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Thought for food

diet and gut health

Quigley, Eamonn M.M.

Current Opinion in Gastroenterology: March 2019 - Volume 35 - Issue 2 - p 99–100
doi: 10.1097/MOG.0000000000000505
NUTRITION: Edited by Eamonn M.M. Quigley

Division of Gastroenterology and Hepatology, Lynda K and David M Underwood Center for Digestive Disorders, Houston Methodist Hospital and Weill Cornell Medical College, Houston, Texas, USA

Correspondence to Eamonn M.M. Quigley, MD, FRCP, FACP, MACG, FRCPI, Gastroenterology and Hepatology, 6550 Fannin St, SM 1201, Houston, TX 77030, USA. E-mail:

It stands to reason that the food that we eat should play critical role in sustaining health and could, equally well, predispose us to various digestive and systemic disorders. Similarly, the roles of food, the products of its digestion (and maldigestion) as well as of the various neural pathways and secretions (such as bile acids) stimulated by food ingestion in the genesis of common gastrointestinal symptoms have now been revealed in some detail [1▪▪]. Obvious as they might seem, relationships between what we eat and our likelihood of developing various gastrointestinal ailments have, for the most part, proven more difficult to unravel. The challenges faced in defining the precise relationship between what we ingest (be it food or alcohol) and diseases as important as cancer are very nicely illustrated by the contributions in this volume from Pan et al. (pp. 101–106) and Capurso et al. (pp. 107–113), respectively. Multiple confounding factors complicate the interpretation of epidemiological studies; is the effect of diet direct or mediated by other lifestyle factors [2]? For colon cancer, for example, only red meat has consistently emerged as a dietary risk factor [3]. With regard to alcohol and gastrointestinal cancer similar confounders and, most notably, cigarette smoking emerge [4]. It is interesting to note how the gut microbiome and its metabolites have emerged as potential cofactors or coconspirators with food and alcohol in gastrointestinal carcinogenesis [4,5▪▪,6▪▪]. Of these metabolites, bile acids (molecules that have enjoyed a true renaissance in homeostasis through multiple pathways) are very much in the limelight [7]. In this volume, Pan et al. urge us to move away from an obsession with individual dietary components and toward an examination of overall dietary patterns and make a strong argument that it is these patterns (e.g., Mediterranean vs. Western) that truly determine risk or confer benefit. Indeed, diet and physical activity may not only help to prevent cancer but prolong survival [8].

Anyone who spends time in a general gastroenterology clinic will be all too familiar with a patient's contention that their symptoms rest entirely on an allergy to certain foods. Unfortunately, there is no shortage of support for this usually unfounded contention in the media and even from healthcare practitioners or those who masquerade as such. Witness the ‘gluten free’ epidemic [9]! When subjected to rigorous evaluation many of these dietary prescriptions fail to pass muster [10]. Dr Lin, in a very timely study, (pp. 114–118) takes us carefully through the definition of food allergy and its diagnosis and in so doing makes it absolutely clear that most gastrointestinal ailments have nothing to do with true food allergy, a potentially fatal and largely systemic issue.

Some unfortunate individuals, whether because of congenital anomaly, trauma, surgical resection, or intestinal disease (or some combination of these insults), can no longer sustain adequate nutrition via the oral or enteral routes and become reliant on parenteral nutrition (formerly referred to as total parenteral nutrition) [11▪▪]. Though fortunately rare, affected individuals require specialist care and intensive monitoring as well laid out in their review by Dibb and Lal (pp. 119–125). They emphasize the basics – attention to the care of the line, regular monitoring of caloric needs and electrolyte status, and a keen eye for the early detection of complications. One of the most feared of these, of course, is liver disease. Formerly, and erroneously, in the dim and distant past, referred to as total parenteral nutrition-related liver disease [12], intestinal failure-associated liver disease (IFALD) is now seen to be multifactorial and not just a consequence of the contents of parenteral nutrition. Rochling and Catron (pp. 126–133) take us through the various factors that may contribute to this potentially disastrous outcome, how they can be prevented, and how IFALD can be detected and reversed as early as possible. There are important messages here for all who care for patients dependent on parenteral nutrition. Here again the microbiome makes an appearance – though data are still incomplete it seems likely that microbes and/or their metabolites and/or their interactions with the host immune system may play an important role in IFALD and other complications of parenteral nutrition [13,14,15▪].

Regrettably, nutrition has ceded its space in many a gastrointestinal curriculum to more ‘exciting’ topics such as endoscopy, inflammatory bowel disease, cancer, and liver disease. The contributions in this volume should serve as a timely reminder of the critical role of nutrition in the everyday practice of the gastroenterologist and the well-being of his or her patients. We must give more thought to food.

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Financial support and sponsorship

Supported in part by a bequest from the Hughes-Sterling Foundation.

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Conflicts of interest

There are no conflicts of interest.

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Papers of particular interest, published within the annual period of review, have been highlighted as:

  • ▪ of special interest
  • ▪▪ of outstanding interest
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1▪▪. Barbara G, Feinle-Bisset C, Ghoshal UC, et al. The intestinal microenvironment and functional gastrointestinal disorders. Gastroenterology 2016; [epub ahead of print].

A comprehensive review of the impact of luminal factors, including food and digesta, in the genesis of common gastrointestinal symptoms.

2. Grosso G, Bella F, Godos J, et al. Possible role of diet in cancer: systematic review and multiple meta-analyses of dietary patterns, lifestyle factors, and cancer risk. Nutr Rev 2017; 75:405–419.
3. Sasso A, Latella G. Dietary components that counteract the increased risk of colorectal cancer related to red meat consumption. Int J Food Sci Nutr 2018; 69:536–548.
4. Capurso G, Lahner E. The interaction between smoking, alcohol and the gut microbiome. Best Pract Res Clin Gastroenterol 2017; 31:579–588.
5▪▪. Wroblewski LE, Peek RM Jr, Coburn LA. The role of the microbiome in gastrointestinal cancer. Gastroenterol Clin North Am 2016; 45:543–556.

A topic for the future: the burgeoning literature on the role of the microbiome in gastrointestinal cancers.

6▪▪. O’Keefe SJ. Diet, microorganisms and their metabolites, and colon cancer. Nat Rev Gastroenterol Hepatol 2016; 13:691–706.

The microbiome strikes again: a well-delineated assessment of the interactions between diet, the microbiome and their metabolites in colon cancer.

7. Di Ciaula A, Wang DQ, Molina-Molina E, et al. Bile acids and cancer: direct and environmental-dependent effects. Ann Hepatol 2017; 16 (Suppl. 1: s3-105):s87–s105.
8. Mehra K, Berkowitz A, Sanft T. Diet, physical activity, and body weight in cancer survivorship. Med Clin North Am 2017; 101:1151–1165.
9. Pearlman M, Casey L. Who should be gluten-free? A review for the general practitioner. Med Clin North Am 2019; 103:89–99.
10. Dionne J, Ford AC, Yuan Y, et al. A systematic review and meta-analysis evaluating the efficacy of a gluten-free diet and a low FODMAPs diet in treating symptoms of irritable bowel syndrome. Am J Gastroenterol 2018; 113:1290–1300.
11▪▪. Lappas BM, Patel D, Kumpf V, et al. Parenteral nutrition: indications, access, and complications. Gastroenterol Clin North Am 2018; 47:39–59.

A comprehensive discussion of the current status of parenteral nutrition.

12. Quigley EM, Marsh MN, Shaffer JL, Markin RS. Hepatobiliary complications of total parenteral nutrition. Gastroenterology 1993; 104:286–301.
13. Pierre JF. Gastrointestinal immune and microbiome changes during parenteral nutrition. Am J Physiol Gastrointest Liver Physiol 2017; 312:G246–G256.
14. Cahova M, Bratova M, Wohl P. Parenteral nutrition-associated liver disease: the role of the gut microbiota. Nutrients 2017; 9: pii: E987.
15▪. Neelis E, de Koning B, Rings E, et al. The gut microbiome in patients with intestinal failure: current evidence and implications for clinical practice. JPEN J Parenter Enteral Nutr 2018; [epub ahead of print].

The microbiota again! This time in relation to intestinal failure.

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