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Part Three SIBO - What next?

By Karen Miller-Lane, ND, L.Ac


In Part One, I provided an overview of small intestinal bacterial overgrowth or SIBO. An important consideration to keep in mind is that SIBO may be an underdiagnosed cause of irritable bowel syndrome (IBS). Then, in Part Two, I reviewed the pathophysiology of SIBO in which the overgrowth of microorganisms in the small intestine can lead to GI symptoms such as bloating, gas, nausea, heartburn, stomach discomfort, diarrhea, and or constipation. Recall that factors such as stress or a GI infection, or when mechanisms that maintain gut health such as gastric acid, and digestive enzymes are impaired, they contribute to microbial overgrowth in the small intestine. These conditions and pre-existing conditions such as hypothyroid or celiac disease can lead to damage and inflammation of the gut mucosal barrier which then sets the stage for additional systemic conditions.


[1]

Small intestinal bacterial overgrowth: the chicken or the egg?



In Part Three, we turn our attention to the consequences of a disrupted small bowel ecology that may affect other systems in the body. For example, when there is low stomach acid or a decrease in digestive enzymes, our natural GI protective mechanisms are compromised. This leads to dysbiosis, a state of microbial imbalance. In addition, changes in gut motility (the muscle contractions that mix and move food along the GI system), mucosal inflammation, decreased absorption of vitamins and minerals and fat-soluble vitamins (such as B12, iron, zinc, Vitamin D, A, and E) and increased intestinal permeability, all affect small bowel ecology. These factors can then set the stage for issues in other systems such as the skin, liver, and vascular systems.


Many human and animal studies suggest that the intestinal microbiome’s influence extends beyond the gut and in fact contributes to the function, and dysfunction, of distant organ systems.[2] We discussed in Part Two that bacterial overgrowth in SIBO may be implicated in inflammation, intestinal permeability, and food sensitivities due to changes in the mucosal lining of the small intestine. In cases of disturbed intestinal barriers, intestinal bacteria as well as the metabolites of these microorganisms have been shown to accumulate in the skin and disrupt the balance of the skin.[3] This state of microbial imbalance may be implicated in acne vulgaris, atopic dermatitis or eczema, and psoriasis.


Symptoms of SIBO have also been present with a variety of liver diseases perhaps due to intestinal permeability and inflammation. In liver disease there can also be increased intestinal permeability which occurs when the gut barrier is compromised and there is a translocation of bacteria, endotoxin, a toxin present inside a bacterial cell, and other inflammatory agents.[4] The bacterial translocation and inflammation involved in SIBO may contribute to conditions such as non-alcoholic fatty liver disease or NAFLD. Further investigation is needed before we can make any final conclusions.


SIBO is also being investigated as a link to subclinical atherosclerosis. There is a protein (matrix Gla) involved in maintaining vascular health. Vitamin K2 is a prerequisite for matrix Gla’s activation and function. Vitamin K is present in two main forms (i) phylloquinone or vitamin K1 and (ii) menaquinone (MK) or vitamin K2. Vitamin K2 is involved in strengthening bone and, via the production of matrix Gla protein, preventing vascular calcification by repairing smooth muscle and endothelium. This means vitamin K2 is involved in preventing plaque formation in our arteries that leads to cardiovascular disease. Early studies show vitamin K2 may also enhance insulin sensitivity thereby supporting healthy blood sugar regulation. Intestinal bacteria are the main source of vitamin K2 in humans and bacterial dysbiosis is associated with altered K2 metabolism and impairing the protein (matrix Gla) required for maintaining vascular health. [5] Humans need gut bacteria in order to fulfill their vitamin K requirements because the dietary intake of vitamin K is often insufficient. SIBO, a condition characterized by gut bacteria imbalance, is also associated with impaired vitamin K metabolism. Therefore, SIBO and/or low vitamin K may hypothetically put someone at increased risk of atherosclerotic disease.[6]

We still have a long way to go to understanding what constitutes the normal bacterial population of our gut – our gut microbiome - along with the challenges and limitations of testing. Our concept of SIBO will most likely change over time with further research and understanding. This is a normal part of scientific investigation. It means that, at times, it is appropriate to twist and pivot from what we think we know to be “true” to what is emerging as new insights and interconnections. Our challenge is to make these pivots consciously rather than reactively. At the moment, I believe SIBO is a useful and valid concept for understanding some of the mechanisms behind the varied symptoms of a form of irritable bowel disease. A diagnosis is always a thing in motion. A diagnosis is often a compilation of symptoms as we learn to understand what lies betwixt and between what we see, how we see, what we measure, and how we interpret. The diagnosis continues to be in flux, along with the tools we use and the way we come to know. This shared learning process between humans and our environment is all in service of a deeper integration of our understanding of how bodies and selves interact in the world.

So, where does this leave us in the treatment of SIBO? The diagram below reminds us of where we began – exploring the factors that protect or go awry in the development of SIBO.


[7]

Treatments for SIBO have predominantly included antibiotic therapy. The above diagram points to the many considerations involved when treating SIBO.


Some of the factors that I investigate and consider when treating SIBO include: proper digestion, healthy gut motility and healthy gut integrity.


Some of the many questions that I ask include:


· Is there an infection that needs to be treated?

· Is there a pre-existing or underlying condition that is contributing to the disordered physiological processes?

· What are the stressors that can be modulated?

· Is there a gut imbalance or a predominance of certain gut bacteria that may be generating symptoms such as pronounced gas?

· What foods aggravate the condition or is gut integrity the cause of food sensitivities? If so, could we experiment with changes in diet?

· How do we calm an inappropriate immune response and inflammation?

Are there nutrients that are being compromised and need to be replaced?

· Are antibiotics and which antibiotics may be most effective?

· Are there herbs or other nutrients that can soothe, and heal the gut, or reduce the bacterial imbalance?

These questions and considerations are just some of what is involved in exploring SIBO in relationship with your doctor. The questions are built on a commitment to be curious and to pull back the lens sufficiently to be able to explore the intersection of our bodies, ourselves and our environment that manifest as our health.


This process provides a dynamic, ever evolving understanding of how to listen, test, experiment, and treat conditions that are complex and that we are still trying to understand. There are some conditions and treatments that are more straightforward than others. As you can see, with SIBO, there are numerous moving parts as we continue to research and understand all of the factors and physiology involved. This again is why you are in relationship with your doctor to determine how to navigate this together with the best information and understanding possible in the moment. For example, there is research into certain herbs such as the Quebracho Colorado from Argentina. It is from the bark of a tree called the axe breaker and it is used to deal with fungus and the organism archaebacter which produces methane in SIBO. Peppermint leaf may be more appropriate than the oil due to the polyphenol content. M. balsameas a specific type of peppermint may be more useful in calming the stomach and small intestine than other forms of peppermint. There may be certain probiotics that may secrete a range of natural antibiotics that target common pathogenic organisms in SIBO such as Bacillus subtilis HU58 and herbs such as licorice flavonoids that protect gastric mucosa and balance H. Pylori levels. One of the unique challenges we face today is we are inundated with information that is limited and that does not include the full context.


How we navigate what ails us is a dynamic process. A dance. Research is ever changing. SIBO is not just one thing - how it is expressed and treated is the art of medicine. Our symptoms may be complex and point in seemingly divergent directions. This is why the relationship between doctor and patient must not be merely transactional, but, rather, relational and grounded in a shared commitment to listen, learn, and explore what health means.



[1] Menees S, Chey W. The gut microbiome and irritable bowel syndrome. F1000Res. 2018 Jul 9;7:F1000 Faculty Rev-1029. doi: 10.12688/f1000research.14592.1. PMID: 30026921; PMCID: PMC6039952.

[2] Salem I, Ramser A, Isham N, Ghannoum MA. The Gut Microbiome as a Major Regulator of the Gut-Skin Axis. Front Microbiol. 2018 Jul 10;9:1459. doi: 10.3389/fmicb.2018.01459. PMID: 30042740; PMCID: PMC6048199.

[3]Ibid.

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

[5] Rakel, D. Integrative Medicine. Elsevier Inc, 4th Edition, Chapter 33, 2018.

[6] Ponziani FR, Pompili M, Di Stasio E, Zocco MA, Gasbarrini A, Flore R. Subclinical atherosclerosis is linked to small intestinal bacterial overgrowth via vitamin K2-dependent mechanisms. World J Gastroenterol. 2017 Feb 21;23(7):1241-1249. doi: 10.3748/wjg.v23.i7.1241. PMID: 28275304; PMCID: PMC5323449.

[7] Bushyhead D, Quigley EMM. Small Intestinal Bacterial Overgrowth-Pathophysiology and Its Implications for Definition and Management. Gastroenterology. 2022 Sep;163(3):593-607. doi: 10.1053/j.gastro.2022.04.002. Epub 2022 Apr 7. PMID: 35398346.


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