While scanning the journals recently, I came across a review by Peter Gibson making the case for the low FODMAP diet as a first line treatment for IBS. He quoted six randomised control clinical trials, three in which all the food was provided and three where the low FODMAP intervention was dietitian led. These also included three trials in which people on a low FODMAP diet showed similar or better outcomes than those on what has hitherto been considered standard dietary treatment for IBS. He also referred to a host of ‘real world’ open studies in which about 70% of patients had shown a reduction in their symptoms. These results similar to the outcomes from hypnotherapy.
It would seem to be, as they say, a ‘no-brainer’ – in other words, so obvious, we don’t need to think about it. Call me old sceptic, but I remain to be convinced. I can clearly remember the enthusiasm for high fibre diets in the 1980s, when GPs and gastroenterologists jumped on the Bran Wagon to extol the virtues of coarse wheat bran. That was before Dr Peter Whorwell broke the back axle by demonstrating in a paper in The Lancet that wheat bran made many people with IBS worse. Theories and treatments follow fashion. It is only since the millennium, we have been gripped by the microbiome and the apparently conflicting cases for probiotics, prebiotics and the low FODMAP diet.
Dr Gibson compares the development of the low FODMAP diet to development of a new drug, which comprises a preclinical phase of laboratory and animal studies, and three clinical phases, the first in healthy volunteers to determine safety and dosage, the second in patient volunteers to establish proof of concept, effectiveness and side effects and the third in a larger cohort of patient volunteers to determine longer term effectiveness and safety. Only about a quarter of all drugs that are evaluated in preclinical studies make it through to marketing, but evaluation does not stop even then. Post marketing surveillance continues to monitor clinical experience and side effects. So, on this yardstick, the low FODMAP diet might seem to have exceeded the requirements for launch (except that being a diet, it was launched years ago – after phase 2).
The reason for such extensive period of drug development is to establish whether: 1) the treatment is safe and 2) whether it is better than placebo. But herein may lie the problems.
In the last few years, it has become apparent that a strict low FODMAP diet depletes the microbiome of beneficial species such as Bifidobacteria that help to maintain the integrity of the lining of the gut and prevent invasion by more harmful bacteria, which might cause excitation of the immune system with inflammation and sensitivity, not only in the gut but in other organs as well. In the last few weeks, Professor Marcus Simren’s group from Gothenburg in Sweden published a randomised controlled clinical trial a low FODMAP diet versus a traditional IBS diet on faecal microbiota and symptom severity. Their results showed that those whose symptoms responded to a low FODMAP diet had more dysbiosis (depletion and instability of the faecal microbiome) both before and after intervention compared with non-responders. This would suggest the already depleted microbiome had made the gut more sensitive and therefore more responsive to the reduced gas production and distension caused by the low FODMAP diet. So, although the low FODMAP diet might win the battle for immediate symptom relief, it may lose the war on the disease by further depleting the microbiome and enhancing visceral sensitivity.
Drugs are evaluated by double blind controlled clinical trials, in which subjects are prescribed either the active treatment or an inactive placebo or sometimes another drug. Diets are not the same as drugs. You cannot conceal the nature of a diet. Although patients may be unaware of the details of the low FODMAP diet, I have yet to meet a patient with IBS who did not have some understanding of what foods upset them. It is therefore difficult to believe they would not have a pretty good idea which was the active diet and which wasn’t. So, we cannot rule out the possibility that the low FODMAP diet worked because more patients believed it would.
The protocol as propounded by the Monash and King’s College, London groups directs patients to undergo a period of dietary exclusion after which it is expected their symptoms will be substantially diminished. Then they undertake a more extended period of trial-and-error piecemeal reintroduction until they find the combination of foods in the amounts they can tolerate without symptoms. Most patients can cope with dietary exclusion for a while, but it’s during the reintroduction phase, when the problems start. It is generally believed that FODMAP foods do not cause IBS, but they trigger symptoms when the gut is sensitive. But the sensitivity of the gut can vary according to what is going on in a person’s life and what that means. This is like hitting a moving target; trigger foods cause more symptoms if a person is stressed and upset. This situation is exacerbated if the exclusion phase also sensitises the gut by depleting the microbiome; the longer they stay in the exclusion phase, the more difficult it may be to get out of it.
Any diet worth its salt should be simple enough to be conducted by the patient herself. Dietitians should work to their own redundancy. In a nationalized health service, dietetics, like medicine, is political practice. Both Monash and King’s College set great store on the assertion that the low FODMAP diet must be administered by a state-registered specialist dietitian, who has attended a FODMAP training course. This is good for GI dietitians because at last they have an ‘effective’ treatment for IBS that they alone can administer. But this very fact may help to consolidate the placebo effect. It is not just the Low Fodmap Diet that is being prescribed, it is also ‘The Dietitian’, who alone can understand its complexity. But is the low FODMAP diet that complicated? Are dietitians disempowering patients who might otherwise learn to adapt their diet to suit them. As Peter Gibson has commented, most patients may be able to manage quite well by reducing their intake of onions, pulses and some fruits, though some may also need to restrict wheat and milk.
But, to be fair, this same caveat applies to any treatment or therapy. The friendly GP who prescribes antispasmodics with a sincere demeanor and reassuring smile is prescribing herself, so is the complementary therapist. And what I do as a psychoanalytical psychotherapist is entirely dependent on the nature and mutability of ‘the therapeutic relationship’. Reports that the results from a low FODMAP diet are similar to those from hypnotherapy might suggest that both are effective because they instil a sense of confidence and belief in the patient, but does that matter?
Whether the effect of a Low FODMAP relies in part on ‘the healing effect’ is immaterial. The fact is that it can work in a lot of patients. Other therapies are equally effective when delivered by a charismatic and trustworthy healer. Apart from exploitation, the only thing that should cause real concern is if the treatment damages the patient in the long term.
It is for this reason, that I remain concerned about the long term effects of a low- FODMAP-depleted microbiome. Insufficient long term studies of The Low FODMAP diet have been carried out. So perhaps judgement on the Low FODMAP diet as a first line treatment for IBS should be withheld awaiting more data on the effects of FODMAP exclusion on the colonic microbiome.
In the meantime, if you are struggling with reintroduction of FODMAPs, find space in your life to relax, consider mindfulness meditation or yoga and talk about the things that may be upsetting you. That may stabilise the sensitivity of your gut. And as far as your diet is concerned, why don’t you and your dietitian nourish your microbiome by getting your teeth into some of the poorly-absorbed long chain carbohydrates that form the basis of dietary fibre and are less rapidly fermented.
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