Objective: To determine the efficacy of a breakfast promotion intervention based on Health Promoting Schools processes. Design: Schools were recruited and randomly allocated into intervention (seven schools) or control (six schools) groups. Intervention schools formed working groups, discussed their specific breakfast issues, and developed, implemented and evaluated their action plans. The students completed a survey on breakfast eating habits and knowledge at baseline (February‐April 2002) and at follow up (November‐December 2002). Subjects: 792 seventh grade students (11–12 years) (n = 341 for the control group; n = 451 for the intervention group). The response rate for completion of the follow up survey was 95% for the intervention group and 96% for the control group. Setting: Thirteen schools, including 12 government and one independent school, with seven located in metropolitan, four in rural and two in remote areas of southern Queensland. Main outcome measures: Proportion of children reporting they usually skip breakfast one or more days per school week; Consumption of selected breakfast food items, including energy‐dense, micronutrient‐poor food or beverage choices; Selection of perceived ‘healthy breakfast meals’ from a list provided. Statistical analyses: Frequencies of responses and cross tabulations were calculated using SPSS version 11.0. Results: Breakfast skipping increased by a greater percentage in the control group compared to the intervention group (20.2% vs 4.5%). The proportion of children reporting that they ate at least one ‘poor food choice’ for breakfast on the day of the survey decreased from 16.4% to 14.8% for the intervention group, while this rate more than doubled (9.7% to 19.9%) for the control group. Conclusion or application: Use of the Health Promoting Schools approach to address the quality of breakfast consumption by upper primary school children is recommended as an effective methodology.

In the healthy colon, sodium nitrite stimulates mucosal metabolism of short-chain fatty acids and absorption of ions, both functions that are impaired in the mucosa of patients with ulcerative colitis (UC). To assess the role of nitrite in colonic inflammatory disease, sodium nitrite was measured in rectal dialysate of 49 subjects (18 controls, 23 UC and 8 other colitis). None of the control or quiescent UC patients had measurable levels of nitrite while 78% of patients with acute UC and 38% of patients with other colitis had measurable nitrite levels (acute UC vs. other colitis eχ² = 5.555, p < 0.02). Functional acitivity of the colonic mucosa, judged by bicarbonate output, was impaired in all subjects with measurable nitrite levels in UC. Detection of nitrite in acute colitis suggests impaired oxidation of nitrite to nitrate in the colonic mucosa or impaired luminal reduction of nitrite to NH₄ by bacteria.

Elevated levels of luminal nitrite and a lowered luminal pH were found in 77 percent of patients with acute ulcerative colitis. No luminal nitrite was found in healthy control subjects. Nitrites are a secretory product of activated macrophages and neutrophils of the lamina propria, whereas the lowered luminal pH is due to diminished bicarbonate formation by impaired colonocytes. A hypothesis is put forward that nitrites, lowered pH, and bacterial amines are conducive to formation of carcinogenic n-nitroso compounds, which reflect a cancer risk in patients with ulcerative colitis dependent on the type and extent of inflammatory cell activation as well as metabolic impairment of colonic epithelial cells.

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