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

• Published in: British journal of nutrition Vol. 92; no. 6; pp. 947 - 955
• Main Authors: Lomer, Miranda C. E., Hutchinson, Carol, Volkert, Sara, Greenfield, Simon M., Catterall, Adrian, Thompson, Richard P. H., Powell, Jonathan J.
• Format: Journal Article
• Language: English
• Published: Cambridge, UK Cambridge University Press 01.12.2004
• Subjects: Adolescent; Adult; Aged; Bacteria; Biocompatible Materials; Biological and medical sciences; Calcium, Dietary - administration & dosage; Crohn Disease - etiology; Crohn's disease; Diet; Dietary fiber; Dietary Fiber - administration & dosage; Dietary microparticles; Dietary Sucrose - administration & dosage; Dietary Supplements; Energy Intake - physiology; Female; Food; Food Additives - administration & dosage; Food Analysis; Gastroenterology; Gastroenterology. Liver. Pancreas. Abdomen; Humans; Male; Medical sciences; Middle Aged; Nutrition research; Other diseases. Semiology; Particulates; Pharmaceutical Preparations - administration & dosage; Silica; Silicates; Silicates - administration & dosage; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Titanium; Titanium - administration & dosage; Titanium - adverse effects; Titanium dioxide; Toothpastes - administration & dosage; United Kingdom > UK; Particulates; Crohn's disease; Silicates; Titanium dioxide; Dietary microparticles; Human; Crohn disease; Dietary microparticles: Crohn's disease: Titanium dioxide: Silicates: Particulates; Food intake; Digestive diseases; Intestinal disease; Microparticle; Endogenous substance; Feeding; Inflammatory disease; Inorganic compound
• ISSN: 0007-1145; 1475-2662
• DOI: 10.1079/BJN20041276

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.