The Relationship Between FODMAPs and IBS Symptoms


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A diet low in Fermentable Oligo-, Di- and Monosaccharides And Polyols (FODMAPs) has been shown to significantly improve IBS symptoms, in particular bloating and diarrhea-type symptoms, even though the health benefits of such a diet when consumed over a prolonged period of time are highly questionable.

FODMAPs are poorly absorbed short-chain carbohydrates including fructose, fructans, lactose, polyols, as well as large complex sugar molecules, so-called galacto-oligosaccharides. They are found in a wide variety of foods, and in certain patients with IBS, may trigger lower gastrointestinal symptoms, in particular bloating, abdominal distension, cramping and a sensation of gas. It has been suggested that these symptoms are triggered by distention of the small bowel as a consequence of the osmotic effects of these foods via fermentation in the colon by the gut microbiota, resulting in increased gas production.

As FODMAPs have been implicated as a major source of certain IBS symptoms, the low FODMAP diet is often recommended by physicians and dietitians as a therapy for IBS. It is worth noticing that increased consumption of many of these foods (except those contained in unprocessed fruits and vegetables) is a hallmark of the Standard American Diet (SAD) and moving to a personalized largely plant-based diet, such as a modified Mediterranean diet, may accomplish the same effect without the negative consequences. So, what is behind this FODMAP frenzy?

Before going into the mechanisms by which FODMAPs worsen IBS symptoms, lets go through a brief FODMAP-101 course, to become aware which components in our diet make up this maligned group of largely plant-based molecules.

Number I. Fructose

Fructose, or “fruit sugar,” is a simple sugar molecule like glucose. It’s naturally found in fruits, most root vegetables, honey, and agave. Importantly, fructose is commonly added to many processed foods in the form of high-fructose corn syrup, which has been identified as an important factor of obesity and metabolic syndrome. Fructose is sourced from sugar cane, sugar beets and corn.

The most significant sources of fructose in the SAD include:

  • High fructose corn syrup added to a large number of foods, including fruit juices and ketchup.
  • Table sugar

Other high-fructose foods include:

  • Most fruits, especially dried fruits and fruits canned in juice or high fructose corn syrup.
  • Vegetables including artichoke, asparagus, broccoli, leeks, mushrooms, okra, onions, peas, red pepper, shallots, and tomato products.
  • Foods with wheat as the main ingredient, such as wheat bread and pasta.

Number II. Fructans

Fructans are large, poorly absorbable complexes (or polymers) of fructose molecules. The human gut is unable digest and absorb fructans, so they are instead fermented by the bacteria in the gut.

The most significant sources of fructans in the SAD include

  • Wheat and onions.

Other fructan containing foods include:

  • Many fruits including watermelon, grapefruit, nectarine, persimmon, plums, pomegranate, ripe bananas, dates, prunes, and raisins.
  • Many vegetables, including onions, shallots, leeks, asparagus, artichoke, beets, Brussels sprouts, savoy cabbage, fennel, and snow peas.

Number III. Lactose

Lactose is a large sugar molecule contained in milk and non-fermented dairy products, which requires the gut-based enzyme lactase to be broken down into absorbable components one molecule of glucose and one of galactose linked together. If lactase is absent or deficient, as it is in the majority of healthy and symptom-free adult humans, unabsorbed lactose travels down the intestine and is fermented by the gut microbes into its constituent molecules.

While human breast milk and cow’s milk is an essential source of nutrients for infants, consumption of large amounts of unfermented dairy products by adults is an unnatural way to improve nutrition and can lead to abdominal discomfort.

Number IV. Polyols

Polyols are a specific group of sugar alcohols that are formed via the enzymatic alterations of certain sugar molecules. They are naturally contained in certain fruits, vegetables, and mushrooms.

However, the most significant sources of polyols in the SAD are sugar-free sweeteners in products such as chewing gum, candies, and sweetened beverages and food items. These products have become a popular replacement for sugar in the SAD, despite the conflicting evidence for their health benefits.

Number V. Galacto-oligosaccharides

Galacto-oligosaccharides are large complex carbohydrates which cannot be absorbed by the human small intestine, but are essential nutrients for our gut microbes, playing a crucial role in assuring a diversity and richness of the gut microbiome.

At first glance it would seem that eating a personalized healthy, diet containing a large variety of fruits and vegetables, without added sugar and sweeteners, the avoidance of high amounts of non-fermented dairy products and ultra-processed food components should have the same beneficial effect as sticking to an unhealthy and unsustainable diet like the low FODMAP diet. At the same time, such a personalized largely plant-based diet would have the additional benefit of nurturing our gut microbes, a generally accepted goal in human health.

A recent study by an international group of investigators under the leadership of Lukas van Oudenhove at the Catholic University Leuven in Belgium provides some interesting answers why the avoidance of fructans is associated with fewer symptoms in IBS patient. In order to unravel the mechanisms within the brain gut microbiome (BGM) system that are responsible for fructan-induced IBS symptoms they randomly assigned 13 IBS patients and 13 healthy, asymptomatic control subjects to 3 conditions in a double-blind, cross-over study. During 3 visits, fructans (40 g/500 mL saline), glucose (40 g/500 mL saline) or saline (500 mL) were infused into the stomach of subjects, while abdominal symptoms were assessed with a rating scale, intestinal distension and gas measured with an abdominal imaging technique and brain activity was assessed using functional magnetic resonance imaging (fMRI) at baseline at 1 h, and 2 h post administration of the fructan solution.

As expected, IBS patients, but not healthy control subjects reported significantly more cramps, pain, flatulence, and nausea compared to glucose infusion. However, fructans increased small bowel contractions as well as gas and volume in the first part of the colon equally in IBS and control subjects. In other words, the microbially increased gas production in response to fructan was identical in IBS and control subjects. However, the difference in colonic gas between fructans and saline was correlated with differences in bloating and cramps in IBS, but not in control subjects. Brain images during the study revealed that IBS patients had greater activation in pain processing regions compared to control subjects and these brain responses were correlated covaried with symptom responses in IBS.

Based on their findings, the authors concluded that fructans increase small bowel motility and colon gas and volume similarly in IBS patients and HC. However, the increased symptom responses to fructans in IBS but not control subjects were correlated with altered brain responses in pain-related regions. Hence, increased sensitivity to normal FODMAP-induced gas production and/or osmotic activity, rather than excessive gas production and water content (which has never been identified as a cause of IBS symptoms), is the most plausible cause for FODMAP-induced symptoms in IBS.

Even though collected in a small sample of patients, the new findings are consistent with a large body of earlier evidence supporting a crucial role of visceral hypersensitivity in IBS symptomatology. While increased sensitivity and subjective responses to signals arising from the gut, related to contractions and distension has been demonstrated in many previous studies, the identification of this mechanism underlying fructan-induced symptoms leads to an important question: Is it more important to focus on therapies which reduce the enhanced perception of food-related gut signals by the brain, OR recommend a diet that is difficult to follow and sustain, and has negative long term effects on gut microbial diversity and richness?

Emeran Mayer, MD is a Distinguished Research Professor in the Departments of Medicine, Physiology and Psychiatry at the David Geffen School of Medicine at UCLA, the Executive Director of the G. Oppenheimer Center for Neurobiology of Stress and Resilience and the Founding Director of the Goodman-Luskin Microbiome Center at UCLA.