Pharmaceutical/food grade titanium dioxide particles are absorbed into the bloodstream of human volunteers.

BACKGROUND: Exposure to persistent engineered nano and micro particles via the oral route is well established. Animal studies have demonstrated that, once ingested, a small proportion of such particles translocate from the gastrointestinal tract to other tissues. Exposure to titanium dioxide is widespread via the oral route, but only one study has provided indirect evidence (total titanium analyses) of absorption into the blood stream in humans. We sought to replicate these observations and to provide additional evidence for particulate uptake. FINDINGS: Human volunteers with normal intestinal permeability were orally administered 100 mg pharmaceutical/food grade titanium dioxide. Blood samples were collected from 0.5 to 10 h post ingestion and analysed for the presence of reflectant bodies (particles) by dark field microscopy, and for total titanium by inductively coupled plasma mass spectrometry (ICP-MS). Blood film analyses implied early absorption of particles (2 h) with a peak maximum at 6 h following ingestion. The presence of these reflectant particles in blood roughly mirrored the levels of total titanium by ICP-MS, providing good evidence for the latter being a measure of whole particle (titanium dioxide) absorption. CONCLUSIONS: This study shows that a fraction of pharmaceutical/food grade titanium dioxide is absorbed systemically by humans following ingestion. It confirms that at least two routes of particle uptake may exist in the human gut- one proximal and one distal. Further work should quantify human exposure and uptake of such persistent particles.

An endogenous nanomineral chaperones luminal antigen and peptidoglycan to intestinal immune cells.

In humans and other mammals it is known that calcium and phosphate ions are secreted from the distal small intestine into the lumen. However, why this secretion occurs is unclear. Here, we show that the process leads to the formation of amorphous magnesium-substituted calcium phosphate nanoparticles that trap soluble macromolecules, such as bacterial peptidoglycan and orally fed protein antigens, in the lumen and transport them to immune cells of the intestinal tissue. The macromolecule-containing nanoparticles utilize epithelial M cells to enter Peyer's patches, small areas of the intestine concentrated with particle-scavenging immune cells. In wild-type mice, intestinal immune cells containing these naturally formed nanoparticles expressed the immune tolerance-associated molecule 'programmed death-ligand 1', whereas in NOD1/2 double knockout mice, which cannot recognize peptidoglycan, programmed death-ligand 1 was undetected. Our results explain a role for constitutively formed calcium phosphate nanoparticles in the gut lumen and show how this helps to shape intestinal immune homeostasis.

The comparative absorption of silicon from different foods and food supplements.

Dietary Si (orthosilicic acid; OSA) appears important in connective tissue health, and although the sources and intakes of Si are well established, its absorption is not. Si absorption was measured from eight high-Si-containing sources: alcohol-free beer; OSA solution (positive control); bananas; green beans; supplemental choline-stabilised OSA (ChOSA); supplemental monomethyl silanetriol (MMST); supplemental colloidal silica (CS); magnesium trisilicate British Pharmacopoeia antacid (MTBP). Two of the supplements and the antacid were pre-selected following an in vitro dissolution assay. Fasting, healthy subjects (CS, n 3; others, n > or = 5) each ingested two of the sources separated by a 1-week wash-out period. Blood and urine were collected and measured for total Si concentrations by inductively coupled plasma optical emission spectrometry. Absorption, based on urinary Si excretion, was highest for MMST and alcohol-free beer (64% of dose), followed by green beans (44%), OSA (43%), ChOSA (17%), bananas and MTBP (4%) and CS (1%). Peak serum concentrations occurred by 0.5 h for MMST and green beans, 1.5 h for OSA and alcohol-free beer, 2 h for ChOSA and CS, and 4 h for MTBP. Area under the serum curves correlated positively with urinary Si output (r 0.82; P < 0.0001). Absorption of Si from supplements and antacids was consistent with their known chemical speciation and kinetics of dissolution under simulated gastrointestinal conditions. Monomeric silicates were readily absorbed, while particulate silicates were decreasingly well absorbed with increasing polymerisation. The present results highlight the need to allow for relative absorption of Si from different foods or supplements in subsequent epidemiological and intervention studies.

Increased longitudinal growth in rats on a silicon-depleted diet.

Silicon-deficiency studies in growing animals in the early 1970s reported stunted growth and profound defects in bone and other connective tissues. However, more recent attempts to replicate these findings have found mild alterations in bone metabolism without any adverse health effects. Thus the biological role of silicon remains unknown. Using a specifically formulated silicon-depleted diet and modern methods for silicon analysis and assessment of skeletal development, we undertook, through international collaboration between silicon researchers, an extensive study of long-term silicon depletion on skeletal development in an animal. 21-day old female Sprague-Dawley rats (n=20) were fed a silicon-depleted diet (3.2 microg Si/g feed) for 26 weeks and their growth and skeletal development were compared with identical rats (n=10) on the same diet but with silicon added as Si(OH)(4) to their drinking water (53.2 microg Si/g water); total silicon intakes were 24 times different. A third group of rats, receiving a standard rodent stock feed (322 microg Si/g feed) and tap water (5 microg Si/g water), served as a reference group for optimal growth. A series of anthropometric and bone quality measures were undertaken during and following the study. Fasting serum silicon concentrations and especially urinary silicon excretion were significantly lower in the silicon-deprived group compared to the supplemented group (P=0.03 and 0.004, respectively). Tibia and soft-tissue silicon contents did not differ between the two groups, but tibia silicon levels were significantly lower compared to the reference group (P<0.0001). Outward adverse health effects were not observed in the silicon-deprived group. However, body lengths from week 18 onwards (P<0.05) and bone lengths at necropsy (P

Low dietary calcium levels modulate mucosal caspase expression and increase disease activity in mice with dextran sulfate sodium induced colitis.

Dietary calcium (Ca) positively modulates the susceptibility to colon cancer, but its effects on related or earlier colonic pathologies, such as inflammation and mucosal dysregulation, are poorly understood. We tested the effects of differing dietary Ca levels on acute dextran sulfate sodium (DSS)-induced colitis in mice. BALB/c mice received a normal Ca (NCa) diet (0.5% Ca), a high Ca (HCa) diet (1.5% Ca), a low Ca (LCa) diet (0.05% Ca), or a very low Ca (VLCa) diet (0.009% Ca) for 3 wk. Mucosal caspases 1, 3, and 9 were assessed by Western blotting, and the histological crypt score was assessed by microscopy. Half of the mice in each group received DSS (1.5%) for 20 d in their drinking water, and disease activity was assessed. Increasing or lowering dietary Ca increased mucosal caspases (P < 0.0001 vs. NCa). Crypt scores increased with decreasing dietary Ca levels (P < 0.0001, r = -0.675), indicating that elevated caspases in LCa groups reflected early subclinical inflammation. DSS-induced disease activity was higher in mice fed low dietary Ca levels [P < 0.0001, VLCa and DSS vs. NCa and DSS (NCaDSS) and P < 0.005, LCa and DSS vs. NCaDSS], and mice from the VLCa group were moribund within 11 d of DSS administration. Those in the HCa group did not differ greatly from controls. Together, these data indicate that Ca protects against DSS-induced colitis in mice. The mechanisms are unclear, but the calcium-sensing receptor and/or luminal precipitates of calcium phosphate microparticles may be involved. Whether these observations can be extended to patients with colitis or infectious diarrhea deserves consideration.

Fine particles that adsorb lipopolysaccharide via bridging calcium cations may mimic bacterial pathogenicity towards cells.

Fine particles (10(2)- to 10(3)-nm diameter) are potentially potent adjuvants in acquired immune responses but little is known about their interaction with pathogen-associated molecular patterns (PAMPs) and impact upon innate immunity. Here we show that 200-nm-sized, food-grade titanium dioxide avidly binds lipopolysaccharide (LPS) with bridging calcium cations, and the complex induces marked proinflammatory signalling in primary human mononuclear phagocytes. In particular, caspase 1-dependent interleukin-1beta (IL-1beta) secretion was induced at levels far greater than for the sum of the individual components, and without concomitant secretion of modulatory cytokines such as interleukin-1 receptor antagonist or transforming growth factor-beta1 (TGF-beta1). Secondly, the conjugate induced apoptotic-like cell death. These responses were inhibited by blockade of both phagocytosis and scavenger receptor uptake. Specific caspase 1-facilitated IL-1beta secretion and apoptosis following phagocytosis are features of cellular responses to certain invasive, enteric pathogens, and hence induction of these events may be mimicked by fine particle-LPS conjugates. The inadvertent adsorption of PAMPs to ingested, inhaled, or "wear" fine particulate matter provides a further potential mechanism for the proinflammatory nature of fine particles.

Serum iron curves can be used to estimate dietary iron bioavailability in humans.

Erythrocyte incorporation of isotopic iron (Fe) is the standard method for assessing iron bioavailability, but the process is expensive, technically difficult, and gives no information on the kinetics of absorption. The main objective of this study was to validate serum Fe curves as measures of dietary iron absorption because previous work demonstrated that serum iron curves can be generated with iron doses as low as 5-20 mg and that up to 20 mg iron can be added to meals without affecting relative absorption. In 3 studies, groups (n = 10, 10, 21) of Fe-deficient, mildly anemic women consumed meals of varying calculated Fe bioavailability, with and without added ferric chloride (10 mg Fe). Blood samples were collected at baseline and every 30 min for 4 h after the meal. Serum Fe concentrations were measured. Areas under the serum Fe curves and peak concentrations were used in different models to estimate Fe absorption and uptake. In 21 subjects, (58)Fe-enriched ferric chloride was added to the meals, and blood was taken 2 wk later to calculate red cell isotope incorporation. The addition of 10 mg Fe to test meals produced measurable serum iron curves even when the meal Fe bioavailability was low. Serum Fe curves were highly reproducible and were affected as expected by food composition. Even the single measurement at the estimated time of peak iron concentration was correlated significantly with erythrocyte incorporation of (58)Fe (r = 0.72, P < 0.0001). Hence the extent and rate of absorption of nonheme iron from meals, rather than in individuals, can be investigated with such subjects without the need for isotopes.

The superior mesenteric artery syndrome; an unusual cause of vomiting.

A 29-year-old female presented with anorexia, vomiting and weight loss. A diagnosis of superior mesenteric artery syndrome was made based upon contrast duodenography and then at laparotomy when the patient was successfully treated with a duodenojejunostomy. Superior mesenteric artery syndrome is a rare cause of vomiting not detectable by endoscopy, but is eminently amenable to treatment.

Lack of efficacy of a reduced microparticle diet in a multi-centred trial of patients with active Crohn's disease.

BACKGROUND AND AIMS: Dietary microparticles, which are bacteria-sized and non-biological, found in the modern Western diet, have been implicated in both the aetiology and pathogenesis of Crohn's disease. Following on from the findings of a previous pilot study, we aimed to confirm whether a reduction in the amount of dietary microparticles facilitates induction of remission in patients with active Crohn's disease, in a single-blind, randomized, multi-centre, placebo controlled trial. METHODS: Eighty-three patients with active Crohn's disease were randomly allocated in a 2 x 2 factorial design to a diet low or normal in microparticles and/or calcium for 16 weeks. All patients received a reducing dose of prednisolone for 6 weeks. Outcome measures were Crohn's disease activity index, Van Hees index, quality of life and a series of objective measures of inflammation including erythrocyte sedimentation rate, C-reactive protein, intestinal permeability and faecal calprotectin. After 16 weeks patients returned to their normal diet and were followed up for a further 36 weeks. RESULTS: Dietary manipulation provided no added effect to corticosteroid treatment on any of the outcome measures during the dietary trial (16 weeks) or follow-up (to 1 year); e.g., for logistic regression of Crohn's disease activity index based rates of remission (P=0.1) and clinical response (P=0.8), in normal versus low microparticle groups. CONCLUSIONS: Our adequately powered and carefully controlled dietary trial found no evidence that reducing microparticle intake aids remission in active Crohn's disease.

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

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 7 d 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 35 mg/individual per d respectively, totalling 10(12)-10(13) 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.

Selective and effective bactericidal activity of the cobalt (II) cation against Helicobacter pylori.

BACKGROUND: Although the anti-Helicobacter pylori activity of bismuth is well established, the therapeutic potential of other metal ions against the organism is not known. MATERIALS AND METHODS: We measured the minimum inhibitory concentrations of a series of metal ions, including several cobalt (II) compounds against four type strains and seven clinical isolates of H. pylori using three standard broth culture media and a defined medium. Other intestinal bacteria were also investigated for specificity of action. RESULTS: Cobalt chloride had marked activity against H. pylori (minimum inhibitory concentration range was 0.03-1.0 mg/l). The effect was specific because other transition metals had no effect and other intestinal bacteria were not affected by cobalt chloride. Activity was attributable to free cobalt ions as ligands inhibited activity in proportion to their affinity for the ions. Inhibition of cobalt activity was also observed in the presence of nickel, in a dose dependent fashion. However, cobalt activity was not directed towards the nickel-dependent urease enzyme because its effect was similar in wild-type and urease negative mutant strains of H. pylori. Finally, the viability of H. pylori was reduced at the same rate with 2 mg/l cobalt as with 1 mg/l amoxicillin. CONCLUSIONS: Cobalt competes for nickel in its acquisition by H. pylori, but mediates toxicity in a nonurease dependent fashion. As cobalt MIC is similar to some antibiotics and 10 to a hundred times lower than for bismuth, cobalt may represent an effective form of therapy for H. pylori infection.

The silicon content of beer and its bioavailability in healthy volunteers.

Dietary Si, as soluble orthosilicic acid (OSA), may be important for the growth and development of bone and connective tissue. Beer appears to be a major contributor to Si intake, although the Si content of beer and its bioavailability in human subjects have not been well established. Here we investigated the Si content of different beers and then estimated Si absorption from beer in healthy volunteers. The Si content of seventy-six different beers was estimated using inductively coupled plasma optical emission spectrometry and one of the beers, used in the ingestion study, was ultrafiltered to determine OSA content. Next, following the ingestion of 0.6 litres beer (22.5 mg Si; 4.6 % (v/v) ethanol), serum and urinary Si levels were measured in nine healthy volunteers over a 6 h period. A solution of OSA was similarly investigated as a positive control and water and 4.6 % ethanol as negative controls. The mean Si level of beer was 19.2 (sd 6.6) mg/l; the median Si level was 18.0 mg/l. There was no significant difference in the Si levels of the different beers by geographical origin or type of beer. Serum and urinary Si levels increased considerably following the ingestion of beer or a solution of OSA but not with the ingestion of either 4.6 % ethanol or water. The ultrafilterability of Si from beer (about 80 %) and its absorption in volunteers (about 55 %) was comparable with that of a solution of OSA suggesting that Si in beer is present chiefly in a monomeric form and is readily bioavailable.

Efficacy and safety of endoscopic dilation of esophageal strictures in epidermolysis bullosa.

BACKGROUND: Epidermolysis bullosa is a rare genetically determined disorder of the stratified squamous epithelium. Patients with the most severe forms develop scarring of the esophagus after ingestion of food. This results in dysphagia, which severely compromises the ability to eat. Maintenance of adequate nutritional intake is a central aim, but the most appropriate method is unknown. METHODS: The results of endoscopic through-the-scope balloon dilation under propofol anesthesia in 53 patients with epidermolysis bullosa and esophageal strictures are reported. RESULTS: Seventy-five percent of patients had a single stricture (range 1 to 6 strictures), most often in the proximal esophagus (median 20 cm from incisors). A total of 182 dilations were performed (median two per patient) over a median follow-up period of 3.5 years. For all but 3 patients, there was an improvement in the dysphagia score. There was a mean increase in weight after the procedure of 2.9 kg: 95% CI[2.0, 3.8]; p<0.001, over a median 29 days. There was no significant post-procedure morbidity. CONCLUSIONS: Endoscopic balloon dilation is a safe and effective treatment for the esophageal strictures of epidermolysis bullosa. In the majority of patients, dilation relieves dysphagia and improves nutritional status.

Intake of dietary iron is low in patients with Crohn's disease: a case-control study.

Patients with Crohn's disease (CD) often experience Fe deficiency (ID) and frequently alter their diet to relieve abdominal symptoms. The present study set out to assess whether patients with CD have dietary habits that lead to low Fe intakes and/or reduced bioavailable Fe compared with control subjects. Patients with asymptomatic CD were matched to controls (n 91/group). Dietary intakes of Fe and contributions from different food groups were compared using a 7 d food diary. Promoters and inhibitors of non-haem Fe absorption were investigated and a recently published algorithm was applied to assess bioavailable Fe. Fewer patients than controls met the reference nutrient intake for Fe (32% CD patients v. 42% controls). Overall, patients had significantly lower mean Fe intakes (by 2.3 mg/d) and Fe density (by 0.26 mg/MJ (1.1 mg/1000 kcal)) compared with controls (both P<0.001). Differences were mainly due to a preference among CD patients for low-fibre non-Fe fortified cereals, particularly breakfast cereals. In particular, control subjects had higher Fe intakes than matched CD subjects for men (P<0.001) and women less than 50 years (P=0.03). Intakes of both ascorbic acid (P<0.001) and phytic acid (P<0.01), but not animal tissue (P=1.0), were lower in patients with CD, but these had no overall effect on the predicted percentage of bioavailable Fe. Thus total bioavailable Fe was reduced in patients with CD due to lower intakes (P<0.01). Dietary Fe intakes are low in CD patients, which may contribute to an increased risk of ID and anaemia. Changing dietary advice may compromise perceived symptoms of the disease so the need for Fe supplementation should be carefully considered.

Neoplasia of the tongue in a patient with Crohn's disease treated with azathioprine: case report.

Azathioprine is now widely used for the maintenance treatment of Crohn's disease, but there are concerns whether azathioprine could predispose to malignancy in patients with inflammatory bowel disease. We report here a case of a 39-year-old non-smoking male with Crohn's disease who had been treated for 3 years with azathioprine and developed a lingual ulcer. Biopsy revealed squamous cell carcinoma, a tumour not previously associated with Crohn's disease.

Selective binding of nucleotide probes by eosinophilic cationic protein during in situ hybridisation.

During in situ hybridisation on frozen and paraffin-embedded sections of bowel for IkappaB alpha, oligodeoxyribonucleotide probes were found to bind more avidly to eosinophils than target mRNA. This binding could not be obviated using strategies previously employed to block either binding of long DNA probes (200-mers) to eosinophils in bone marrow smears, or of riboprobes to eosinophils in sections of bowel, without removing specific hybridisation of probes. That this binding could arise through interaction of anionic oligodeoxyribonucleotides with eosinophil cationic protein, which has an unusually high pI, and is abundant in cytoplasmic granules of eosinophils, was demonstrated in vitro using real-time biomolecular interaction analysis with a BiacoreX instrument. Finally, a relationship between probe hydrophobicity, measured by reverse phase ion-pair high performance liquid chromatography, and in situ binding of individual probes to eosinophils was demonstrated. Effective tissue penetration by hydrophobic probes and subsequent strong probe-eosinophilic cationic protein interactions therefore may confound the interpretation of in situ hybridisation performed with oligonucleotide probes in eosinophil-containing tissues, such as bowel and nasal polyps.

The role of dietary microparticles and calcium in apoptosis and interleukin-1beta release of intestinal macrophages.

BACKGROUND & AIMS: The intestinal mucosa is exposed to micron-sized, man-made exogenous particles (e.g., titanium dioxide) and freshly formed endogenous particles (calcium phosphate). A role for such microparticles in inflammation has been proposed, and here we examined their effects on lamina propria mononuclear cells. METHODS: Lamina propria mononuclear cells were isolated from patients with and without inflammatory bowel disease and incubated with lipopolysaccharide, titanium dioxide, and calcium +/- citrate, as well as a conjugate of lipopolysaccharide, calcium, and titanium dioxide. Interleukin-1beta and interleukin-1 receptor antagonist were measured by enzyme-linked immunosorbent assay in culture supernatants and macrophage apoptosis by flow cytometry. Mechanistic studies were undertaken in normal peripheral blood mononuclear cells. RESULTS: Baseline levels of interleukin-1beta and macrophage apoptosis were greater in inflammatory bowel disease than in normal lamina propria mononuclear cells. Lipopolysaccharide and titanium dioxide had no additional effect, but calcium, and more so the conjugate, induced interleukin-1beta release in proportion to the degree of inflammation. Citrate, used to prevent in situ calcium phosphate formation, negated lamina propria mononuclear cell stimulation. Macrophage apoptosis was also increased by calcium and the conjugate. In peripheral blood mononuclear cells, inhibition of caspase 1 reduced interleukin-1beta secretion, whereas blockade of phagocytosis inhibited calcium-induced apoptosis and interleukin-1beta release. CONCLUSIONS: The endogenous luminal microparticle calcium phosphate Promotes apoptosis of intestinal macrophages. Concomitantly, interleukin-1beta is released, which is enhanced in the presence of inflamed cells and/or exogenous dietary microparticles. Endogenous or exogenous microparticles could aggravate the ongoing inflammation of inflammatory bowel disease.

Fine and ultrafine particles of the diet: influence on the mucosal immune response and association with Crohn's disease.

Crohn's disease is a modern Western disease characterised by transmural inflammation of the gastrointestinal tract. It is of unknown aetiology, but evidence suggests that it results from a combination of genetic predisposition and environmental factors. Bacterial-sized microparticles (0.1-1.0 microm) are potent adjuvants in model antigen-mediated immune responses and are increasingly associated with disease. Microparticles of TiO2 and aluminosilicate accumulate in macrophages of human gut-associated lymphoid tissue where the earliest signs of lesions in Crohn's disease are observed. Dietary microparticles are of endogenous or exogenous origin. Endogenous microparticles dominate and are calcium phosphate (most probably hydroxyapatite), which precipitates in the lumen of the mid-distal gastrointestinal tract due to secretion of Ca and phosphate in the succus entericus. Exogenous dietary microparticles are contaminants (soil and/or dust) and food additives. TiO2, for example, is a food colourant, and aluminosilicates are anti-caking agents, although some aluminosilicates occur as natural contaminants. Food additives alone account for ingestion of approximately 10(12) particles/person per d. Possible mechanisms for the role of exogenous and endogenous dietary microparticles in promoting toleragenic or immune responses of gastrointestinal mucosal phagocytosis are discussed. In a double-blind randomised pilot study we have shown that a diet low in Ca and exogenous microparticles appears to alleviate the symptoms of ileal Crohn's disease, with a significant (P= 0.002) improvement in the Crohn's disease activity index. A multi-centre trial and further mechanistic studies at the cellular level are underway.

Dietary silicon intake and absorption.

BACKGROUND: Increasing evidence suggests that silicon is important in bone formation. The main source of silicon for humans is the diet, but the bioavailability of silicon from solid foods is not well understood. OBJECTIVE: We estimated the dietary intake of silicon by adults, separately for men and women and for different age groups. Foods that were major contributors to silicon intake were identified. We then estimated the gastrointestinal uptake of silicon from major food sources and studied how uptake correlated with the silicon contents of the foods. DESIGN: Silicon intakes were determined in cohorts from the original Framingham Study and the Framingham Offspring Study by using a 126-item food-frequency questionnaire. Gastrointestinal uptake of silicon from foods was estimated in 3-8 healthy subjects by using urinary silicon excretion as a surrogate measure of silicon uptake. RESULTS: Mean silicon intakes in men (30 and 33 mg/d in the original Framingham and Framingham Offspring cohorts, respectively) were significantly higher than those in women (24 and 25 mg/d in the 2 cohorts, respectively; P = 0.0001). Silicon intake decreased with age (P < 0.001, adjusted for sex). The major food sources were beer and bananas in men and bananas and string beans in women. Silicon was readily available from foods; a mean of 41% of the ingested silicon was excreted in urine. The silicon content of the foods consumed was significantly correlated with urinary silicon excretion (P = 0.019). CONCLUSIONS: Solid foods are a major source of available silicon. The association between dietary silicon intake and bone health should now be investigated.