SIBO SERIES PART 1: Is SIBO The Hidden Cause of Your IBS?

This post is personal. As a SIBO sufferer I am pretty passionate about getting the word out about this under-diagnosed IBS condition. It wrecked my life for 2 years, so I’m dedicating a three-part series to it, to give you the most up-to-date science and everything you need to know about what it is, and how to get started with testing and treatment so it doesn’t wreck yours.

Here is a summary of what we are going to cover:
Part 1:
>  What is SIBO and how it can ruin your health
>  Why it’s important to know which ‘type’ of SIBO you have
>  Symptoms to look out for and why SIBO is often the cause of IBS
>  The most common underlying root causes of SIBO?

Part 2:
>  The science (and art) of testing for SIBO

Part 3:
>  Latest SIBO treatment protocols that actually work


Small Intestinal Bacterial Overgrowth (SIBO) is defined as an increased number and/or abnormal type of bacteria in the small intestine (1). While bacteria are normally found in huge numbers in the large intestine, what is unique about SIBO is that these bacteria move to where they don’t belong and colonise the small intestine, a region that should contain very limited numbers of bacteria (2).

Because these bacteria are supposed to be in the large intestine, they are mostly species that ferment carbohydrates into hydrogen gas (H2) or archaea (not technically bacteria) that produce methane gas (CH4). While both types will usually result in abdominal bloating and distention, SIBO sufferers are usually divided into one of three different categories;  diarrhoea-dominant (D), constipation-dominant (C) or alternating variations of both.

bacteria numbers intestine stomach bowel

bacteria numbers intestine stomach bowel

SIBO-D: Diarrhoea and Hydrogen-Producing Bacteria

Diarrhoea-dominant SIBO is the more common form of diagnosed SIBO and is the result of carbohydrate-fermenting bacteria that produce hydrogen gas in the small intestine. And unlike the large intestine, the small intestine is super sensitive to the production of hydrogen. This excessive production of hydrogen in the small intestine is what causes the abdominal bloating and the diarrhoea (1).

SIBO-C: Constipation and Methane-Producing Archaea

It’s not technically bacteria, but single-celled organisms called archaea, that are mostly responsible for the constipation-dominant form of SIBO. Interestingly, only half of the world’s population are thought to have detectable levels of archaea in their gastrointestinal tract, and only from about three years of age (3). Archaea, such as Methanobrevibacter smithii, feed off the hydrogen produced by bacteria during the fermentation of carbohydrates and produce a by-product of their own; methane (4). As with hydrogen in the small intestine, methane gas will also cause abdominal bloating, plus a much bigger problem; it slows down transit time which leads to constipation (3). While you might think constipation is preferable to diarrhoea, and symptomatically in the short-term you might be right, constipation caused by these methanogens can create a vicious cycle of SIBO that is harder to break than the traditional SIBO-D type. This was my issue so let me explain some more.

You see, methane slows transit time and causes constipation, and constipation allows more bacteria to grow, which causes more methane and more constipation… and so on, and so forth. And to make matters worse, archaea are more stubborn and difficult to treat with antibiotics and antimicrobials (5). They can also survive for a while without hydrogen, so killing their food source can also have minimal short-term benefits. Basically, methanogens are tough critters to kill… But more on that in Part 3 of this series.

A third type of SIBO? Hydrogen Sulphide-Producing Bacteria and ‘Rotten Egg’ Gas

While less common, a third type of SIBO is gaining attention because of its prevalence amongst those with SIBO symptoms, who test negative on traditional breath testing (6). Sulphate-reducing bacteria (SRB) in the small intestine produce hydrogen sulphide, a highly toxic gas to the cells of the intestinal wall, best known for its distinctively foul odour of rotten eggs (7, 8). Because they also consume hydrogen, these bacteria compete with methanogenic archaea (SIBO-C type) and may keep levels of each other in-check (8). But for those with both types, this means that killing only one species may allow the other to overgrow further.


Symptoms of SIBO closely mirror those of IBS and for good reason. It is estimated that up to 85% of IBS cases are actually caused by SIBO (9) . As discussed above, most SIBO sufferers are categorised as constipation or diarrhoea-dominant. But of all the symptoms, the most frequent and distinguishable in clinical practice seems to be that of excessive bloating within 5-60 minutes after eating.

The most common symptoms of SIBO are:

  • Bloating within 1 hour after meals

  • Chronic diarrhoea or chronic constipation or alternating constipation and diarrhoea

  • Burping or reflux after meals

  • Foul smelling gas

  • Stomach gurgling and discomfort or cramping

Secondary symptoms that often accompany the most common symptoms of SIBO are:

  • Restless legs at night

  • Joint pain

  • Mood changes

  • Multiple food sensitivities

  • Respiratory symptoms such as asthma

  • Acne or skin rashes

  • Memory issues and foggy thinking

  • Chronic iron and/or B12 deficiency

  • Weight gain or loss

  • Difficulty sleeping

Another symptomatic clue might be that digestive symptoms improve while using antibiotics, even for unrelated issues. Or, using fibre products such as Metamucil, or taking pre- and probiotics makes you feel worse, not better. 


Beyond the frustrating and often embarrassing symptoms, the biggest health issues you are likely to face if you suffer from SIBO are as a result of improper digestion and absorption of vitamins and nutrients (10). This can happen in one of two ways:

> Damage to the intestinal wall (the intestinal mucosa) - the bacteria, their biofilms and toxic by-products can all damage the lining of the small intestine, blocking the absorption of nutrients and causing a leaky gut.

> Bacteria absorb the nutrients before your own cells - most digestive processes happen in the small intestine, while most bacteria live in the large intestine (11). But, if you have an overgrowth of bacteria into the small intestine, now there is competition between your own cells, and the bacteria. In particular, bacteria may take up certain vitamins such as B12 and minerals such as magnesium, iron and calcium before your own cells have the chance. The bacteria may also consume amino acids from protein, the building blocks for growth and repair.

For SIBO-D sufferers in particular, malnutrition is also a common side-effect from gut irritation, with many being diagnosed with iron and B12 deficiencies. While for SIBO-C sufferers, the opposite is often true. Methanogens that cause constipation are also associated with obesity and weight gain, thought to be a result of slow transit time and overly-efficient digestion of short-chain fatty acids (12).


As mentioned, SIBO is the result of certain bacteria and archaea moving from the large intestine, and setting up shop in the small intestine. But how do they make the move - especially since the body has a number of different protective mechanisms to prevent this happening, including;

> Stomach acid secretion - maintains an acidic environment for killing off bad bacteria before they enter the small intestine.

> Bile secretion - produced in the liver, stored in the gallbladder and released into the small intestine, bile protects against bad bugs within the small intestine.

> Migrating motor complex (MMC) - waves of small intestinal wall muscular activity, that happens about every 90-120 minutes and typically between meals, moves waste and unwanted bacteria through the digestive tract and to the colon. The MMC is not the same as peristalsis that happens in the large intestines.

> Immune system - the fluid in the small intestine contains immunoglobulins that act as antibodies to fight bacteria and other pathogens.

> Ileocecal valve -  a one-way valve that allows the flow of contents into the large intestine but prevents them from refluxing back into the small intestine.

sibo prevention mechanisms

sibo prevention mechanisms

Basically, to get SIBO, one or more of these protective mechanisms needs to fail. There are many causes of SIBO, most of which are complex and affect more than one of the protective mechanisms discussed above. However, they can be grouped into three main categories; MMC damage, Structural and Functional.

1. Damage to the migrating motor complex (MMC). This is where bacteria are not cleared or swept away from the small intestine correctly. Conditions that increase the risk of impaired MMC function include:
> Gastroenteritis, caused by a parasite, bacteria, yeast, etc.
> Lyme disease
> Clostridium difficile
> Inflammatory bowel disease
> Scleroderma
> Diabetes
> Ehlers-Danlos syndrome
> Hypothyroidism
> Medications such as opiates or the recurrent use of antibiotics
> Surgery or injury resulting in muscle or nerve damage
> Autonomic nervous system dysfunction resulting in sympathetic dominance

2. Altered anatomy (Structural). Anatomical changes can result in bacterial clearance being blocked within the small intestine or allow migration of bacteria from the large intestine back up into the small intestine. These include conditions such as:
> Adhesions or obstructions from abdominal surgery or nonsurgical causes such as trauma
> Inflammatory bowel disease stricture
> Ileocecal valve removal or impairment
> Volvulus
> Cancer
> Superior mesenteric artery syndrome
> Non-draining pockets

3. Altered physiology (Functional). In this situation, the function of the body has been altered, and bacteria are not killed off in the stomach or small intestine as they should be, often as a result of:
> Hypochlorhydria
> Altered bile flow and enzyme production
> Medications such as proton pump inhibitors
> Immunodeficiency
> Leaky gut (damage to the small intestinal walls)

And the winner for the most common cause of SIBO goes to…

Post-infectious SIBO: the result of an impaired migrating motor complex caused by an episode of acute gastroenteritis. I’m looking at you my travel-loving friends, because this was most likely from a very memorable bout of food poisoning. I remember mine clearly - five star seafood buffet in Africa, an extra-dodgy prawn, followed by 4 days of being chained to the loo. The bout of gastro was likely caused by one or more of the four common infectious organisms responsible for food poisoning: Campylobacter jejuni, Salmonella, Escherichia coli or Shigella (13). Basically, once you have had a bout of infectious gastroenteritis, your risk of getting IBS/SIBO increases by as much as six fold (14).

For those of you who love the science as much as I do, I’m going to summarise what happens within the body and why post-infectious SIBO is a special kind of nasty. The four organisms I mentioned above secrete a substance called cytolethal distending toxin B (CdtB), which is very toxic to the human body. This means the body wants to protect itself and produces an antibody called anti-CdtB in response to the infection.

Unfortunately, CdtB is very similar in structure to vinculin, an important component of the nerve cells of the migrating motor complex. The problem with this situation is that the body misinterprets what is happening and also produces anti-vinculin antibodies that damage the migrating motor complex (15, 16). Without this cleansing wave to move the bad bacteria through, an overgrowth can occur. This also presents an ongoing problem with autoimmunity, where the immune system is constantly attacking the migrating motor complex - an issue that I am sure will be studied further.

sibo postinfectious pathophysiology

sibo postinfectious pathophysiology


SIBO is strongly associated with chronic relapse (9), largely because
1) killing off the overgrown bacteria (or archaea) can be difficult, even with a comprehensive protocol that covers antimicrobials/antibiotics, diet and lifestyle factors; and
2) killing the bacteria itself doesn’t necessarily fix the root cause of why you have the SIBO to begin with.

This is particularly important when it comes to the migrating motor complex. If you have managed to kill off almost all the bacteria but still have slow motility or constipation, there is a risk that the bacteria will overgrow, again. We will talk more about the importance of targeted and tailored treatment protocols in Part 3.


SIBO is certainly an under-diagnosed and poorly understood condition for most health professionals. The best way to know if you have SIBO, is to test for it. And we are going to discuss assessment and testing in great detail in Part 2. For all my IBS sufferers, I hope you have found this post informative. I also hope it inspires you to consider the root cause of your IBS because we know that up to 85% of IBS is SIBO - maybe that is you.

As always, I am here for you and if you are ready to find out about testing, please get in touch. Healing SIBO is a journey. If you are ready to begin yours, please head to the Work With Us page to learn more about how we work online with clients in many countries to test for and treat the many root causes of IBS symptoms and other GI conditions.

Jump to:
>  SIBO SERIES PART 2: The Science (and Art) of SIBO Testing
>  SIBO SERIES PART 3: Latest SIBO Treatment Protocols That Actually Work


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  2. Gorbach SL. Microbiology of the Gastrointestinal Tract. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Chapter 95.

  3. Triantafyllou, K., Chang, C., Pimentel, M. (2013). Methanogens, methane and gastrointestinal motility. J Neurogastroenterol Motil, 20(1), 31-40

  4. Gaci, N., et al. (2014). Archaea and the human gut: New beginning of an old story. World Journal of Gastroenterology : WJG, 20(43), 16062–16078

  5. Dridi, B., et al. (2011). The antimicrobial resistance pattern of cultured human methanogens reflects the unique phylogenetic position of archaea. J Antimicrob Chemother, 66(9), 2038-44

  6. Banik, G., et al. (2016). Hydrogen sulphide in exhaled breath: a potential biomarker for small intestinal bacterial overgrowth in IBS. J Breath Res, 10(2), 026010

  7. Lewis. S., et al. (2005). Effects of metronidazole and oligofructose on faecal concentrations of sulphate-reducing bacteria and their activity in human volunteers. Scand J Gastroenterol, 40(11), 1296-303

  8. Gottlieb, K., Wacher, V., Sliman, J., & Pimentel, M. (2016). Review article: inhibition of methanogenic archaea by statins as a targeted management strategy for constipation and related disorders. Alimentary Pharmacology & Therapeutics, 43(2), 197–212

  9. Bures, J., et al. (2010). Small intestinal bacterial overgrowth syndrome. World Journal of Gastroenterology : WJG, 16(24), 2978–2990

  10. Dukowicz, A. C., Lacy, B. E., & Levine, G. M. (2007). Small Intestinal Bacterial Overgrowth: A Comprehensive Review. Gastroenterology & Hepatology, 3(2), 112–122

  11. Krajmalnik-Brown, R., Ilhan, Z.-E., Kang, D.-W., & DiBaise, J. K. (2012). Effects of Gut Microbes on Nutrient Absorption and Energy Regulation. Nutrition in Clinical Practice, 27(2), 201–214

  12. Basseri, R., et al. (2012). Intestinal Methane Production in Obese Individuals Is Associated with a Higher Body Mass Index. Gastroenterology & Hepatology, 8(1), 22–28

  13. Buchan, B., et al. (2013). Clinical Evaluation of a Real-Time PCR Assay for Identification of Salmonella, Shigella, Campylobacter (Campylobacter jejuni and C. coli), and Shiga Toxin-Producing Escherichia coli Isolates in Stool Specimens. Journal of Clinical Microbiology, 51(12), 4001–4007

  14. Thabane, M., & Marshall, J. K. (2009). Post-infectious irritable bowel syndrome. World Journal of Gastroenterology : WJG, 15(29), 3591–3596

  15. Pimentel M., et al. (2015). Autoimmunity Links Vinculin to the Pathophysiology of Chronic Functional Bowel Changes Following Campylobacter jejuni Infection in a Rat Model. Dig Dis Sci, 60(5), 1195-205

  16. Pimentel, M., et al. (2015). Development and Validation of a Biomarker for Diarrhea-Predominant Irritable Bowel Syndrome in Human Subjects. PLoS ONE, 10(5), e0126438