Wednesday, April 30, 2014

Cereal fibre – key to healthy living

A walk down the ‘health aisle’ of your local supermarket is a powerful demonstration of the popularity of the ‘free-from’ movement, including gluten-free and grain-free. But in the pursuit of health by cutting out grains many people may be missing out on a key source of fibre and actually increasing their risk of chronic disease.

A recent study in the US found a diet higher in whole grain foods is more likely to be higher in fibre. While this may not seem like new news to most health care professionals, it seems many consumers may have forgotten the importance of these foods as a source of fibre.

The study found a strong association between the intake of whole grain foods, such as bread and breakfast cereal, with total dietary fibre intake for both children and adults. Compared to those who ate no whole grain, adults who ate at least 3 serves per day were 76 times more likely to fall into the highest fibre intake group. The major whole grain sources included bread/rolls, oatmeal, breakfast cereals, and popcorn. Among those with the highest whole grain intake, whole grain breakfast cereals were the greatest contributor to total dietary fibre.

To help Australians boost their fibre intake it is important to remind people of the importance of eating whole grain foods and high fibre grain foods in line with the Australian Dietary Guidelines recommendation to enjoy grain foods each day, choosing mostly whole grain and/or higher fibre varieties.

While fruit and veggies are an important part of the diet and key sources of fibre, two recent study highlight the importance of cereal fibre in the diet. These studies add to the significant body of evidence that higher intakes of cereal fibre reduce risk of a range of chronic conditions including obesity, heart disease, diabetes and colorectal cancer.

In the first study, a meta analysis of 17 prospective cohort studies found higher cereal fibre intakes were associated with a 23% reduced risk of type 2 diabetes. The risk reduction from cereal fibre was stronger than both total fibre (19%) and fruit fibre (6%). In comparison, there was no significant reduced risk with higher fibre intakes from vegetables.

Interestingly, this is the first study to determine the dose of fibre associated with reduced risk of type 2 diabetes. A reduced risk was seen with as little as 3 grams of cereal fibre per day and the risk decreased by 6 % for each additional 2 grams per day.  In comparison a threshold of 25 grams of total fibre was needed before a significant risk reduction was seen.

The second study, an analysis of two large US cohort studies, found heart attack survivors with higher cereal fibre intake had a 25% lower risk of dying in the nine years following their heart attack. Cereal fibre intake in particular demonstrated the greatest protection compared to other sources of fibre.

The current Nutrient Reference Values for dietary fibre are based on an estimated adequate intake for gastrointestinal function and adequate laxation. However this study adds to the significant body of evidence that higher intakes of cereal fibre reduce risk of a range of chronic conditions including obesity, heart disease, diabetes and colorectal cancer. Encouraging Australians to choose foods high in cereal fibre more often and ensuring whole grain foods are available may assist people to meet and/or exceed the adequate intakes for dietary fibre and achieve health benefits beyond the effects of fibre on gastrointestinal function and laxation.

  1. Li S, Flint A, Pai J, Forman J, Hu F, Willett W, Rexrode K, Mukamal K, Rimm E. Dietary fiber intake and mortality among survivors of myocardial infarction: prospective cohort study. BMJ 2014; 348 doi: (Published 29 April 2014)
  2. Reicks M, Jonnalagadda S, Albertson AM, Joshi N. Total dietary fibre intakes in the US population are related to whole grain consumption: results from the National Health and Nutrition Examination Survey 2009 to 2010. Nutrition Research. 2014,34(3):226-234. 
  3. Yao B1, Fang H, Xu W, Yan Y, Xu H, Liu Y, Mo M, Zhang H, Zhao Y. Dietary fiber intake and risk of type 2 diabetes: a dose-response analysis of prospective studies. Eur J Epidemiol. 2014,29(2):79-88.

Non-Coeliac Gluten Sensitivity – A Scientific Update

Grains & Legumes Nutrition Council
Written by Jessica Biesiekierski

The avoidance of wheat- and gluten-containing products is a worldwide phenomenon, where more than one million Australians purchase gluten-free products for health reasons.1 The Australian gluten-free market is growing up to 20% annually1 and in the USA, it is suggested that as high as 8% of the population purchase gluten- and wheat-free products.2 While coeliac disease is a well-established entity, the evidence-base for gluten as a trigger of symptoms in patients without coeliac disease is minimal (so-called ‘non-coeliac gluten sensitivity’; NCGS). Gluten has been putatively linked to a wide range of conditions including various skin problems,3 fatigue and migraine,4 weight gain5 and autism,6 but most often blamed for gastrointestinal (GI) symptoms.7 Recent data has suggested NCGS may exist, however much remains unknown and important considerations are required before diagnosis. This update discusses the latest scientific evidence in our current understanding of NCGS.

The most well understood gluten intolerance is coeliac disease, an autoimmune GI disease estimated to affect 1% or more of Western populations.8 It occurs when genetically susceptible patients are exposed to dietary gluten, the major protein in wheat, rye, barley and related grains, activating a specific immune response. This leads to small intestinal villous atrophy, intraepithelial lymphocytosis and the development of GI symptoms.9 The only known treatment is a lifelong, strict gluten-free diet (GFD).

Many of the GI symptoms seen in coeliac disease (such as diarrhoea, abdominal pain, bloating, wind, distension and altered bowel habit) can mimic irritable bowel syndrome (IBS). IBS is a disorder characterised by GI symptoms but with no abnormal pathology and affects 15% of the population.10

There is an emerging belief that gluten sensitivity might mediate IBS symptoms.11 Until recently, there were no controlled clinical studies investigating NCGS and the scientific evidence assessing the effects of gluten outside of coeliac disease had focused on animal models or cancer cell lines.12,13 Regardless, the GFD is increasingly prescribed by alternative health practitioners and recommended on Internet sites.

Is it really gluten?
Other components of wheat have been studied in detail, such as the carbohydrate or more specifically, the fructan component.14 Fructans are one of a group of short-chain carbohydrates poorly absorbed in the small intestine. The poor absorption, by virtue of their small molecular size and rapid fermentability, increases delivery of water and fermentable substrates to the colon.15,16 These effects result in increased gas production and GI symptoms in patients with IBS.16-18 This group have been termed FODMAPs, which stands for Fermentable Oligo-, Di-, and Mono-saccharides And Polyols.19 A diet low in FODMAPs has become a well-understood and evidence-based strategy, leading to symptomatic improvement in 70 to 74% of patients with IBS.17,20,21

FODMAPs are found in a wide variety of foods and include lactose (in milk), excess fructose (in pears, apples), fructans and fructo-oligosaccharides (FOS; in artichoke, garlic, onions, wheat and rye), galacto-oligosaccharides (GOS; stachyose and raffinose in legumes), and sugar polyols (sorbitol and mannitol in stone fruits and artificial sweeteners).22,23 Recent grain and cereal composition data has highlighted that wheat- and rye-derived products contain the highest FODMAP content, predominantly fructans and GOS.24 Cereal products with the lowest FODMAP contents are mostly gluten-free, based on rice, oat, quinoa and corn ingredients.24 Therefore, choosing ‘gluten-free’ products is likely to result in automatically selecting a low-FODMAP diet.

What is so wrong with being gluten-free?
Exclusion of coeliac disease – The prescription of a GFD for gut and other symptoms may lead to the under diagnosis of coeliac disease. Two in three patients with self-perceived NCGS do not have coeliac disease adequately excluded,25 which increases patients’ risk of inadequate management and screening of associated complications if left untreated (i.e., reduced bone health,26 long-term mortality27).

Nutritional concerns – The GFD is markedly restrictive, presents challenges when eating at places other than home and can be two to three times more expensive than that of a standard diet.28 It can also be nutritionally inadequate, especially in fiber and B-vitamins.29 In addition, at least 45% of patients with self-perceived NCGS self-initiate the GFD and have not undergone dietetic education to ensure maintained nutritional adequacy.25 Long-term restrictive diets, particularly avoidance of wheat- and gluten-based products, are likely to have health implications given their important role in bowel health.

What is the current evidence behind NCGS?
Evaluation of exclusion diets has previously shown wheat-induced gut symptoms,30 but given wheat is also high in fructans, such evidence for NCGS has been inconclusive. Other studies, mostly completed in animal models31 or uncontrolled clinical trials have found some evidence for the efficacy of a GFD. In these published studies, however, either the patients have had coeliac-associated antibodies or intraepithelial lymphocytosis in the duodenum32,33 and, therefore, have not been convincingly defined as NCGS.

The first definitive experiment where the effect of gluten, free from contamination from carbohydrates, was evaluated in patients with IBS where coeliac disease had been definitively excluded was published in 2011.34 This study was a randomised double-blind, placebo-controlled trial of a single dose of gluten (16 g/day for 6 wk) without a controlled background in parallel groups (n=34). The results showed gluten specifically induced GI symptoms and tiredness in those who have NCGS. Although these results were exciting, they must be reproduced to confirm the existence of NCGS.

The same research group went onto conduct another dietary trial using a crossover design and supplying a controlled diet.35 Following a 2-week run-in period on a low FODMAP diet, 40 patients with NCGS and IBS who were symptomatically controlled on a GFD underwent a double-blind, placebo-controlled, randomised crossover trial of placebo, low-gluten (2g/day) or high-gluten (16g/day) for 1 week, followed by a 2-week washout period, before crossing over to the next diet. Protein levels were balanced with whey protein. No evidence of specific or dose-dependent effects of gluten was observed, but FODMAP restriction uniformly reduced residual symptoms. There were no changes in markers of potential mechanism including intestinal inflammation/injury, immune activation or by-products of protein metabolism.

A separate gluten (16g/day) and whey (16g/day) re-challenge in 22 of these patients showed poor reproducibility of symptom induction to a specific protein. A very high placebo response was found in both trials, regardless of all background dietary triggers being controlled. Either the patients do not have NCGS as self-reported or the trial design precluded its recognition. A better understanding is warranted for the diagnosis of NCGS where self-reporting is probably inaccurate.

Future research directions for NCGS
Current research is focusing on non-GI symptoms reported to improve with the GFD and continues to investigate the effects of gluten on intestinal inflammation, permeability, and other pathways of both innate and adaptive immunity in patients who do not have coeliac disease.

How common NCGS is, how it can be reliably identified and what its underlying mechanisms are, warrant further evaluation. Without convincing results showing effects on inflammatory or immune markers, NCGS should be regarded as a sub-group of IBS and distinct from coeliac disease.

Concluding comments
We have some evidence for the existence of NCGS, but this group remains poorly understood. We have no evidence to allow a plausible explanation of the pathogenesis of NCGS and more definitive research is needed to fulfill our understanding. Although the use of dietary gluten restriction in the management of patients with functional gut symptoms may benefit a small number of people, lowering the dietary intake of FODMAPs continues to be the first line therapy for IBS. Conducting well-controlled dietary studies are complex; the most valid study design of verifying the existence of NCGS remains unsubstantiated. Public health agencies and the food industry must not perpetuate public demand and consumer trends for the GFD without sufficient evidence first supporting the existence of NCGS.

Identifying patients with NCGS
Medical advice and dietetic supervision (ideally someone trained in the low FODMAP dietary method) is imperative throughout this process.

Key messages: 

  • Self-reported NCGS and improved symptoms on a GFD may not be an accurate indication of the condition
  • Prevalence and diagnostic procedures including biomarkers are not yet clearly defined
  • Widespread promotion of GFD to treat gluten intolerance without first excluding coeliac disease may lead to coeliac disease not being detected and increase the risk of related consequences
  • Lowering the dietary intake of FODMAPs continues to be first line therapy for managing GI symptoms
  • Recommend referral of patients to a specialist dietitian


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