulbourn Road, Cambridge, CB1 9NL, UK
*
*Corresponding author: Dr Miranda C. E. Lomer, fax +44 20 7188 2510, email, [email protected]
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Abstract

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Dietary microparticles are non-biological, bacterial-sized particles. Endogenous sources are derived from intestinal Ca and phosphate secretion. Exogenous sources are mainly titanium dioxide (TiO2) and mixed silicates (Psil); they are resistant to degradation and accumulate in human Peyer's patch macrophages and there is some evidence that they exacerbate inflammation in Crohn's disease (CD). However, whether their intake differs between those with and without CD has not been studied. We aimed to identify dietary microparticle sources and intakes in subjects with and without CD. Patients with inactive CD and matched general practice-based controls (ninety-one per group) completed 7d food diaries. Intake data for dietary fibre and sucrose were compared as positive controls. All foods, pharmaceuticals and toothpastes were examined for microparticle content, and intakes of Ca and exogenous microparticles were compared between the two groups. Dietary intakes were significantly different between cases and controls for dietary fibre (12 (SD 5) v. 14 (sd 5) g/d; P=0.001) and sucrose (52 (sd 27) v. 45 (sd 18) g/d; P=0·04) but not for Ca. Estimated median TiO2 and Psil intakes (2·5 and 35mg/individual per d respectively, totalling 1012–1013 microparticles/individual per d) were broadly similar to per capita estimates and while there was wide variation in intakes between individuals there was no significant difference between subjects with CD and controls. Hence, if exposure to microparticles is associated with the inflammation of CD, then the present study rules out excess intake as the problem. Nonetheless, microparticle-containing foods have now been identified which allows a low-microparticle diet to be further assessed in CD.

Keywords

Dietary microparticlesCrohn's diseaseTitanium dioxideSilicatesParticulates
Type
Review Article
Information
British Journal of Nutrition , Volume 92 , Issue 6 , December 2004 , pp. 947 - 955
Copyright
Copyright © The Nutrition Society 2004

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