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Chronic subclinical bowel inflammation may explain increased risk of colorectal cancer in obese people
  1. Biku J John,
  2. Al Mutaz Abulafi,
  3. Andrew Poullis,
  4. Michael Anthony Mendall
  1. Mayday University Hospital, Croydon, UK
  1. Correspondence to:
    B J John
    Mayday University Hospital, London Road, Croydon CR7 7YE, UK; biku.john{at}

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We read with interest the recent articles on obesity, inflammation and colorectal cancer (CRC).1–3 Although insulin resistance is the most widely accepted underlying mechanism explaining the association between obesity and CRC, recent evidence suggests that the effects of obesity on the immune system in general and on the gut in particular may play a role. We propose that obesity predisposes to CRC through its effects on innate immune activation (IIA) and consequent subclinical bowel inflammation. We further propose that the role of insulin resistance is either complementary or might merely represent an epiphenomenon. The justification of our argument is explained below.

Recently, we studied the determinants of whole gut inflammation in a normal middle-aged population by determining levels of calprotectin in faeces. Calprotectin is a calcium-binding protein found only in neutrophils and monocytes. Levels in faeces correlate well with faecal levels of indium-labelled white cells and inflammatory bowel disease activity. It is well established that many risk factors for CRC influence levels of IIA in a healthy individual. Lack of physical exercise, for instance, is associated with increased serum levels of C reactive protein, as are body mass index, smoking and increasing age.4 We confirmed that faecal levels of calprotectin also correlated directly with increasing age, obesity, …

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  • Competing interests: None declared.