Micropathology of SIBO: Bridging a Gap Between Research & Clinical Practice
Manoji-Tharaka Gamaralalage, BSc
Chris Hergesheimer, BA, MA
Karrin Fairman-Young, ND
The human-gut microbiome is illuminated as a multifactorial signature of aging and a modulator of health and disease. Small intestinal bacterial overgrowth (SIBO) and its putative links to lifestyle and microbiome dysbiosis remains poorly understood in the absence of strict research methodology. Attempts to understand SIBO, a relatively poorly defined condition, require a closer investigation into controversies regarding treatment, including the concept of bacterial overgrowth as a root cause, complication, or predisposing factor of SIBO. This article presents key points gathered from metagenomics and existing literature and proposes a new avenue of research and treatment by exploring SIBO micropathology. This approach may help bridge a gap between research and clinical practice.
Humans are becoming increasingly susceptible to a sedentary lifestyle encumbered by morbidity and chronic diseases.1-3 Disruption of work-life balance places a heavy burden on the individual who suffers from lack of sleep, proper nutrition, and daily physical activity. Not surprisingly, lifestyle may be largely responsible for increasing prevalence of SIBO. Beyond an oversimplified definition of SIBO as an abnormally large population of coliform bacteria in the small intestine,4,5 this heterogeneous syndrome4,6 is shaped by environmental, structural, and age-related changes to the gut over the course of the human lifespan.
The cause of SIBO is controversial within the scientific community, which adds to the challenge of advancing knowledge about clinical treatment. Research and scientific speculation highlight the role of host-gut microbiome dysbiosis in SIBO,7,8 while other studies describe SIBO as resulting from a combination of motility disorders, breakdown of endogenous defense mechanisms9 that disrupts digestion, malabsorption of food, and altered gut physiology.6,10 These findings suggest that there is no one sole cause of SIBO; rather, it is a combination of associated complications, risk factors, and symptoms unique to each patient.6 Therefore, commonly reported symptoms such as bloating, constipation, diarrhea, malnutrition, and abdominal distension do not represent the entire repertoire of possible SIBO-related symptoms and complications.6,11 This may help explain the high number of under-diagnosed cases.4,6
Inhibiting our ability to identify underlying factors of SIBO is limited awareness of multifactorial12,13 and age-related complications6,9,14 and their association with microbiome dysbiosis,7,15 as well as putative contributions by lifestyle,6,7 diet,4,6 preexisting medical conditions, polypharmacy,16,17 psychological stress18 and mental illness19 (via disruption of the gut-brain axis13), motility disorders such as absence or prolonged migrating motor complex (MCC), postprandial gastric emptying,20 and changes in orocecal transit time.21 With age, smooth functioning of the gastrointestinal (GI) tract becomes compromised.14,22 Deterioration of peristalsis can occur as early as 40 years of age,23 and may be accompanied by reduced trituration and gastric emptying.24 Impaired peristalsis increases the likelihood of SIBO due to delayed gastric emptying and stasis of food and bacteria in the upper GI tract.9 Type of diet can also affect orocecal transit time (OCTT).4,6 Short transit time is often attributed to inflammation and/or food allergies, whereas long transit time is frequently attributed to refined foods, dehydration, and lack of dietary fiber.25
Additionally, impaired acid secretion, such as in achlorhydria, which is common in aging,26,27 is a risk factor for SIBO.28 Although a research study reported a greater incidence (10-20%) of achlorhydria in elderly compared to younger subjects (<1%),29 age isn’t the only contributing factor. Long-term ingestion of proton-pump inhibitors (PPI) can cause persistence of achlorhydria,30 increasing the incidence of SIBO. PPIs promote duodenal bacterial growth,6 implicating the role of gastric acid sterilization of the upper GI tract. The effects of multiple risk factors and their relationship with SIBO should be closely examined in the context of individual case studies.
SIBO & the Gut Microbiome
In the last 20 years, metagenomics research continues to provide insights into the role of gut bacteria in human health. Host-gut microbiome dysbiosis is characterized by an imbalance in gut microbiota that favors colonization by opportunistic pathogens.31 These opportunistic microorganisms are widely documented in metagenomics research as a contributing factor to the development of chronic diseases such as obesity, cardiovascular disease, and type 2 diabetes.32
Despite emerging evidence of links between SIBO and host-gut microbiome dysbiosis, the micropathology of SIBO, as it relates to environmental and age-related changes, is not well understood. However, this research provides clues about gut health, associated complications, risk factors, and symptoms. For example, mechanical changes in gut physiology, such as spasm or resection of the ileocecal valve (IV),9,33 can cause retrograde translocation of large bowel aerobes and anaerobes into the small intestine.9 Gram-negative Bacteriodes, Klebsiella,34 and enterococci35,36 in the small intestine have been associated with malabsorption, malnutrition, and weight loss.36,37 Identification of pathogenic and commensal strains may help to map out bacteria responsible for symptoms underlying SIBO pathology and contributing to comorbidity.
During intestinal transit, gut flora deconjugate primary bile acids (free bile acids), freeing taurine and glycine.38 Some of these unconjugated bile acids are recycled in the liver after ileal absorption into the enterohepatic bloodstream,39,40 whereas others enter the large bowel.40,41 In a healthy individual, probiotic strains with cholesterol-reducing effects, such as Lactobacillus, reduce serum lipids via elimination of deconjugated bile acids in feces.42 However, jejunal absorption of deconjugated bile acids in SIBO patients cause impaired micelle formation, contributing to malabsorption of dietary fat and deficiencies of fat-soluble vitamins.6,9 In other words, if bile salts are not efficiently absorbed in the ileum,43 bacterial overgrowth can increase toxicity of free intestinal bile acids, which contributes to mucosal inflammation and nutrient malabsorption.6
It is common for patients with SIBO to have various comorbidities that are either contributing factors or consequences of SIBO. For example, chronic pancreatitis (CP), which commonly causes pancreatic exocrine insufficiency, increases the risk of SIBO.44 According to a meta-analysis, one-third of CP patients were found positive for SIBO.45 Alcohol abuse is a commonly reported risk factor associated with both CP and SIBO. Alcohol ingestion is also known to increase intestinal permeability.46 During chronic alcohol consumption, release of pro-inflammatory cytokines in the GI tract in response to lipopolysaccharides (LPS) from gram-negative bacteria47 cause the accumulation of plasma LPS and acetaldehyde.48 These endotoxins also weaken the intestinal barrier, increase susceptibility to bacterial overgrowth, and, ultimately, increase the risk of alcohol-induced organ damage.48 The challenge is to understand if and how toxin-producing bacteria are exacerbating symptoms of SIBO.
Microbiome dysbiosis in comorbidities may be a feature of shared pathophysiology. GI symptoms are common among patients with type 2 diabetes mellitus (T2DM), possibly due to factors such as delayed transit time.49 In turn, dysbiosis in diabetics might influence metabolic risk. In a clinical study, SIBO was diagnosed in 43% of diabetic patients with chronic diarrhea.50 Among patients with T2DM, the concentration of trimethylamine N-oxide (TMAO), a byproduct of bacterial metabolism of L-carnitine and lecithin from animal protein,51 was found in one study to be dose-dependently related to insulin-resistance.52 Interestingly, high TMAO levels correlate with increased risk of cardiovascular disease (CVD),51 thus another possible comorbidity.
In clinical practice, micropathology of SIBO may provide a framework with which to analyze bacterial manipulation of gut physiology, comorbidity, and its relationship with a combination of underlying risk factors previously discussed.
Fecal analysis from metagenomics research and bioinformatics using Next-Generation DNA sequencing (NGS) methods can serve to identify overabundant commensal or opportunistic strains contributing to dysbiosis, aging, and disease. Metagenomics and bioinformatics can help identify key factors of research necessary to make clinical advancements; they may also redirect our attention to whether the goal of treatment should be to starve gut bacteria or to induce gut-healing mechanisms that intrinsically restrict bacterial overgrowth.
Along with metagenomics studies of the gut microbiome, fecal color and form using Bristol stool chart (BSC) analysis (commonly used in IBS studies) are also useful clinical indicators of gut health. Different colors may represent various possible complications in SIBO patients, such as ulcers (black/red), cancers (red), celiac disease or fat malabsorption (yellow), bile duct obstruction (white/clay color), or rapid transit time (green).53 The BSC can help monitor changes in transit time, diarrhea, and constipation54 in SIBO patients.
The common approach of treating SIBO with using non-FDA-approved, gold-standard antibiotics such as rifaximin may serve to exacerbate the condition or cause relapse of SIBO if mucosal biofilms allow bacteria to develop resistance to antibiotics.55 Additionally, rare adverse side effects of rifaximin, ie, nausea, diarrhea, vomiting, abdominal discomfort, or flatulence,56 can mimic common symptoms of SIBO. For some individuals, rifaximin may only complicate treatment. The use of combined naturopathic modalities that treat the whole person (tolle totum) is underutilized and may be much more effective for long-term relief than a simple allopathic approach using prescription antibiotics or a restricted low-FODMAP diet. Additionally, starving gut bacteria with repeated administration of an antibiotic may be an induced environmental stress that favors growth of resistant mucosal biofilms.55 The long-term outcome of this bacteria-starvation approach has not been thoroughly explored in studies.
A better long-term goal in SIBO than broad-spectrum antibiotic treatment that sometimes includes the elimination of many beneficial species is to reverse gut-microbiome dysbiosis. This goal can be accomplished by re-establishing homeostasis, ie, altering the gut environment to make conditions unfavorable for bacterial overgrowth and pathogenesis. Many herbal antibiotics with antibacterial and anti-inflammatory properties are underused in SIBO. Examples include oil of oregano (Origanum vulgare), berberine extracts, and garden thyme (Thymus vulgaris).57 Equisetum arvense L also demonstrates antimicrobial activity for a broad spectrum of bacteria, eg, Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Salmonella enteritidis, and Candida albicans.57
Malnutrition, a common SIBO complication, can be addressed by eating a diet rich in protein and plant-based sources of anti-inflammatory omega-3 fatty acids, including cold-water fish, flaxseeds and walnuts, and meats from grass-fed cattle.58,59 In contrast, omega-6 fatty acids, eg, sunflower and safflower oils, which are common in the typical Western diet, may promote inflammation. Foods rich in vitamins A, B6, B12, D, E, K, iron, zinc, and selenium (such as in grass-fed beef60) should also be consumed regularly and/or administered intravenously. Deficiencies of fat-soluble vitamins – such as vitamins A, D, and E, in particular – can result from fat malabsorption and contribute to steatorrhea.9 Additional useful interventions for SIBO patients may include probiotics, diet counseling, stress relief through yoga, acupuncture, and cognitive behavioral therapy (CBT) – measures that have also been used for IBS patients.61
Reduction of clinical symptoms should be systematically recorded along with specific interventions/goals. Gut health and healing might be monitored carefully using non-invasive ultrasonography62,63 to target healing of mucosal and deep lesions of the intestinal wall, observe motility, and identify biomechanical abnormalities.64,65 In other words, this diagnostic tool over the course of treatment may help determine whether a combination of herbs, prokinetic motility agents, and measures such as CBT are working effectively to restore gut health and physiology. In attempting to reverse dysbiosis, SIBO should ideally not be addressed using a standalone treatment. A future direction in research can explore trouble-shooting effects and efficacies of different combinations of natural remedies, fermented food, fiber, probiotics, prebiotics, prokinetic agents and antibiotics using matched-based cohort studies. Furthermore, renewed interest in alternative medications should reflect scientific rigor regarding its usefulness rather than subjective opinions or ambiguity about use and efficacies. There may not be any one gold-standard treatment if treatment is effectively custom-tailored to meet a patient’s specific needs.
Insights from metagenomics research may unlock potential for understanding how microbiome dysbiosis interacts with lifestyle and age-related changes in patients suffering from SIBO. This may be an effective vehicle for increasing scientific methodology, rigor, and recognition of alternative medicine in research and clinical treatment of SIBO. Additionally, effective treatment for long-term relief should draw evidence from clinical trials and case studies to inform an integrative naturopathic treatment with flexibility to adopt modifications to diet, and treatment that is individualized to each patient. Bottom line, a healthy merging of disciplines such as metagenomics and naturopathic medicine may be necessary to elucidate the multifactorial profile of SIBO, minimize refractory symptoms, and to establish long-term relief with gradual improvement over time.
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Manoji-Tharaka Gamaralalage, BSc (Co-operative Education), obtained her undergraduate degree from Simon Fraser University in molecular biology and biochemistry and minored in psychology. While pursuing naturopathic medicine, she completed a Co-op Work-term at the Boucher Institute of Naturopathic Medicine (BINM). By pioneering SIBO research at BINM, she aspires to bring fresh ideas, insight, and scientific rigor to a better understanding of SIBO through clinical studies and practice.
Chris Hergesheimer BA, MA, is a PhD candidate in the Faculty of Land and Food Systems at the University of British Columbia. His work there revolves around small-scale agriculture and value chains in the tropics. He is also the Director of Research Education and is an academic instructor at the Boucher Institute of Naturopathic Medicine in New Westminster, BC.
Karrin Fairman-Young, ND, is a 2004 graduate of the Canadian College of Naturopathic Medicine (CCNM) and practices in Vancouver, BC. She is Associate Dean of Clinical Studies and Chief Medical Officer at the Boucher Institute of Naturopathic Medical (BINM). She joined BINM in 2008 as Adjunct Clinic Faculty and continues to dedicate her time and skills to the direction of the clinic as well as ensuring clinical excellence through her contributions and direction of the clinical education program.