Irritable bowel syndrome or IBS is identified as a significant condition because its symptoms bring profound negative impacts on a patient’s life. IBS is a complex condition and is classified with many subtypes such as diarrhea-predominant IBS (IBS-D), Mixed diarrhea and constipation IBS (IBS-M), unspecified IBS (IBS-U), and constipation-predominant IBS (IBS-C). Many underlying factors may lead one to suffer from IBS. Infections, digestive insufficiencies, adverse food reactions, etc.

There are a few options for treatment for IBS depending on the individual’s clinical recognition of primary causes and initial presentation. Learning the different factors that affect the development of IBS and symptom severity is important to help create a more effective treatment plan.    

Root causes and the potential triggers for IBS

Studies theorize that patients with IBS may suffer from increased inflammation, altered gut microbiome, systemic immune reactivity, and intestinal permeability. Research is getting better in finding the etiological factors that may induce IBS.

The following entries represent samples of known primary triggers and causes for IBS.

Digestive Insufficiencies: Focus on Bile Acid

Malabsorption and digestive imbalance issues may be a contributing factor to IBS development or can make the symptoms worse.  An example has some studies that theorize abnormal changes in bile acid (BA) metabolism may have a close connection with IBS3 and that BA malabsorption may predispose patients towards IBS symptoms such as diarrhea and loose stools.

Bile acids are created in the liver, which is then converted from primary Bile acids to secondary Bile acids in an individual’s intestines. Bile acids play an important role in promoting lipid absorption during digestion, and it helps maintain homeostasis of the gut microbiota. The Bile acids may affect inflammatory response regulation and intestinal permeability.          

Even in patients without an overt Bile Acids malabsorption, the Bile acids still affect the colon’s transit time and fecal weight, which strengthens the hypothesis that Bile acids play an important role in IBS symptomology. Evidence suggests that IBS-D is identified by an increase in primary Bile Acids and a decrease in secondary Bile acids with the higher primary Bile acid levels similarly with more severe diarrhea. Recent studies have shown that patients suffering from IBS-C also had higher levels of amino-conjugated BA levels and serum but a decrease in Bile acid deconjugation activity when compared to a healthy volunteer. Abdominal pain in both IBS-D and IBS-C may share a connection with fecal primary Bile acid levels and serum.     


A disruption in gut homeostasis is usually seen in patients with IBS. A study from 2020 for patients with IBS-D has found that other than dysbiosis, the gut microbiota’s diversity was reduced for patients when compared to the healthy control group. Results from a small observational study from 2021 suggest that individuals whose gut composition changes with IBS can lead to alterations in their bacterial functions such as transformation in bile acid and induced inflammation.     

Small intestinal bacteria or SIBO and the fungal overgrowth or SIFO are conditions of dysbiosis. Studies theorize that an increase in SIBO for patients suffering from IBS and common symptoms, such as distention, bloating, abdominal pain, diarrhea. Gut fungal dysbiosis has been linked to IBS. An observational study made in 2020 has found that while some of the patients with IBS-D showed dysbiosis in their fecal bacterial structure and diversity when compared to the healthy control group. All the patients with IBS-D showed fecal fungal dysbiosis when compared to the healthy control group. Dysbiosis was not the only finding for patients with IBS-D, they also had altered bacterial-fungal interactions.  

Pathobionts VS Acquired Infectious Agents

Research shows that gastrointestinal or GI infection is a very common risk factor for IBS development. A cohort study of military personnel has found an antecedent for the many cases of IBS. Having previously suffered from infectious gastroenteritis increased the risk by two-threefold versus the healthy control group. The pathogen type may also play a role in risk, the protozoal agents that demonstrate the highest prevalence followed by bacteria and then viruses. Most of the post infections for IBS cases are usually mixed or diarrheal-predominant. This information suggests that disease mechanisms include mucosal barrier dysfunction, dysbiosis, neuronal hypersensitivity, and immune dysregulation. 

Pathobionts are different from the acquired infectious agents because they are the commensal gut microbiota and are benign but have pathogenic potential under certain environmental pressures when exposed to toxicants, overuse of antibiotics, and unhealthy diets. Perturbed microbiota may also assist in the formation of overgrowths of these pathogens that include parasites, viruses, and bacteria. These pathogens may release disease-triggering products that may modify an individual’s microbiota components, potentially immune functions such as pro-inflammatory T-cell mediated responses and the mucosal barrier. Research continues to check the connections between IBS symptomology and pathobiont mechanisms.   


Adverse Food Reactions

Many patients with IBS report certain symptoms after eating certain foods. The foods that cause symptoms are often made with fermentable oligo-, di-, and polyols (FODMAPs), monosaccharides, fructose in excess of glucose, lactose, gluten, and fructans. Some patients that test negative for celiac disease may still experience IBS symptoms by ingesting gluten-containing food. This phenomenon indicates an overlap between non-celiac gluten sensitivity and IBS. The insufficient degradation of gluten and other proteins like casein may increase the number of un-neutralized or undigested particles and may activate the innate immune reaction and increase inflammatory triggers. 


Anxiety and Stress

There are multiple environmental and lifestyle factors that affect both the severity and emergence of IBS, which include psychiatric stress and depression. Research theorizes that negative emotions like anxiety play a big role in GI functioning because of the bidirectional communication between the brain and gut. Some data theorizes that mood disorders may even cause GI symptoms. The epidemiological data provide strong evidence in subset cases wherein GI symptoms manifest first, and then mood disorders follow. In 2021, a meta-analysis was done to check how prevalent anxiety and depression were for those individuals suffering from different subtypes of IBS. Results show that people with IBS-C suffer the most from anxiety and depression. When compared to the healthy control group. Individuals suffering from IBS-C, IBS-D, and IBS-M all had high depressive symptoms, with the IBS-M mostly showing the highest levels of anxiety and depressive symptoms. Emotions being related to an individual’s gut homeostasis is an area that requires more research for better understanding.      



Even when taking into account the primary considerations discussed in the article, there are still other factors that may be relevant to an individual’s development of IBS. An example would be low vitamin D which has been observed to share a connection with some GI disorders including IBS. Genetic risk factors for IBS have also been suggested. IBS triggers are go-betweens for increased intestinal permeability for some individuals. IBS is a potential pathway for different systematic dysfunctions and complaints. 

Irritable bowel syndrome can be a course of significant dysfunction, including the discomfort and pain that comes with it. Working with an experienced functional medicine physician trained in treating gut microbiome dysfunction may help you to develop personalized treatment options for intestinal permeability and gut dysfunction.

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