Clinical Study

British Journal of Cancer (2005) 93, 639–646. doi:10.1038/sj.bjc.6602770 www.bjcancer.com
Published online 30 August 2005

A pilot randomised controlled trial to reduce colorectal cancer risk markers associated with B-vitamin deficiency, insulin resistance and colonic inflammation

W R Bruce1, M Cirocco2, A Giacca3, Y-I Kim1,2,4, N Marcon2,4 and S Minkin5

  1. 1Department of Nutritional Sciences, University of Toronto, 150 College Street, Toronto, Ontario, Canada M5S 2E3
  2. 2Division of Gastroenterology, St Michael's Hospital, 30 Bond Street, Toronto, Ontario, Canada M3B 3R8
  3. 3Department of Physiology, University of Toronto, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
  4. 4Department of Medicine, University of Toronto, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
  5. 5Department of Public Health Sciences, University of Toronto, 12 Queen's Park Crescent, Toronto, Ontario, Canada M5S 1A8

Correspondence: Dr W Robert Bruce, E-mail: wr.bruce@utoronto.ca

Received 25 May 2005; Revised 4 August 2005; Accepted 4 August 2005; Published online 30 August 2005.

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Abstract

Colorectal cancer risk is associated with biochemical markers for B-vitamin deficiency, insulin resistance and colonic inflammation, suggesting that these three conditions are each involved in colon carcinogenesis. We expected that dietary supplements of folic acid, n-3 fatty acids and calcium would reduce the markers and thus possibly cancer risk. We therefore randomised 98 participants, with previous colonic polyps or intramucosal carcinomas, to a combined treatment of supplementary folic acid, fish oil and calcium carbonate, or placebos for 28 days. Blood and faecal samples were obtained prior to and at the conclusion of the intervention and analysed for plasma folate, homocysteine, insulin, free fatty acids, triglycerides and faecal calprotectin. In addition, plasma vitamin B12, thiamin, glucose and C-reactive protein were assessed. Our supplemental strategy modestly affected some of the biomarkers associated with folate metabolism and insulin resistance, but had no effect on those associated with colonic inflammation. This pilot study demonstrates the feasibility and practicality of clinical trials aimed at reducing diet-related biochemical risk markers for colon cancer. We suggest that long-term intervention studies with tumour-related end points should be undertaken when the intervention agents used are found effective in short-term biochemical risk marker trials.

Keywords:

homocysteine, folate, insulin, free fatty acids, triacylglycerol, calprotectin, C-reactive protein, n-3 fatty acids, calcium

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