Fodmaps veg

From Fibre to Fermentation: The FODMAPs Revolution

Dr Nick Read, MD, FRCP.  Physician, Psychotherapist, Nutritionist, Medical Adviser to The IBS Network

There was a time and not so long ago when doctors, dietitians and scientists recommended the use of dietary fibre for the treatment of Irritable Bowel Syndrome.  The message was clear.  Our diet had become too refined, we were not eating enough fruit and vegetables and the cereals had been stripped of their unabsorbable polysaccharides to yield highly refined starches and sugars. 

The idea resonated with the culture; we had become too soft, too refined, too civilised.  There was not enough roughage for the bacteria in our colons to work on. It stood to reason: lack of fibre (moral or dietary)  was the cause of many of the diseases of civilisation. 

The Bran Wagon rolls on...

So almost overnight, patients with IBS  were told to go out and buy bags of coarse wheat bran, the coarser the better.  Many complained that their pain and bloating got worse but were largely ignored; bran was good and they were not taking enough. Well, The Bran Wagon trundled on for another twenty years despite papers confirming that those patients, who complained, were correct (Cann et al, 1984, Francis and Whorwell, 1994). Fibre particularly, the insoluble husks of wheat, oats, and barley, the skins of fruits and vegetable stalks could irritate the colon and make IBS worse. 
  
Fermentation and 'hot gas'

But the enthusiasm for fibre did not just produce bulkier stools, it also generated a lot of heated  gas. In the ruts of the bran wagon, came an understanding of colonic microflora; an appreciation of fermentation. So, hot on the trail of Blazing Saddles and the laxative properties of prune juice, the gastroenterologist, Peter Gibson and his team in Melbourne developed a new concept (Gibson et al, 2006).  

Poorly absorbed, low molecular weight sugars, present in many foods, could be partially fermented in the colon,  producing gas and causing symptoms of bloating with flatulence and abdominal pain in people with the Irritable Bowel Syndrome, while other short chain, osmotically- active sugars, which were less rapidly fermented, caused diarrhoea (Barrett et al, 2010). 

The birth of FODMAPs
   
With exemplary straight talking, the Australian group coined a brand new term to describe these fermentable foods - FODMAPs: Fermentable Oligosaccharides, Disaccharides, Monosaccharides And Polyols; to my mind an unfortunate acronym, which sounds more like a streetguide to Melbourne restaurants.  

Some of these FODMAP foods were already well recognised. It is part of folk history that sprouts, beans and Jerusalem artichoke cause flatulence and too many plums, prunes and figs can give you the runs. And the flatulent patient, the eponymous Mr Sutalf, cured his affliction in the late seventies by a diet very similar to a low FODMAP diet (Sutalf and Levitt, 1979). 

Impaired absorption of lactose had been known to be a cause of diarrhoea and bloating for the last half century, but although most of the world’s population, with the notable exception of those of Northern European origin, lose their lactase enzyme after weaning, the vast majority, perhaps those with no proclivity to IBS, can drink modest amounts of milk with impunity and not get bloating or diarrhoea. We also knew that fructose was only slowly absorbed and fruits could be a problem in people with IBS, but not those without that diagnosis. Wheat could also be a problem in people with IBS, but only 4% of them had undiagnosed coeliac disease.

Something else afoot... 
So there must be something else going on. Ong and his colleagues clearly showed that high FODMAP foods could be tolerated by people who did not have IBS; they had less symptoms and less production of hydrogen gas (Ong et al, 2010).  

As Gibson and his colleagues explained in their recent review (Gibson and Shepherd, 2012), the other factor is likely to be ‘the sensitive gut’, though the possible role of colonic microflora in influencing bowel sensitivity requires further investigation.   

An increase in intestinal sensitivity is the nearest we get to a biomarker in patients with IBS but it is by no means specific (Delvaux, 2002) or that sensitive, perhaps because Irritable Bowel Syndrome is a concept rather than a disease and may turn out to include several different pathological processes. Intestinal sensitisation can be caused by stress, infection (post infectious IBS), inflammation as in Crohn’s or Colitis (Gearry, Irving and Barrett, 2009), bile acid malabsorption, coeliac disease and allergy.   

Food intolerance in IBS is never a specific or fixed entity. It can involve many different foods, not just high FODMAP foods, it can come and go according to what is happening in a person’s life, and the foods implicated often convey context and meaning for that individual. So it’s not the food to which the person is intolerant, it is the gut that is intolerant of a number of different foods. In-depth interviews of patients so frequently reveal that food and mood work in concert to cause abdominal upset.    
  
FODMAPs and IBS

Using High Performance Liquid Chromatography, Gibson and his colleagues provided an inventory of Australian foods with high FODMAP content. They then put patients with IBS on a diet restricted in FODMAPs and noted a marked improvement in symptoms (Shepherd and Gibson, 2007). They followed this up with a more definitive double blind challenge study in IBS patients known to be intolerant of FODMAPs, and observed that reintroducing fructose, fructans, and a combination of the two reproduced their symptoms while equivalent quantities of glucose did not (Shepherd et al, 2008). Often the proof of the efficacy of a new concept is that it travels. 

The group at Kings College Hospital, London, have modified the FODMAP inventory for an English diet and shown significant reductions in bloating, flatulence and abdominal pain when people with IBS were put on a low FODMAP diet compared with a NICE recommended diet for IBS (Staudacher et al, 2010). 

The placebo effect

People with IBS are highly suggestible. The placebo effect in randomised controlled trials of drugs for IBS is up around the rate of 40% or more, and responses to complementary therapies in which there is no proven scientific principle are as good as those where there is. It is not always what is so that counts but what people think is so. The number of suggested treatments for IBS far outweigh those that have survived the rigours of scientific evidence. The more complicated the treatment, the greater the involvement of the health professional, the more focussed the attention on the patient, the more customised the treatment, the better the result. This is the way many therapists harness the healing effect. If the patient feels hopeful and confident, it would seem probably that the gut will become less sensitive. This might explain the effects of hypnotherapy, psychotherapy and antidepressants on gut symptoms. 

FODMAPs and the DBPCT

Double blind, randomised studies of dietary intervention are notoriously difficult to conduct and evaluate, especially for a diet as pervasive and complicated as low FODMAPs. FODMAP foods coincide with common knowledge, have been so widely publicised and cannot be concealed, so it is impossible to avoid the effect that expectation may have on the results. Nevertheless, the data is as good as it gets, and the re-challenge studies have been conducted with impressive scientific rigour (Shepherd et al, 2008). 

One of the best open studies is a comparison of low FODMAPs diet versus dietary advice for IBS, directed by NICE guidelines (Staudacher et al, 2010). This showed a significant benefit for low FODMAPs for bloating, abdominal pain and flatulence. The data look convincing, but illness and fashion are fickle and the treatments of IBS is littered with discarded enthusiasms.  

The sensitive gut

Poorly absorbed fermentable carbohydrates are not the only food constituents to which the sensitive gut reacts. There is fibre, fats, hot spices and coffee. It seems that anything which stimulates contraction or causes distension is going to make the sensitive gut react with pain, bloating and diarrhoea. Resistant starch (as in bananas or reheated cooked potatoes or rice) is another dietary component that is poorly absorbed and encourages fermentation. 

Poorly absorbed proteins are also fermented. This may occur after consumption of meat that has not been cooked through, and in people with rapid small bowel transit. In this context it may be relevant that people with IBS who have diarrhoea, exhibit abnormally rapid small bowel transit of a meal (Cann et al, 1983). 

Multiple causes; multiple treatments

IBS is not a disease. There is no pathology, no specific cause and no definitive treatment. It is a syndrome, a collection of unexplained gut symptoms that may or may not fit together as a single illness. As far as FODMAPs are concerned, it may just complicate matters to expect reduction in all the IBS symptoms or to target patients who do not have gas bloat, flatulence or diarrhoea. In fact, some patients with constipation have an insensitive gut (De Medici et al, 1989) and find that a diet rich in insoluble fibre, coffee, and high FODMAP foods such as beetroot, fruit juices and prunes helps their constipation but may increase bloating and flatulence.   

In the UK, The King’s College Hospital group advocate that patients with unresolved moderate to severe IBS symptoms should undertake a process of dietary exclusion and re-introduction, supervised by a dietitian who has been instructed according to their method and understands the risks of nutritional deficiency.  But to test the effectiveness of a dietary regimen that excludes so many food constituents, when the condition itself constantly fluctuates, is never straightforward and might seem to disempower and frustrate patients.  The ultimate success of any dietary regime depends on the extent to which patients can understand and adapt it to suit themselves. In that respect, the group from Monash University are to be applauded for bringing out an inexpensive mobile app on the low FODMAPs diet.    

The IBS Network encourages patient self help and favours a pragmatic solution. Rather like Mr Sutalf, patients suffering from gassy symptoms of bloating and flatulence would be well advised to keep a detailed food diary, identify which FODMAP foods are represented prominently and cut these down, preferably under supervision from their health care professional. 

Food intolerance is not the same as food allergy. People can tolerate a modest amount of high FODMAP foods and can learn to identify which ones feature prominently in their diet and are associated with symptoms. Some FODMAPs generate more gas in some people than others, depending on strain, ripening, preparation and cooking and presumably also the composition of their own bacterial flora. The inventory of the FODMAP content of foods is unlikely to be as exhaustive as the McCance and Widdowson database (Church, 2002).    

There is even evidence, for example, that the artificial transgalactans in Bimuno, are fermentable oligosaccharides that do not produce gas during fermentation and reduce bloating and abdominal pain (Silk et al, 2009). Instead they act as prebiotics encouraging the growth of bifidobacteria. The low FODMAP diet, by contrast, reduces bifidobacteria (Staudacher et al, 2012). Clearly, the implications of this run counter to the therapeutic principles of pre- and probiotics and will need further investigation and clinical experience.
   
FODMAP foods are not the cause of IBS

FODMAP foods are not the cause of IBS, but they may generate symptoms if the bowel is sensitive. Adhering to a diet that involves so many different foods is not easy. The most direct therapeutic endeavour must be to reduce sensitivity. If stress is a major factor, then relaxation, finding space, taking time out and finding help to deal with whatever might be going on will reduce both sensitivity and symptoms and as the symptoms recede, then patients can in time return to a more normal diet. 

Any treatment undergoes a trajectory, the initial enthusiasm that accompanies the first few papers, then scepticism when the failures start being reported with longer term treatment, then reappraisal and closer definition of responders. The low FODMAPs diet is still on its upward trajectory. The British Dietetic Association guidelines for IBS, published in 2012 (McKenzie et al, 2012), approved the low FODMAPs diet as second line treatment, but recognised that it required specialist knowledge in the dietary management of IBS and particular expertise in the dietary sources of fermentable carbohydrates and their effects on the gut. 

Only experience and the passage of time will tell how much The Low FODMAP diet will revolutionise the management of IBS. A recent prospective follow up study showed sustained improvements, of an average of 17 months, in bloating, flatulence, diarrhoea and abdominal pain in patients, most of whom had impaired fructose or lactose absorption on breath testing (Roest et al, 2013). More long term studies are needed.  
     

References

• Cann PA, Read NW, Brown C, Hobson N, Holdsworth CD (1983). Irritable bowel syndrome: relationship of disorders in the transit of a single solid meal to symptom patterns. Gut. 1983 24(5):405–411. 
• Cann PA, Read NW, Holdsworth CD (1984). What is the benefit of coarse wheat bran in patients with irritable bowel syndrome? Gut. 25:168–173.
• Church S. (Ed) (2002) McCance and Widdowson’s the Composition of Foods: Summary Edition (6th edition) Food Standards Agency (UK).
• Delvaux, M. (2002), Role of visceral sensitivity in the pathophysiology of irritable bowel syndrome. Gut 51 i67-i71.
• De Medici  A, Badioli D,  Corraziari E, et al (1989) Rectal sensitivity in chronic constipation.  Dig Dis Sci 34: 747-753.
• De Roest, RH, Dobbs, BR, Chapman BA et al (2013). The low FODMAP diet improves gastrointestinal symptoms in patients with IBS: A prospective study.  Int. J. Clin. Practice 67. 895-903. 
• Francis CY and Whorwell PJ (1994) Brain and Irritable Bowel Syndrome.  Time for reappraisal. Lancet. 344, 39-40.
• Gearry RB, Irving PM, Barrett, JS et al (2009).  Reduction of dietary, poorly absorbed short chain carbohydrates (FODMAPs) improves abdominal symptoms in patients with inflammatory bowel disease – a pilot study.  J Crohn’s and colitis 2009. 3. 8-14. 
• Gibson PR, Newnham E, Barrett JS et al (2007) Review article: fructose malabsorption and the bigger picture.  Al. Pharm. Ther. 25, 349-363.  
• Gibson PR and Shepherd (2012) Food Choice as a management strategy for Irritable Bowel Syndrome.  Am J . Gastroenterology, 2012.  107.  655-666.
• McKenzie YA, Alder A, Anderson W. et al (2012) BDA evidence based guidelines for the dietary management of Irritable Bowel Syndrome.  J.Hum. Nutr. Diet. 25. 260-274.
• Ong DK, Mitchell SB, Barrett, S et al (2010) Manipulation of dietary short chain carbohydrates alters pattern of gas production and genesis of symptoms in IBS.  J. Gast. Hep. 25. 1306-1373.  
• Shepherd SJ and Gibson P (2006) Fructose malabsorption and symptoms of Irritable Bowel Syndrome.  Guidelines for effective dietary management.  J.Am. Diet Assn 106. 1631-1639.

Shepherd SJ , Parker FC , Muir JG et al. Dietary triggers of abdominal symptoms in patients with irritable bowel syndrome: randomized placebo-controlled evidence . Clin Gastroenterol Hepatol 2008 ; 6 : 765 – 71 .
Silk, DBA, Davis, A, Vulevic, J, Tzortiss G and Gibson, GR (2009).  Clinical trial: the effects of a trans-galactooligosaccharide prebiotic on faecal microbiota and symptoms in irritable bowel syndrome.  Al. Pharm. Ther. 29. 508-518
• Staudacher HM, Whelan K, Irving PM, Lomer MC. (2011) Comparison of symptom response following advice for a diet low in fermentable carbohydrates (FODMAPs) versus standard dietary advice in patients with irritable bowel syndrome..  J Hum Nutr Diet. 24:487-95. 
• Staudacher HM, Lomer, MCE, Anderson,JS  et al (2012) Fermentable Carbohydrate Restriction Reduces Luminal Bifidobacteria and Gastrointestinal Symptoms in Patients with Irritable Bowel Syndrome.  J. Nutr.  142. 1510-1518
Sutalf LO, Levitt MD (1979) Follow up of a flatulent patient. Dig. Dis. Sci. 24. 652-655.

First published January 2014

 

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