Review Article

Review Article: Dietary Fibre in the era of Microbiome Science

John O'Grady; Eibhlís M. O'Connor; Fergus Shanahan

Disclosures

Aliment Pharmacol Ther. 2019;49(5):506-515. 

In This Article

Challenges and Disappointments

In the past, several factors undermined enthusiasm for the health benefits of fibre. First was the undue emphasis on gastrointestinal pathology rather than metabolic disease. Second, some challenged Burkitt's enthusiasm for fibre by pointing to confounding variables such as healthy lifestyle factors including reduced smoking, greater exercise and consumption of nonfibre nutrients found in fruit and vegetables.[3] Third, there were exaggerated expectations for the therapeutic potential of fibre in reversing gastrointestinal pathology.[3,77,78] The potential for fibre to prevent rather than treat infectious, diverticular and neoplastic disorders would have been a more realistic objective. Changes in the microbiota in the peri-diverticular region may be an important step in diverticular disease pathogenesis and inflammation and a more appropriate target for fibre intervention.[79]

Inconsistent and confusing results from trials investigating dietary fibre and colorectal cancer risk led some to further question Burkitt's early claims.[3,80,81,82] However, much of the available prospective data have demonstrated an inverse relationship between fibre intake and incident colorectal cancer risk.[80,83,84,85,86] The previous discrepancies are likely explained by a lack of evidence for fibre in reducing the risk of recurrent adenomatous colorectal polyps.[78,86,87] Proposed mechanisms for a protective fibre effect on colorectal cancer risk include dilution of faecal carcinogens, quicker gut transit times, SCFA production and binding of carcinogenic bile acids.[80,81] In addition, butyrate can improve colonic atrophy by providing an energy source and as the primary source of energy for cancer cells is glucose, butyrate does not influence cancer cell proliferation.[33] Furthermore, the expression of GPR109A and GPR43 receptors is markedly reduced in colon cancer, suggesting a protective role of SCFA signalling.[33]

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