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Beyond Breath Testing: Using the GI-MAP to Uncover the Other Players in SIBO

Woman suffering from SIBO

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Dear Colleagues,

SIBO is on the top of everyone’s mind these days. In this sponsored blog by Dr. Amy Rolfsen, ND at Diagnostic Solutions Laboratory, we review why SIBO breath testing by itself just isn’t enough. To design an effective treatment protocol the first time, we need the whole picture of gut health, including digestion, immunity, commensals, pathogens, opportunists, and more. There are many useful scientific tidbits in this well-referenced blog, and I hope you read, comment, and share! Enjoy! ~DrKF

Diagnostic Solutions Laboratory

Website: www.diagnosticsolutionslab.com

Beyond Breath Testing: Using the GI-MAP® to Uncover the Other Players in SIBO

Small intestinal bacterial overgrowth (SIBO) describes the state of abnormal concentrations of bacterial and/or archaeal growth in the small intestine. Although the classic definition of SIBO refers to the overgrowth of commensal organisms, opportunistic, and pathogenic organisms are often involved.

The current diagnostic standard for SIBO within the medical community is a three-hour lactulose breath test. This test is useful in identifying dysfunctional gas production in the upper gastrointestinal (GI) tract. Beyond gas production, however, the lactulose breath test does not provide a complete assessment of GI function and other infections.[i] Many clinicians will stop searching when a lactulose breath test comes back with positive findings. However, the absence of deeper assessment of the gastrointestinal health of our patients is one of the biggest pitfalls in the long-term management of SIBO cases.

Most clinicians are acutely aware of the common SIBO symptoms and associated clinical conditions. Still, it can be puzzling when patients return with an incomplete relief of symptoms despite reasonable SIBO protocols. These persistent cases are all too common. In these situations, your practice and your patients could benefit greatly from GI-MAP’s deeper investigation into GI ecology, microbiome status, and assessment of digestive health.

 

Using GI-MAP (Gastrointestinal Microbial Assay Plus) to Clarify SIBO Cases

GI-MAP is perfectly suited as an adjunct to the 3-hour breath test to decode your most complicated and unremitting SIBO cases. In addition to detecting common hydrogen and methane-producing organisms, the GI-MAP can also identify many other confounding factors that can be present in patients with SIBO, including many hydrogen sulfide (H2S) producing organisms.

This comprehensive stool analysis employs quantitative PCR technology to detect gastrointestinal organisms, allowing for extremely sensitive detection at both high and low levels of pathogenic, commensal, and opportunistic organisms.

The following data provide insights and clinically relevant information to help you use the GI-MAP test to add depth to your treatment approach in SIBO cases.

 

Assessing GI-MAP for Common SIBO Findings

Identifying Hydrogen (H2) Producing Organisms

The GI-MAP report measures several H2 producers, some of which are likely to be found in the large intestine and some of which favor the small intestine.

 

Hydrogen Producing Bacteria on the GI-MAP Report That Favor Small Intestinal Colonization [ii]

Normal Bacterial Flora

·         Enterococcus spp.

·         Lactobacillus spp.

 

Opportunistic Bacteria

·         Bacillus spp.

·         Enterococcus faecalis

·         Enterococcus faecium

·         Staphylococcus spp.

·         Streptococcus spp.

 

Identifying Methane (CH4) Producing Organisms

Methanobacteriaceae family is a normal finding in the distal colon. These archaea can become problematic when they are displaced proximally into the small intestine.[iii]

Methane Producing Archaea on the GI-MAP Report

Methanobacteriaceae

 

Identifying Hydrogen Sulfide (H2S) Producing Organisms

The GI-MAP also tests for several hydrogen sulfide producing bacteria, many of which preferentially colonize the small intestine. There is great importance in assessing these as they can be extremely inflammatory in nature and can increase symptoms in the GI tract.[iv] [v] [vi]

 

Hydrogen Sulfide Producing Bacteria on the GI-MAP Report [vii] [viii] [ix] [x] [xi]

Pathogenic Bacteria

·         Campylobacter spp.

·         Escherichia coli

·         Salmonella spp.

·         Vibrio cholerae

·         Yersinia enterocolitica

Normal Bacterial Flora

·         Escherichia spp.

·         Enterobacter spp.

 

Opportunistic Bacteria

·         Helicobacter pylori

·         Morganella spp.

·         Pseudomonas spp.

·         Citrobacter spp.

·         Klebsiella spp.

·         Prevotella spp.

·         Proteus spp.

·         Fusobacterium spp.

 

Underlying Causes of SIBO

To successfully treat SIBO, a clinician must first identify and correct the underlying cause (or causes). In a normally functioning small intestine, regular peristalsis, host immunity, and tightly controlled pH ensure that bacteria are unable to grow in large quantities. Any aberration in these factors could result in bacterial colonization in the proximal GI tract. A considerable list of medications and underlying medical conditions can predispose to dysbiosis.[xii] Beyond these, GI-MAP can detect several factors that can play significant roles in the persistence and recurrence of SIBO.

For optimal patient outcomes, identifying and addressing all gut dysfunction is best practice. Stool testing with the GI-MAP can provide critical information on gut health status that breath testing alone may miss. The GI-MAP provides insight into the following areas of gut health that are commonly found in patients suspected of SIBO or resistant to SIBO treatment:

 

Helicobacter pylori

Chronic H. pylori can impact the human body far beyond the classic upper GI signs and symptoms. Some of the most impactful effects of H. pylori are elicited through changes in gastric pH and alterations in host immunity.[xiii] [xiv]

The net effect of chronic H. pylori infections is usually an increase in gastric pH, which can contribute to dysbiosis in several ways.[xv]  Low pH is required to prevent bacterial entry into the GI tract and is also required to elicit pancreatic enzyme release.[xvi] Increased pH in the proximal small intestine provides favorable conditions for rampant bacterial growth and may predispose patients to dysbiosis, especially in conjunction with dysfunctional motility. [xvii] Deficiency of hydrochloric acid can also result in undigested proteins and nutrients, which can provide a food source for bacterial growth. [xviii]

 

Digestive Insufficiency

Deficient hydrochloric acid (HCl), enzyme, or bile secretion can predispose patients to dysbiosis in numerous ways. Decreased HCl output is discussed above under “Helicobacter pylori.

The GI-MAP test report measures steatocrit and elastase-1 as markers for digestive function. Steatocrit is a measure of fecal fat, which can represent bile flow and fat absorption.

Elastase-1 is a marker of pancreatic exocrine, or enzyme, output. The optimal level of elastase-1 is >500. Any finding below this level represents suboptimal pancreatic function.

Significant bacterial growth can also contribute to carbohydrate and protein malabsorption by degrading brush border enzymes.[xix] [xx]

 

Low Immunity

Treating immune deficiency can increase success rates when treating dysbiosis. A functional immune system is a requirement for a healthy microbiota balance.[xxi] [xxii] The immune system must be active and discerning to simultaneously identify and eliminate pathogens and recognize beneficial organisms. Low secretory IgA (sIgA) indicates a deficiency of innate immunity in the GI tract.

 

When SIBO is More Than Just SIBO

In clinical practice, SIBO is rarely just SIBO. In addition to the underlying causes discussed above, bacterial overgrowth is often accompanied by other gastrointestinal phenomena. When the GI tract is treated as a dynamic, multi-faceted system, patients are more likely to achieve remission and lasting relief from their gastrointestinal symptoms.

 

Pathogenic Bacteria

It is common to find low levels of pathogenic bacteria in patients with SIBO. Most of the bacteria found on the first page of GI-MAP (with the exception of C. difficile) are hydrogen sulfide producing organisms, and many favor the distal ileum.[xxiii] [xxiv]  Pathogenic bacteria may contribute to persistent dysbiosis, may be associated with more severe symptoms, and may require intensive treatment.

 

Yeast/Fungi

Candida and other fungal infections can be involved in small intestine dysbiosis.[xxv] Symptoms associated with a fungal infection have many commonalities with SIBO symptoms.

 

Parasites

Parasites are commonly found alongside bacterial dysbiosis.[xxvi] Pathogenic and opportunistic parasitic infection can alter immunity to favor bacterial growth, especially the growth of gram-negative organisms.[xxvii]

 

Deficient Normal Flora

Normal flora play a pivotal role in overall GI health, including motility, metabolism, barrier function, and immunity.[xxviii] [xxix] [xxx]  [xxxi] When normal flora are deficient in the colon, we frequently see immune dysfunction, nutrient malabsorption, inflammation, and GI symptoms (such as irregular stools, gas, and bloating). Decreased bacterial diversity is also a common finding in SIBO.[xxxii]

 

GI Lining Dysfunction

SIBO and barrier dysfunction can operate in a vicious cycle. Bacterial overgrowth has been shown to result in epithelial cell damage and villous blunting in some people, which can contribute to deficient production of brush border enzymes.[xxxiii] [xxxiv]  This deficiency frequently leads to undigested carbohydrates and proteins, which are likely to provide food substrate to bacteria, leading to excessive growth.

 

GI-MAP Report Findings That Can Suggest Barrier Dysfunction

Deficiency of the following normal flora:

·         Enterococcus spp.

·         Escherichia spp.

·         Lactobacillus spp.

·         Enterobacter spp.

·         Akkermansia muciniphila

·         Bacteroidetes phylum

Intestinal Health Markers

·         Low elastase-1

·         Low secretory IgA

·         High zonulin (add-on test)

 

Blood, Inflammation, and Inflammatory Disorders

When a patient presents with SIBO-type symptoms alongside more significant symptoms such as blood or mucus in the stool, a more thorough investigation is warranted. Small intestinal dysbiosis is an extremely common finding in both Crohn’s disease and colitis.[xxxv] Although SIBO can exacerbate inflammatory bowel disease, it is rarely the driving force behind the pathogenesis of these conditions. The GI-MAP includes a fecal immunochemical test (FIT) to assess for occult blood as well as calprotectin to evaluate inflammation.

 

SIBO Breath Testing Alone May Miss Common Areas of GI Dysfunction

Patients who are suspected of having SIBO can benefit from adjunct GI-MAP® stool testing that uses quantitative PCR technology to accurately identify other underlying or comorbid GI dysfunction that a breath test alone would miss.

 

To Build Your Proficiency in GI-MAP® Testing:

If you are new to GI-MAP, please visit our website: https://www.diagnosticsolutionslab.com/tests/gi-map.

Discover the GI-MAP Interpretive Guide.

Diagnostic Solutions Laboratory has produced two webinars on small intestinal dysbiosis, which can be found here:

 

Works Cited

D’Elios, M. M., Codolo, G., Amedei, A., Mazzi, P., Berton, G., Zanotti, G., … & De Bernard, M. (2009). Helicobacter pylori, asthma and allergy. FEMS Immunology & Medical Microbiology, 56(1), 1-8.

Dukowicz, A. C., Lacy, B. E., & Levine, G. M. (2007). Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterology & hepatology, 3(2), 112.

DuPont, A. W., & DuPont, H. L. (2011). The intestinal microbiota and chronic disorders of the gut. Nature reviews Gastroenterology & hepatology, 8(9), 523-531.

Erdogan, A., & Rao, S. S. (2015). Small intestinal fungal overgrowth. Current gastroenterology reports, 17(4), 1-7.

Guilliams, T. G., & Drake, L. E. (2020). Meal-Time Supplementation with Betaine HCl for Functional Hypochlorhydria: What is the Evidence?. Integrative Medicine: A Clinician’s Journal, 19(1).

Hasni, S. A. (2012). Role of Helicobacter pylori infection in autoimmune diseases. Current opinion in rheumatology, 24(4), 429.

Kalantar-Zadeh, K., Berean, K. J., Burgell, R. E., Muir, J. G., & Gibson, P. R. (2019). Intestinal gases: influence on gut disorders and the role of dietary manipulations. Nature Reviews Gastroenterology & Hepatology, 16(12), 733-747.

Kastl Jr, A. J., Terry, N. A., Wu, G. D., & Albenberg, L. G. (2020). The structure and function of the human small intestinal microbiota: current understanding and future directions. Cellular and molecular gastroenterology and hepatology, 9(1), 33-45.

Lappinga, P. J., Abraham, S. C., Murray, J. A., Vetter, E. A., Patel, R., & Wu, T. T. (2010). Small Intestinal Bacterial Overgrowth. Archives of Pathology & Laboratory Medicine, 134(2).

Leite, G., Morales, W., Weitsman, S., Celly, S., Parodi, G., Mathur, R., … & Pimentel, M. (2020). The duodenal microbiome is altered in small intestinal bacterial overgrowth. PloS one, 15(7), e0234906.

Mukherjee, P. K., Zhou, G., Munyon, R., & Ghannoum, M. A. (2005). Candida biofilm: a well-designed protected environment. Medical mycology, 43(3), 191-208.

Pimentel, M., Saad, R. J., Long, M. D., & Rao, S. S. (2020). ACG clinical guideline: small intestinal bacterial overgrowth. American Journal of Gastroenterology, 115(2), 165-178.

Quigley, E. M. (2011). Microflora modulation of motility. Journal of neurogastroenterology and motility, 17(2), 140.

Quigley, E. M. (2019). Symptoms and the small intestinal microbiome—The unknown explored. Nature Reviews Gastroenterology & Hepatology, 16(8), 457-458.

Rausch, S., Held, J., Fischer, A., Heimesaat, M. M., Kühl, A. A., Bereswill, S., & Hartmann, S. (2013). Small intestinal nematode infection of mice is associated with increased enterobacterial loads alongside the intestinal tract. PloS one, 8(9), e74026.

Sachdev, A. H., & Pimentel, M. (2013). Gastrointestinal bacterial overgrowth: pathogenesis and clinical significance. Therapeutic advances in chronic disease, 4(5), 223-231.

Shea-Donohue, T., Fasano, A., Smith, A., & Zhao, A. (2010). Enteric pathogens and gut function: Role of cytokines and STATs. Gut Microbes, 1(5), 316-324.

Simrén, M., Barbara, G., Flint, H. J., Spiegel, B. M., Spiller, R. C., Vanner, S., … & Zoetendal, E. G. (2013). Intestinal microbiota in functional bowel disorders: a Rome foundation report. Gut, 62(1), 159-176.

Singh, S. B., & Lin, H.C. (2015). Hydrogen sulfide in physiology and diseases of the digestive tract. Microorganisms, 3(4), 866-889.

Sundin, O. H., Mendoza-Ladd, A., Zeng, M., Diaz-Arévalo, D., Morales, E., Fagan, B. M., … & McCallum, R. W. (2017). The human jejunum has an endogenous microbiota that differs from those in the oral cavity and colon. BMC microbiology, 17(1), 1-17.

Tlaskalová-Hogenová, H., Štěpánková, R., Hudcovic, T., Tučková, L., Cukrowska, B., Lodinová-Žádnıková, R., … & Kokešová, A. (2004). Commensal bacteria (normal microflora), mucosal immunity and chronic inflammatory and autoimmune diseases. Immunology letters, 93(2-3), 97-108.

Tomasova, L., Konopelski, P., & Ufnal, M. (2016). Gut bacteria and hydrogen sulfide: the new old players in circulatory system homeostasis. Molecules, 21(11), 1558.

 

[i] Leite et al. 2020

[ii] Kastl et al 2020

[iii] Kalantar-Zadeh et al. 2019

[iv] Leite et al. 2020

[v] Sachdev & Pimentel 2013

[vi] Dupont & Dupont 2011

[vii] Pimentel et al. 2020

[viii] Kastl et al 2020

[ix] Singh & Lin 2015

[x] Tomasova et al. 2016

[xi] Sundin et al. 2017

[xii] Dukowicz et al. 2007

[xiii] Hasni 2012

[xiv] D’Elios et al. 2009

[xv] Dukowicz et al. 2007

[xvi] Guilliams & Drake 2020

[xvii] Guilliams & Drake 2020

[xviii] Guilliams & Drake 2020

[xix] Kalantar-Zadeh et al. 2019

[xx] Lappinga et al. 2010

[xxi] Pimentel et al. 2020

[xxii] Dukowicz et al. 2007

[xxiii] Kastl et al 2020

[xxiv] Sundin et al. 2017

[xxv] Erdogan & Rao 2015

[xxvi] Shea-Donohue et al. 2010

[xxvii] Rausch et al 2013

[xxviii] Quigley 2011

[xxix] Kalantar-Zadeh et al. 2019

[xxx] Tlaskalová-Hogenová et al. 2004

[xxxi] Dupont & Dupont 2011

[xxxii] Leite et al. 2020

[xxxiii] Dukowicz et al. 2007

[xxxiv] Lappinga et al. 2010

[xxxv] Kalantar-Zadeh et al. 2019

By: Dr. Amy Rolfson

Dr. Amy Rolfsen is a naturopathic doctor and medical consultant. Her areas of clinical interest and expertise are women’s wellness, children’s health, immunology and gastrointestinal health. Dr. Rolfsen is continually working on mastering her craft. She is drawn to gentle, non-invasive techniques and will incorporate a combination of nutrition, botanicals, Chinese medicine, manual therapies, energetic therapies and pharmaceuticals, tailoring treatment plans to each individual.

Dr. Rolfsen runs her own clinic where she sees patients in-person and also consults with international clients. She works with people who are seeking guidance in understanding their health and taking steps toward perfecting their physical, mental and emotional health.

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