Small intestinal bacterial overgrowth (SIBO) is defined as the presence of excessive bacteria in the small intestine. SIBO is frequently found to be the cause of chronic diarrhea and malabsorption. Patients with SIBO may also suffer from unintentional weight loss, nutritional deficiencies, and osteoporosis. A common misconception is that SIBO affects only a limited number of patients, such as those with an anatomic abnormality of the gastrointestinal (GI) tract or those with a motility disorder. However, the recent literature shows that SIBO may be more prevalent than previously thought. This apparent increase in prevalence may have occurred partly due to readily available diagnostic tests which have improved our ability to diagnose SIBO.
Only limited data are available regarding the prevalence of SIBO in healthy populations but age appears to be an important risk factor. In a study of 294 non-hospitalized older adults in which 34 younger adults (mean age 33.6 years) served as healthy controls, the prevalence of SIBO, as determined by glucose breath test, was 5.9% in the control group versus 15.6% in the older group. Healthy elderly volunteers from the United Kingdom had a 14.5% prevalence rate for SIBO based on a positive glucose breath test.
“Small bowel bacterial overgrowth is an important and under-recognized clinical syndrome in the elderly. It is the most common cause of malabsorption among older adults”
Irritable bowel syndrome (IBS) is another known risk factor for SIBO. Studies have shown that up to 78% to 84% of patients who met the Rome I criteria for IBS had an abnormal lactulose breath test suggestive of SIBO compared to 20% of healthy volunteers.[507,508] In summary, although data are limited, the prevalence rates of SIBO appear to be consistently higher in patients with IBS. However, it is also common in children with chronic gastrointestinal symptoms and abdominal pain.
“Similar to adults with irritable bowel syndrome, there is a significantly higher prevalence of SIBO in children with chronic abdominal pain”
“…SIBO may be more common in children with gastrointestinal symptoms and apparent carbohydrate malabsorption than previously recognized”
- 3% of patients with celiac disease
- 66% of patients with celiac disease with persistent GI symptoms
- 15% of elderly population
- 53% of patients with antacid medication use
- 78% of patients with IBS
- 33% of patients with chronic diarrhea
- 34% of patients with chronic pancreatitis
- 90% of alcoholics 
Causes of SIBO
“SIBO can result from failure of the gastric acid barrier, failure of small intestinal motility, anatomic alterations or impairment of systemic and local immunity”
“In the intact intestine, small intestinal bacterial overgrowth is prevented by the actions of gastric acid, pancreatic enzyme activity, small intestinal motility, and the ileocecal valve”
Intestinal bacterial overgrowth develops when the normal homeostatic mechanisms that control gut bacterial populations are disrupted. The two most common conditions that predispose to bacterial overgrowth are diminished gastric acid secretion (hypochlorhydria) and decreased small intestinal motility (sluggish bowels). Let’s take a brief look at how these conditions lead to SIBO.
SIBO: Low Gastric Acid Production
As discussed in Common Stomach Disorders: Hypochlorhydria, gastric acid suppresses the growth of ingested bacteria, thereby limiting bacterial counts in the stomach and upper small intestine. Diminished acid production (hypochlorhydria) is a risk factor for bacterial overgrowth simply because there is less acid available to prevent bacteria from growing. As discussed in the hypochlorhydria section, there are a number of factors that can lead to this condition, including colonization with H. pylori, stress and as a consequence of aging. SIBO can also result from PPI use in the treatment of GERD. A prospective study of 47 outpatients treated with either omeprazole (20 mg/day) or cimetidine (800 mg/day) found that bacterial overgrowth was present in 53% of patients who received omeprazole (PPI), compared to only 17% who received cimetidine (a weaker acid-suppressing medication). In another study, 20 patients treated with 4 weeks of omeprazole had a significant increase in duodenal bacterial counts (compared to baseline) as measured by endoscopic aspiration. These studies clearly show the importance of stomach acid production in preventing bacterial overgrowth.
Normal GI motility involves a complex, tightly coordinated series of events designed to move material through the GI tract. During periods of fasting, a migrating motor complex (MMC) develops approximately every 90-120 minutes to sweep residual debris through the GI tract. Several studies have demonstrated that abnormalities in the MMC may predispose to the development of SIBO.[515-517] There are a number of conditions that can lead to decreased motility including hypothyroidism, age-related enteric nervous system degeneration, brain injury leading to poor vagal tone, neurodegenerative disease, chronic pancreatitis and chronic diabetes.
Small bowel motility disorders predispose to the development of SIBO simply because bacteria (and any undigested food which the bacteria need to flourish) may not be effectively swept from the small intestine into the colon for elimination. Gastroparesis, a chronic disorder of delayed gastric emptying, can also lead to SIBO due to stasis of food and bacteria in the upper GI tract. Patients with chronic renal failure have neuropathic-like motor abnormalities in the small intestine and are more likely to develop bacterial overgrowth as well. In addition, neuropathic processes, such as chronic intestinal pseudo-obstruction (CIP), and myopathic processes, such as scleroderma and polymyositis, are likely to be associated with SIBO.
There are various underlying conditions that can lead to alterations in the amount of gastric acid available to neutralize bacteria or lead to motility disorders via an altered migrating motor complex (MMC) which predispose to bacterial overgrowth. SIBO can also result from anatomical defects leading to bacteria pooling and scarring of intestinal wall from chronic inflammation. Below is a list of some of these conditions that appear to be risk factors for SIBO.
- Hypochlorhydria: lack of acidity to neutralize bacteria and pH homeostasis of small intestine
- Proton pump inhibitor use for gastric reflux: lack of acidity to neutralize bacteria and pH homeostasis of small intestine
- Hypothyroidism: lack of thyroid hormone activation of vagal motor nuclei and migrating motor complex
- Age-related enteric nervous system degeneration: lack of brainstem vagal motor nuclei to stimulate enteric nervous system
- Brain injury leading to poor vagal tone: lack of brainstem vagal motor nuclei to stimulate enteric nervous system
- Neurodegenerative disease: alpha synuclein or Lewy body infiltration of intestinal migrating motor complex
- Chronic pancreatitis: neuropathic destruction of migrating motor complex from oxidative stress
- Chronic diabetes: neuropathic destruction of migrating motor complex from oxidative stress
- Abdominal anatomical disturbances: anatomical location for bacteria pooling
- Fistula: anatomical location for bacteria pooling
- Diverticula: anatomical location for bacteria pooling
- Postsurgical alteration: damage of ileocecal valve or promotion of anatomical location for bacteria pooling
- Scleroderma: scarring of intestinal wall from chronic inflammation
- Celiac disease: scarring of intestinal wall from chronic inflammation
- Significant immunodeficiency: immunodeficiency to regulate to regulate enteric bacterial populations of small intestine
- Radiation-induced enteropathy: oxidative damage to migrating motor complex of intestines 
Hypothyroidism is a major risk factor for the development of bacterial overgrowth in the small bowel. Thyroid hormone is critical for normal activity of the enteric motor complex and vagal motor complex that regulate intestinal motility and ileocecal valve control. Low levels of thyroid hormone in the gut leads to decreased thyroid hormone activation of enteric and vagal motor complex and decreased intestinal motility. It also leads to decreased vagal activation of gastric acid production which prevents bacterial overgrowth. In summary, hypothyroidism leads to the following:
- Decreased ileocecal valve control of trafficking bacteria from large intestine to small intestine
- Decreased gut motility leading to bacteriostasis in small intestine
- Decreased vagal activation of HCl release leading to inability to suppress bacterial growth
All of these dysfunctions lead to SIBO as well as the following conditions:
- Bacterial disruption in the small intestinal lumen
- Interference with thyroid medication absorption
- Decreased thyroid response on receptor sites
There is a significant amount of interest in the connection between SIBO and IBS and in particular, the role of SIBO in the development of IBS. First, many IBS symptoms are nonspecific (bloating, distention, cramping, abdominal discomfort) and can mimic symptoms of SIBO. Delayed transit, disordered motility, or abnormalities in the MMC, all of which can occur in IBS patients, could potentially predispose these patients to SIBO. Additionally, studies show a high prevalence of SIBO in IBS patients. In an uncontrolled study, Pimentel and colleagues found that 157 of 202 patients (78%) who met the Rome I criteria for IBS had an abnormal lactulose breath test suggestive of SIBO. A blinded, randomized study found that 84% of patients who met Rome I criteria for IBS had an abnormal lactulose breath test consistent with SIBO, compared to 20% of healthy volunteers, while another group reported a SIBO prevalence rate of 65% in 98 consecutive IBS patients.
Another line of evidence in support of SIBO contributing to IBS is evidence of IBS symptoms improving when treated for bacterial overgrowth. In the above study which showed 78% of IBS patients having SIBO, these patients were then treated with antibiotics. Of the 47 patients that had follow-up testing after antibiotic treatment, 25 of the 47 subjects (53%) had eradication of their bacterial overgrowth. Those that had the SIBO condition eradicated revealed a statistically significant improvement in IBS symptoms of diarrhea and abdominal pain compared to those that failed to eradicate SIBO. 48% of the patients who eradicated SIBO no longer met criteria for IBS. The researchers concluded the following:
“Small intestinal bacterial overgrowth is associated with irritable bowel syndrome. Eradication of the overgrowth eliminates irritable bowel syndrome by study criteria in 48% of subjects.”
The overlap of shared symptoms between SIBO and IBS, the high incidence of SIBO in IBS and the high percentage of elimination of IBS in the eradication of SIBO is compelling evidence that SIBO is a contributing factor in a large percentage of IBS patients.[507,487-489] Additionally, research has shown a high incidence of IBS in patients with GERD. A study performed at the GI Motility Center at Cedars-Sinai Medical Center in 2002 found that 71% of GERD patients tested positive for IBS – double the percentage seen in non-GERD patients examined. The researchers concluded:
“There is a higher prevalence of IBS in subjects with GERD compared with subjects without GERD.”
Based on these findings that most IBS patients have SIBO and most GERD patients have IBS, we would expect to see a high prevalence of SIBO in GERD patients. This is consistent with some of the most recent literature that is starting to examine this connection. In the largest retrospective cohort study done to date, risk factors for SIBO were assessed and correlated with diagnosis of small intestinal bacterial overgrowth (SIBO). Diagnostic testing for SIBO was performed using the D-xylose breath test (XBT). The XBT was performed on 932 patients with symptoms of bloating, abdominal pain, abdominal distension, weight loss, diarrhea, and/or constipation based on a clinical suspicion for SIBO. In the 932 subjects studied, 513 had a positive XBT. Medical records of the 932 patients who completed the XBT were reviewed. The researchers found a significant correlation between a documented history of GERD (P = 0.04) or peptic ulcer disease (PUD) (P ≤ 0.01) and a positive XBT indicating SIBO. Recall from the previous sections on GERD and peptic ulcer disease (PUD), both of these conditions have been associated with low stomach acid production (hypochlorhydria) which explains the high incidence of SIBO, as this is a known cause of SIBO. The researchers made the following remarks that might explain the results of the study:
“Many of these (SIBO and PUD) patients are placed on lifelong acid suppression therapy, often using high-potency pharmacotherapies (ie: PPIs). A less acidic gastric milieu could create an environment more conducive to SIBO.”
Based on the above studies, it is evident that hypochlorhydria induces SIBO and there appears to be a significant correlation between GERD, IBS and SIBO. Taken together, these data support the theory presented earlier in the Hypochlorhydria section above that hypochlorhydria induces GERD and may be involved in the pathophysiology of IBS as well. Which begs the question: Why are acid-suppressing medications, such as PPIs, being used in the treatment of GERD?
If hypochlorhydria induces both GERD and SIBO, we would expect to see a higher prevalence of SIBO in GERD patients with increased suppression of stomach acid production by PPI therapy. This is consistent with the current literature on PPI use in GERD patients and risk of SIBO. In one study, two groups of patients with GERD were studied. One group was given omeprazole (PPI) and the other group acted as a control group and were not given omeprazole. 37% of the PPI-treated group of GERD patients developed SIBO within 3 months compared to 10% of the GERD patients not treated with the PPI. The researchers concluded the following:
“Proton pump inhibitor therapy in patients with GERD results in a high prevalence of gastric bacterial overgrowth. These findings may have implications in the pathophysiology of gastroesophageal mucosal injury.”
Another more recent larger study confirmed the earlier results that the use of PPIs was associated with increased risk of SIBO. In this study, glucose hydrogen breath tests (GHBTs) were used to assess for SIBO. These GHBTs were given to 450 consecutive patients (200 with gastroesophageal reflux disease (GERD) who received PPIs for an average of 36 months; 200 with irritable bowel syndrome (IBS) with no PPI treatment for at least 3 years; and 50 healthy control subjects that had not received PPIs for at least 10 years). SIBO was detected in 50% of patients using PPIs, 24.5% of patients with IBS, and 6% of healthy control subjects. There was a statistically significant difference between GERD patients using PPIs and those with IBS or healthy control subjects (P < .001). The prevalence of SIBO increased after 1 year of treatment with PPIs. The researchers concluded the following:
“SIBO, assessed by GHBT, occurs significantly more frequently among long term PPI users than patients with IBS or control subjects.”
A large meta-analysis conducted in 2013, which reviewed all the studies available showing a correlation between the use of PPIs and risk of SIBO, concluded the following:
“Use of proton pump inhibitors (PPIs) could predispose individuals to small intestinal bacterial overgrowth (SIBO) by altering the intraluminal environment and bacterial flora”
Small intestinal bacterial overgrowth causes various disruptions to normal physiology which lead to a wide range of symptoms and signs, such as increased gas formation leading to abdominal distension and bowel irregularity, constipation and diarrhea (as a result of fermentation of undigested food in GI tract); protein deficiency and ammonia production (as a result of excess intestinal bacteria leading to bacterial competition with host for protein); nutrient malabsorption (as a result of enterotoxin production from excess gram-negative intestinal bacteria and damage to brush border mucosa); fat malabsorption (as a result of excess intestinal bacteria metabolizing bile salts to unconjugated or insoluble compounds, leading to impairment of bile salt micelle complex and fat malabsorption); production of lithocholic acid and enteric nervous system degeneration (as a result of excess bacteria in small intestine metabolizing bile salts to unconjugated or insoluble compounds); and destruction of intestinal tight junctions, systemic inflammation and destruction of intestinal migrating motor complex (as a result of excess bacteria in small intestine leading to enterotoxin production from gram-negative bacteria and destruction of intestinal tight junctions). Destruction of intestinal tight junctions leads to lipopolysaccharide (LPS) translocation and activation of hepatic macrophages leading to release of hepatotoxic factors and increased systemic and local intestinal inflammation.
Summary of Disruptions to Normal Physiology Caused by SIBO
- Increased gas formation leading to abdominal distension and bowel irregularity, such as constipation and diarrhea (as a result of fermentation of undigested food in GI tract)
- Protein deficiency and ammonia production (as a result of excess intestinal bacteria leading to bacterial competition with host for protein)
- Nutrient malabsorption (as a result of excess enterotoxin production from gram-negative intestinal bacteria and leading to damage to brush border mucosa)
- Fat malabsorption (as a result of excess intestinal bacteria metabolizing bile salts to unconjugated or insoluble compounds, leading to impairment of bile salt micelle complex formation and fat malabsorption)
- Production of lithocholic acid and enteric nervous system degeneration (as a result of excess intestinal bacteria metabolizing bile salts to unconjugated or insoluble compounds)
- Destruction of intestinal tight junctions, systemic inflammation and destruction of intestinal migrating motor complex (as a result of enterotoxin production from excess gram-negative intestinal bacteria and destruction of intestinal tight junctions)
- Destruction of intestinal tight junctions leads to lipopolysaccharide (LPS) translocation and activation of hepatic macrophages leading to release of hepatotoxic factors and increased systemic and local intestinal inflammation
Assessment of SIBO
“The diagnosis of SIBO is controversial. There is substantial disagreement in the literature regarding which test is the most appropriate in either the clinical or research setting. Two tests are commonly employed: bacterial culture and breath tests.”
Two tests are commonly used to assess for SIBO: bacterial culture and breath tests. The most direct method of assessing the bacterial population of the gut is to perform bacterial colony counts of small bowel contents on aspiration; however, the cost of endoscopy and the invasive nature of this procedure with its low but measurable risk, makes this approach less than ideal. There are also several technical hurdles which make this test impractical in many cases. First, many bacterial species do not grow in routine culture media, and quantitative culture may underestimate the bacterial population. Additionally, there are multiple problems inherent in performing this procedure including contamination of the endoscope and catheter as the instrument is passed through the GI tract, difficulty aspirating a sufficient sample, and other issues such as proper specimen handing which affects accurate sampling.
For these reasons, hydrogen breath tests are the most common diagnostic tool for SIBO since they are noninvasive, cheap, simple and safe. These tests are based on the measurement of hydrogen and methane in breath samples. These gases are produced by bacteria as a consequence of carbohydrate fermentation after oral ingestion of glucose and lactulose, and pass through the blood circulation where they are expelled in the lungs. The diagnosis of SIBO is established on the increase of hydrogen and methane gases with respect to the baseline sample. Unfortunately, breath tests have not yet been standardized, in terms of substrate concentration, duration of tests, time intervals of breath sampling and cut-off values. As a result, hydrogen breath tests are still not well-accepted as a specific test for SIBO in the field of gastroenterology. However, hydrogen breath tests remain the most common diagnostic tool for SIBO.
“Although not without shortcomings, hydrogen breath testing provides the simplest non-invasive and widely available diagnostic modality for suspected SIBO. Diagnostic accuracy of hydrogen breath testing in SIBO can be maximized by careful patient selection for testing, proper test preparation, and standardization of test performance as well as test interpretation.”
Conventional treatment aimed at correcting the underlying cause of SIBO primarily includes surgical and drug therapies. Surgical revision of altered small bowel anatomy may be beneficial in patients with SIBO secondary to small bowel diverticulosis, fistulas, or strictures. Medications should be reviewed to determine if they are playing a role in the development of symptoms. Prokinetic drugs (to increase intestinal peristalsis) are used in cases of dysmotility or gastroparesis. The mainstay of conventional treatment for SIBO remains antibiotic therapy. A variety of antibiotics have been used in the treatment of SIBO, most with little supporting evidence. Ideally, antibiotic therapy would be based on bacterial culture and sensitivity data. However, this approach is impractical in the clinical setting and treatment is thus directed at likely organisms based on reports of culture data from SIBO patients. Early antibiotics used in the treatment of SIBO included tetracycline and its derivatives and other broad-spectrum antibiotics such as amoxicillin/clavulanate, ciprofloxacin, and doxycycline. However, these recommendations were based on uncontrolled data. More recently, antimicrobials such as Rifaximin and metronidazole have shown efficacy in improving hydrogen breath test results and symptoms of SIBO. [531-533]
The optimal duration of antibiotic therapy is not known, and most trials employed a 7- to 10-day course. However, one of the drawbacks to the use of antibiotics in the treatment of SIBO is recurrence of SIBO and the need for additional courses of antibiotics. In fact, one trial demonstrated an average duration of symptom improvement of only 22 days, which translates into a need for at least 12 courses (presuming 7 days) of antibiotics per year to provide persistent symptom relief.
“Glucose breath test positivity recurrence rate was high after antibiotic treatment”
“Patients with evidence of GBT positivity recurrence showed gastrointestinal symptoms relapse thus suggesting SIBO recurrence.”
“Inadequate or incomplete response to antibiotic therapy is common…”
In the functional medicine model, we address the underlying causes that lead to this condition as well as the pathophysiology involved in bacterial overgrowth using botanical and other natural compounds. As we learned earlier, SIBO is prevented by the following physiologic functions:
- Actions of gastric acid
- Pancreatic enzyme activity
- Small intestinal motility
- Normal activity of the ileocecal valve
Therefore, it is important to assess these bodily functions in the individual and support them when deficient. As discussed earlier, the most common causes of this condition are hypochlorhydria (low stomach acid) and decreased intestinal motility (sluggish bowels). Hypochlorhydria and pancreatic enzyme deficiency can usually be addressed by supplementing with hydrochloric acid (HCl) and pancreatic enzymes. Discontinuation of PPI therapy in the treatment of GERD is also important in the treatment of SIBO and this can be accomplished by supporting gastric acid levels and pancreatic enzyme levels which as we have seen are at the root cause of both GERD and SIBO. There are a number of factors that can contribute to decreased intestinal motility as discussed above, such as hypothyroidism and decreased vagal activation, so assessing for these underlying conditions and addressing these causes when present is important. Thyroid hormone levels must be normalized prior to addressing the bacterial overgrowth. Decreased vagal activation can be supported by providing the patient exercises to increase vagal output, such as gargling with water throughout the day and promoting the gag reflex. Coffee enemas can also be used to induce activation of enteric motility and activate the brain-gut axis.
As discussed above, there are a number of physiologic imbalances that take place in SIBO, including increased gas formation leading to abdominal distension and bowel irregularity, constipation and diarrhea, protein deficiency and ammonia production, nutrient malabsorption, fat malabsorption, production of lithocholic acid and enteric nervous system degeneration, destruction of intestinal tight junctions, systemic inflammation and destruction of intestinal migrating motor complex, lipopolysaccharide (LPS) translocation and activation of hepatic macrophages. All of these conditions should be assessed and supported when indicated. This can be done with herbal/botanical and nutritional compounds shown in the literature to support these physiologic imbalances in most cases. In some cases of severe or chronic SIBO, anti-microbial therapy is indicated. Nutritional support, particularly in those patients with weight loss or vitamin and mineral deficiencies, is an important component of SIBO treatment. Supplementation and maintenance of vitamin B12 and fat-soluble vitamins, with correction of calcium and magnesium deficiencies, are key components of treatment.
Recent studies have shown that patients with bacterial overgrowth conditions can benefit from the use of probiotics although further studies are needed to define the role of probiotic therapy in SIBO. A randomized, double-blind, placebo-controlled study on 22 patients with proven bacterial overgrowth and chronic diarrhea showed improvement in frequency of symptoms after 15 days and 21 days and the effect was sustained at 7 days and 15 days after withdrawal. The strains used were Lactobacillus casei and L. acidophillus strains (LC). A significant decrease in hydrogen gas concentration was noted in hydrogen breath testing at 7 days (p < 0.005) at 15 days, and 21 days (p < 0.0001) with these probiotics and at 7 days after withdrawal. The researchers concluded the following:
“In summary, this study provides evidence that LC are effective for treatment of bacterial overgrowth–related chronic diarrhea, and suggest that probiotics must be used with continuity.”
In another randomized study of 50 patients with chronic abdominal distension and diagnosis of SIBO made by a lactulose hydrogen breath test, the effects of probiotics were compared to metronidazole, a common antimicrobial medication used to treat SIBO. The probiotic administered to the treatment group contained Lactobacillus casei, Lactobacillus plantarum, Streptococcus faecalis, and Bifidobacterium brevis (Bioflora) for 5 days. The population was divided into two treatment groups of 25 patients in each group. Both groups went on the same diet, which consisted in reduced consumption of alcohol, legumes, dairy products and leafy green vegetables. 13 subjects (52%) receiving metronidazol and 20 (82%) receiving the probiotic showed improvement in symptoms after the treatment. The probiotic group showed a statistically significant difference in symptoms (P = 0.036). The researchers concluded:
“Based on this pilot study results, we can suggest that the probiotic herein used has a higher efficacy than metronidazole in the early clinical response of patients with chronic abdominal distension and SIBO.”
Other studies have shown the following:
“In uncomplicated cases, symptom-free condition could be reached with probiotics, whereas in long lasting, chronic small intestinal bacterial overgrowth, antibiotic treatment should be considered”
“Decontamination of the small intestine is more successful when probiotics are prescribed (both after antibiotics and independently), which suppress the opportunistic flora, protect the mucous coat, improve digestion and arrest diarrhea”
Diet is critical in the bacterial overgrowth patient since many of the overgrowth problems result directly from incomplete carbohydrate digestion and absorption. Some types of carbohydrates such as sugars (fructose, lactose, galactose, etc.), grains (including gluten and gluten-free grains, rice and corn products), dairy (lactose and casein), legumes (galactans) and certain fruits (high-fructose) and vegetables (high-fructan, high starch vegetables) induce bacterial overgrowth. Therefore, eliminating these foods from the diet is an important part of recovering from bacterial overgrowth. For a more detailed list of the specific-carbohydrate diet (SCD) we recommend, please read the upcoming article on SIBO in part 8 of the Successful Aging series.
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