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Digestive disorders are among the most common chronic ailments experienced by individuals in modern society. Perhaps the most prevalent is irritable bowel syndrome (IBS), which is thought to affect 10 to 20% of adults in America. IBS is a gastrointestinal pathology characterized by a combination of symptoms that can include:
Clinically, IBS is often classified into different subtypes based on symptomology.
IBS preferentially affects women and individuals suffering from other gastrointestinal issues such as constipation and acid reflux, and although there is no clear-cut answer as to the mechanism underlying disease onset and progression, there are multiple factors that show a relationship to IBS symptom onset. These include:
Here, we will focus on the role of factors from the diet and microbiome that contribute to the development and persistence of IBS, and how these factors can be modulated to alleviate symptoms.
There are multiple suggested mechanisms by which dietary inputs can trigger the onset of IBS symptoms:
The consumption of fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (also known as FODMAPs) in individuals with gut inflammation or dysbiosis is known to cause gastrointestinal discomfort [1]. FODMAPs cannot be digested by human digestive enzymes and, as a result, they spill over into the colon where they are metabolized by the microbiome. In individuals with inflamed dysbiotic guts, colon cells lose the ability to effectively import the short chain fatty acids (SCFAs) produced from the microbial breakdown of FODMAPs. The result is gas build up in the lower GI tract, which creates bloating, pain, distension, and changes to gut motility.
Dairy products can cause issues for some individuals who lack the enzyme responsible for breaking down lactose as an adult. In this case, the undigested lactose can create an osmotic shift in the gut, which can lead to bloating and diarrhea [1].
A sugar found in fruits and honey—is transported with glucose from the gut into the bloodstream in a 1:1 ratio. Thus, if fructose consumption exceeds glucose consumption (as may occur with consumption of high fructose corn syrup), glucose can spill over into the large intestine where microbes feast upon it and generate gases that cause bloating [1]. Similarly, sugar alcohols like sorbitol, xylitol, and mannitol undergo somewhat slow absorption by the small intestine, which means that consumption of moderate-to-high quantities will result in passage into the colon where the microbiome breaks them down into gases [1].
Additionally, in individuals with sub-clinical food allergies, consumption of particular foods can trigger low-grade inflammation within the gut and incite IBS symptoms [1]. However, food allergy testing can be inaccurate or inconclusive in many cases. Thus, if an individual suspects that a specific food is inciting IBS symptoms, an elimination diet should be performed where the suspected food is avoided for at least two weeks and symptoms are closely monitored. If an individual is unsure if they have a dietary trigger, a food journal should be kept for at least two weeks with notes regarding any symptoms experienced each day to identify a potential trigger.
In clinical studies, wheat (gluten) was identified as a major trigger of sub-clinical gastrointestinal inflammation in a significant portion of IBS patients tested [2]. In fact, pre-clinical research suggests that gluten as well as other proteins in wheat have the potential to activate the innate immune system (i.e. inflammation), increase gut permeability, and create changes in gut motility [3]. The research also suggests that the presence of key bacteria in the microbiome, including Pseudomonas and Lactobacillus, can mitigate the negative effects of wheat consumption by breaking down these proteins before they can interact with immune cells [4]. Thus, targeted microbiome modulation may hold promise for individuals to mitigate the effects of dietary triggers on IBS flares.
A 2019 systematic review of the IBS-microbiome literature found an association between certain microbiome signatures and IBS onset and severity [5]. The most prominent observation across all of the compiled studies was a decrease in the levels of Bifidobacteria and increases in the levels of Bacteroides and species of Enterobacteriaceae in patients with IBS.
Bifidobacteria play a crucial role in immune system regulation, gut health, and maintenance of a healthy, diverse microbiome. Bifidobacteria break down indigestible carbohydrates, like FODMAPs, fibers, and polyphenols, into the metabolites acetate and lactate. These two metabolites serve as important food sources for other beneficial bacteria in the gut including the butyrate-producing bacteria. Butyrate is not only the primary fuel source for colon cells, but also helps to maintain gut barrier integrity and spin down inflammation at the level of both the gut and the whole body. Declines in the levels of Bifidobacteria in the gut occur during aging, and are associated with the development of age-related diseases, most of which arise from low-grade inflammation sustained over decades. The anti-inflammatory activities that Bifidobacteria support by bolstering butyrate production help to mitigate this low-level inflammation and support a healthy aging process.
Although species of Bacteroides often play a beneficial role in the gut, they can also act like pathogens in certain contexts. For instance, some species of Bacteroides can secrete a toxin known as fragilysin, which has been associated with the development of gastric disorders like ulcerative colitis [6]. Additionally, Bacteroides can also create factors known as hemolysins and cytolysins that can harm host cells [6]. Interestingly, the expression of these factors increases in oxygen-rich environments [6]. Bacteroides generally thrive in very low-oxygen environments; however, in the presence of gut inflammation, the oxygen content of the gut lining increases which may subsequently trigger the production of hemolysins and cytolysins that can further damage the cells of the colon.
The most abundant species of Enterobacteriaceae in the colon is E. coli and, in general, high abundance of bacteria within this phylum is associated with weight gain, inflammation, and gastric disease.
Importantly, although reduced FODMAP intake can result in acute symptom relief, a low-FODMAP diet is associated with declines in the levels of Bifidobacteria and reductions in the total bacterial biomass of gut both—two markers that correspond closely with poor gut health [1]. Thus, the elimination of FODMAPs from the diet is not a viable solution to the problem, but only a temporary means to prevent acute discomfort. Instead, a focus on spinning down inflammation in the gut should be prioritized as this will help the colon to restore its ability to effectively burn butyrate. Once butyrate burning is optimized, dietary and supplemental strategies to bolster Bifidobacteria levels can be implemented. To learn about strategies to reduce gut inflammation and optimize for Bifidobacteria, check out our previous blog.
Additionally, clinical research also suggests that IBS and inflammatory bowel disease (IBD) are both associated with increased gap size between the epithelial cells of the gut [7]. These gaps, known as tight junctions, are crucial for regulating intestinal permeability and preventing harmful microbes and toxins from leeching into the bloodstream. Thus, the optimization of Akkermansia muciniphila in the gut may be prudent for individuals with IBS, as Akkermansia play a major role in the maintenance of tight junction integrity. See our previous blog on the topic to learn about ways to boost your levels of Akkermansia.
IBS is a disease characterized by various forms of gastric discomfort, and the mechanism by which it develops remains largely elusive. However, dietary triggers and unfavorable changes to the microbiome are likely two of the most prominent factors driving symptomology. Although a low FODMAP diet can provide acute relief, it is associated with poor markers of gut health, and should thus only be used in the short-to-moderate term. As a long-term solution, individuals may:
Author:
Dr. Alexis Cowan, a Princeton-trained PhD specializing in the metabolic physiology of nutritional and exercise interventions.
Follow Dr. Cowan on Instagram: @dralexisjazmyn
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