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Part Two - What's Behind Small Intestinal Bacterial Overgrowth (SIBO)?

Updated: Mar 10, 2023

Karen Miller-Lane, ND, L.Ac

My intent in providing these summaries is to strike a balance between what can be the overwhelming technicality of a research article in a professional medical journal and the oversimplification of important, albeit complex topics, in mainstream news sources. To be clear, there is technical information in these summaries because I believe that when we are able to access meaningful, scientific information, we are better able to make informed health decisions. However, hopefully, you will find these summaries clear enough to be meaningful and helpful. I look forward to having further conversations.

As we discussed in Part One, SIBO is a common cause of irritable bowel syndrome or IBS. Symptoms of SIBO often include bloating, abdominal gas, flatulence, belching, heartburn, abdominal pain, constipation, diarrhea, or a mixture of the two. That said, there is often a varied presentation of SIBO. In other words, SIBO may look different depending on the individual's past medical history, underlying conditions, and present health concerns. In this article, we will look at the pathophysiology of SIBO which may shed light on its varied presentation and provide insight into how to approach its treatment.

In SIBO, bacteria grow in our small intestine due to an infection, antibiotics, or stress for example. The small intestine should be relatively sterile, whereas the large intestine has a dense and varied microbiome. Along with stressors such as an infection or antibiotics, motility disorders account for a high percentage of SIBO cases. Motility is a term to describe the muscle contractions that mix and move food along the GI system. We have a migrating motor complex (MMC) which acts as a housekeeper in the gut. The MMC creates movements that clear the intestines at regular cycles between meals. It is also responsible for clearing bacteria from the small intestine to the large intestine and inhibiting bacteria from the large intestine entering the small intestine. Anything that impairs MMC function can be a risk factor for SIBO. The MMC is triggered by the fasting state, so MMC can be impaired if you aren’t allowing enough time (three to four hours) between meals. In a vicious cycle, the overgrowth of bacteria in SIBO can also exacerbate impairment of MMC function.

Other risk factors for SIBO include decreased stomach acid, decreased digestive enzymes, and ileocecal valve dysfunction (IVD)--a condition that can occur when the valve that separates the small and large intestine ceases to function correctly. What follows describes a story in which factors affecting digestion, absorption, and the movements within the GI system cause imbalances and dysfunctions that create a landscape hospitable for SIBO. Stomach acid eliminates most of the bacteria that enters the body in our food. Digestive enzymes support efficient digestion of food thereby leaving less substrate for bacteria to ferment and the digestive enzymes also play a role in eliminating bacteria not meant for the small intestine. Bile acids break down fatty acids and are necessary in the absorption of fat-soluble vitamins. As detergents, they can alter bacterial membranes, reducing numbers. The ileocecal valve is a sphincter muscle located at the junction of where our small intestine and large intestine meet. If there is a dysfunction in the valve, then materials from the large intestine can back up into the small intestine. A healthy functioning GI system ensures appropriate digestion, absorption, and maintenance of a healthy gut ecology. Also, pre-existing conditions such as hypothyroid, diabetes, celiac disease, fibromyalgia, or lactose intolerance can lead to bacteria populating the small intestine and cause fermentation.

The by-products of this fermentation, particularly of carbohydrates, are methane, hydrogen, or hydrogen sulfide, which account for the three types of SIBO. The hydrogen dominant type often causes diarrhea. The methane dominant often causes constipation. And the hydrogen sulfide results in diarrhea or constipation.

Besides bacteria, the human microbiome consists of organisms called Archaea which are methanogens, meaning that the microbes belonging to this genus or category of organisms in the gut produce methane. The most prevalent species from this genus is Methanobrevibacter smithii. M. smithii is a methanogen, an organism that soaks up hydrogen and produces methane. Modern day antibiotics will not work on this organism. Methanobrevibacter smithii resides in the large intestine but is found in the small intestine of individuals with SIBO. Methane is relevant, not only because it generates significant gas, but because the methane works as a local paralytic. Methane slows everything down creating gut motility issues. This creates and exacerbates bacterial overgrowth.

It’s worth pausing and recognizing that the space within our esophagus, stomach, small and large intestine is, in fact, the outside world. The mucosal barrier of our digestive system determines what enters our body, similar to our lungs and skin. Literally the space in the tube that extends from the mouth to the anus is the outside world. The mucosal barrier that lines our gastrointestinal tract is literally that, a barrier to the outside world. The reason I am pointing this out is because we often presume that everything that is inside us is our own inner world. Yet, our gut, is the space where the inside and outside world dance. The mucosal barrier of the GI system is there to determine which partners we are meant to dance with. Everything we eat and drink is of the “outside” world, yet, what we need to recognize is that the distinction between outside and inside is far more porous than we generally realize. Our GI system is both inside and outside–this relationship is central to our health.

The increased bacterial overgrowth leads to inflammation within the lumen or cavity of the intestines. Within the lumen - or central cavity of this tube - are dendritic cells that reach up through the intestinal wall and sample the outside world – they are called B cells. B cells determine friend or foe (our dance partner). When bacterial overgrowth occurs the B cells trigger a larger immune response now comprising T cells, and memory cells. This initiates a further immune response. With SIBO there is an inappropriate immune response. This inappropriate immune response can generate chronic inflammation, intestinal permeability, and food sensitivities.

The imbalance of microorganisms and bacteria in the small intestine generates an inappropriate immune response which causes changes to the mucosal lining of the small intestine. Here we find ourselves, once again, at the junction of where our body meets the outside world. When there are imbalances in the ecology of the outside world it affects the ecology of our internal world. This imbalance shows up as inflammation and malabsorption. As a result, inflammatory changes to the lamina propria and villous atrophy often occur in SIBO. The lamina propria is a type of connective tissue found under the thin layer of tissues covering the mucous membrane of the small intestine. Villi are the microscopic, finger-like tentacles that line the wall of your small intestine that absorb nutrients. Chronic inflammation, changes in bowel motility, and overgrowth cause the villi to atrophy and erode, leaving a virtually flat surface of the small intestine which causes malabsorption. This cycle can also cause malnutrition in other ways. The bacteria alter bile, which creates fat malabsorption (steatorrhea, fat-soluble vitamin deficiency). Along with a deficiency of fat-soluble vitamins there are also decreased levels of nutrients such as vitamin B12 and iron. The overgrowth of bacteria affects enzymes that are involved in digestion leading to carbohydrate malabsorption, fermentation, and gas. Thus, SIBO is involved in a cycle that provokes an inappropriate immune response within the mucosal lining of the intestines generating inflammation which can then initiate additional systemic symptoms which we will discuss in Part Three.

Below is a diagram, by Dr. Allison Siebecker an advocate and educator in the understanding and treatment of SIBO. It provides an overview of the pathophysiology of SIBO that I have discussed above. The diagram provides a quick snapshot into the symptoms and conditions that can arise due to changes in the gut caused by SIBO.

In the third and final article in this series, we will explore the effects that SIBO can have on other systems in the body and as a result other conditions that may be associated with SIBO such as rosacea or nonalcoholic fatty liver disease (NAFLD). In conclusion, we will look at approaches to addressing SIBO.

For Further Reading:

Pimentel M, Saad RJ, Long MD, Rao SSC. ACG Clinical Guideline: Small Intestinal Bacterial Overgrowth. Am J Gastroenterol. 2020 Feb;115(2):165-178. doi: 10.14309/ajg.0000000000000501. PMID: 32023228.

Quigley EM. Gut bacteria in health and disease. Gastroenterol Hepatol (N Y). 2013 Sep;9(9):560-9. PMID: 24729765; PMCID: PMC3983973.



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