Small intestinal bacterial overgrowth, or SIBO as an acronym, is one of many modern ways of handling and, in some cases, explaining irritable bowel syndrome and its symptoms.
A meta-analysis and systematic review (where researchers combine studies for better conclusions) brought together twenty-five separate studies confirming the link between IBS and SIBO.[1]
Some estimates have SIBO positive in up to seventy per cent of IBS cases.[2]
One study diagnosed SIBO in almost eighty per cent of people living with IBS.[3]
So what the hell is SIBO?
Why is it important to investigate if you have irritable bowel symptoms such as bloating, diarrhoea, constipation and abdominal discomfort?
That’s what this article is all about. We’ll be looking at the answers to these questions and some ideas about how people develop SIBO and the process of testing and treating it.
For some people, including my patients, the concept of SIBO is new.
Its development, however, has been almost two decades in the making. Its connection largely came about via an evolution of how imbalances in different types of bacteria in the digestive tract affect health.
If you’ve been reading about your digestion and irritable bowel syndrome for a while, you may already be familiar with the term “intestinal dysbiosis.” It’s just the medical or scientific term for the imbalanced bacteria to which we’re referring.
The intestinal dysbiosis in SIBO is an imbalance between desirable “probiotic” bacteria and less desirable species of bacteria and a broader increased volume of bacteria in the small intestine.
Whilst this imbalance can cause the inflammation associated with many other conditions, let’s focus more on what happens when the volume of bacteria gets too high and how this happens.
Recent studies in 2020 showed people positive for SIBO had four times the usual amount of bacteria in parts of the small intestine compared with healthy subjects. In contrast to the colon, this increase in bacteria in the small intestine is one of the primary features of SIBO.
The same study found higher levels of specific families of bacteria associated with bloating (Enterobacteriaceae) and urgency with bowel movements (Aeromondaceae).[4]
This study begins to explain the underlying features of the bacterial environment that causes bloating and altered bowels in IBS. It also led to the agreed definition of SIBO, the presence of excessive numbers in the small intestine causing gastrointestinal symptoms.[5]
Similarly to IBS, signs and symptoms can present differently in different people.
Evidence points to bloating, gas, fullness (also known as distension), flatulence and diarrhoea as the most common symptoms in up to two-thirds of people experiencing SIBO.[6]
Other symptoms of SIBO can include nausea, abdominal cramping, constipation, and poor energy and concentration.[7]
In more severe cases, some nutritional deficiencies can occur; for example, vitamin B12, iron and vitamin D can be affected. An important note here is that conditions that coexist with SIBO, such as low stomach acid and poor digestion of fats, most likely contribute to these deficiencies.[8]
How does SIBO occur?
Causation is where it seems we still need to know more. SIBO appears to align with the title, “functional digestive disorder.” I say this because most of the credible reasons for the development of SIBO originate from a breakdown in function.
For example, the digestive system relies on the mouth and the gastric juice (think hydrochloric acid) in the stomach to do the mechanical part of the digestive process. An easy way to think about this is stomach is preparing the food to be deconstructed into its components. From here, it can then be distributed into the body when it reaches the small intestine.
The mouth starts the process with chewing, and the stomach finishes the job by churning it all up and beginning the process of digestion.
For most, the problems begin with not chewing our food enough. An immediate consequence is that the digestive enzymes in the saliva responsible for breaking down some vegetable fibres whilst chewing don’t get exposed to the food sufficiently. The food leaves the mouth inadequately digested before it gets to the stomach.
This insufficient exposure to the saliva in the mouth also has immune system consequences—another possible cause of SIBO, which we’ll get to later.
Moving into the stomach, the gastric juice, which houses the acidity and the enzymes to continue the breakdown process of the food from the mouth, can also be less effective.
This dilute acidity can have significant effects on the origin of SIBO.
The first is that the gastric juice in the stomach continues to do a suboptimal job of breaking down your food. A condition called achlorhydria or low stomach acid.[9] The food then leaves the stomach for the small intestine, not ready to leave the digestive tract and enter the body.
Unfortunately, there are only minimal measures to continue the breakdown process of your food in the small intestine.
A consequence of this is the food then sits in the small intestine instead of entering the body. It remains in the small intestine and ferments, helping bacteria to thrive in the process. This flourish in bacteria occurs because the undigested food leaves nutrients for the bacteria to feed on, reflecting a lack of pancreatic enzymes.[10]
We’ll revisit this shortly.
Did someone say all you can eat?
From here, the food can continue to travel in the small intestine until it settles at the junction between the small intestine and the large intestine. This part of the small intestine is situated around the belly button and goes some way to explain why people develop symptoms two to three hours after eating (it takes this long for your food to reach this far in digestion) with the fullness feeling lower in the abdomen.
All this to say that SIBO can often reflect the digestive system’s ability to deconstruct your food.
I’ve written an entire article on why function may be more important than food, which you can read here.
What else can cause SIBO?
Within this suboptimal general function we’ve talked about above, a few focused processes are going on that can be isolated, tested for and treated. Let’s look at these processes through the lens of their role in the immune system.
The first is a component of the immune system called Secretory IgA. This immune cell is abundant in the saliva and the digestive tract. Secretory IgA plays a critical role in maintaining the immune response, especially when screening for bacteria in our food. It’s often considered the first line of defence against bacteria coming into our bodies from the outside world.[11]
This first line of defence can break down in two ways.
The first we touched on above is that if we don’t chew our food enough, the immune cells can’t get the exposure they need to screen the contents, and bacteria then slip through the cracks and enter the stomach.
This job is called “immune exclusion” and is one of the main functions of secretory IgA.
The second way this can break down is via a stress-induced deficiency in secretory IgA. Different forms of stress can play a massive role in the immune system, and this can cause significant drops in this critical immune first responder.[12]
The acidity of the gastric juice in your stomach should handle the bacteria that the secretory IgA missed.
Yep, we don’t often think about the acidity in our stomach and how important it is when it comes to our protection from bacteria and other allergens. It is, however, crucially important.[13] Most of the time, it’s hard to fathom just how much it takes care of.
Bacteria such as Streptococcus and Escherichia coli are the main offenders, and their entry into the small and large intestine can often be a precursor to both SIBO and IBS.
Enzymes secreted from the pancreas into the beginning of the small intestine don’t just break down your food.
Sometimes these enzymes don’t get secreted as well as they can be, giving bacteria another opportunity to dodge the immune system’s response.[14]
Aside from the function of digestion and the breakdown of the immune response, a process called motility is also a critical factor in SIBO forming.[15]
In terms of the digestive system, motility is peristalsis.
To best visualise this, I ask patients to think of motility as a conveyor belt. Sometimes at different points on the conveyor belt, things can slow down. Now it just so happens that if some of the processes discussed above aren’t as effective as they could be, this slows down the motility process.
How does the slowing of the conveyor belt cause SIBO?
Well, the slower the transit of food on the conveyor belt, the easier it is for the food to ferment, feed bacteria and cause gas and bloating.
In contrast to diarrhoea, we often see slower motility in people with SIBO who have constipation.
Interestingly, the brain, specifically serotonin, plays a significant role in motility.[16] This connection between the brain and digestion has been well-researched. Evidence confirms that people living with constipation and the IBS symptoms that come with it have lower levels of serotonin when compared to healthy people.[17]
If this is the case for you, then you’ll often find that a big part of your treatment, if confirmed with SIBO, is the modulation of serotonin and motility via herbal and nutritional formulas that play a role in stabilising your serotonin levels.
What’s the process of determining if your digestive symptoms are down to SIBO?
You may remember earlier in the article that we can test and treat everything. Let’s explore this now!
Two main tests can help you to gain some clarity.
The first test is the most important, a lactulose breath test. This test helps to diagnose the overgrowth in the first place and is critical mainly because, even after reading all of this and being convinced you have SIBO, you may not.
The lactulose breath test for SIBO involves a three-hour process of tracking gas formation as it occurs in the small intestine and down towards and into the large intestine.
This gas formation is where the lactulose comes in. Drinking the lactulose syrup sends a figurative buffet into the small intestine for the bacteria to feast. This process makes gases, hydrogen, and methane appear as a by-product. At different points during the three-hour process, you breathe into a sample collection tube so that we can measure the amount of hydrogen and methane present as the buffet transits towards the large intestine.
Once we get these samples collected, a lab then plots the amount of hydrogen and methane on the graph together with the timing and position of the measurements as it relates to the small and large intestine.
SIBO is present if the levels of hydrogen increase by 20 and methane levels (classically lower in volume) grow comparatively to that.
A comprehensive stool exam can help to explain how the SIBO might have formed in the first place.
Ok, so it can be challenging to glamourise pooing in a box, but is it ok if it helps to explain how the SIBO formed?
It’s within the stool that we can check your secretory IgA levels, check on your stomach acidity, and look at how you’re absorbing your fat and carbohydrates.
The stool exam can also give clues as to which bacteria are causing the problems and the current situation regarding your fibre intake and probiotic and prebiotic levels.
These markers combine to create a more personalised treatment plan that considers the nuanced origins of SIBO and how they cause your IBS symptoms.
What happens if the lactulose breath test shows I’m positive for SIBO?
Start treatment straight away!
One of the ways SIBO was initially confirmed was through antibiotic treatment reducing the presence of the overgrowth on retesting and IBS symptoms resolving.[18] Whilst this was predominantly for people with SIBO and diarrhoea, evidence shows that a natural approach combining different herbal formulas along with dietary intervention can be just as effective as antibiotic treatment.[19]
Unbeknownst to many, there is a specific SIBO-oriented prescriptive diet named the Bi-phasic diet created by Dr Nirala Jacobi. This diet is ten to twelve weeks long as a prescription and has helped many people clear their symptoms and their SIBO (confirmed on retest) in perpetuity.
The most important part of this guide is the following.
We’ve covered a lot of ground here. From the origins of SIBO to its causes, how to determine if you have it and what treatment looks like, I’ve tried to give you a full review of how to begin exploring things yourself.
But I don’t think any of this is the essential part.
From me to you, the most important part of this guide is that there are answers and explanations. Especially for those struggling with gut issues for as long as they can remember and feel the chance of solving things is lost.
Hope this helps x
References
[1] Shah A, Talley NJ, Jones M, et al. Small Intestinal Bacterial Overgrowth in Irritable Bowel Syndrome: A Systematic Review and Meta-Analysis of Case-Control Studies. Am J Gastroenterol. 2020;115(2):190-201. doi:10.14309/ajg.0000000000000504
[2] Bures J, Cyrany J, Kohoutova D, et al. Small intestinal bacterial overgrowth syndrome. World J Gastroenterol. 2010;16(24):2978-2990. doi:10.3748/wjg.v16.i24.2978
[3] Pimentel M, Chow EJ, Lin HC. Eradication of small intestinal bacterial overgrowth reduces symptoms of irritable bowel syndrome. Am J Gastroenterol. 2000;95(12):3503-3506. doi:10.1111/j.1572-0241.2000.03368.x
[4] Leite G, Morales W, Weitsman S, et al. The duodenal microbiome is altered in small intestinal bacterial overgrowth. PLoS One. 2020;15(7):e0234906. Published 2020 Jul 9. doi:10.1371/journal.pone.0234906
[5] Pimentel M, Saad RJ, Long MD, Rao SSC. ACG Clinical Guideline: Small Intestinal Bacterial Overgrowth. Am J Gastroenterol. 2020;115(2):165-178. doi:10.14309/ajg.0000000000000501
[6] Pimentel M, Saad RJ, Long MD, Rao SSC. ACG Clinical Guideline: Small Intestinal Bacterial Overgrowth. Am J Gastroenterol. 2020;115(2):165-178. doi:10.14309/ajg.0000000000000501
[7] Rao SSC, Rehman A, Yu S, Andino NM. Brain fogginess, gas and bloating: a link between SIBO, probiotics and metabolic acidosis. Clin Transl Gastroenterol. 2018;9(6):162. Published 2018 Jun 19. doi:10.1038/s41424-018-0030-7
[8] Zaidel O, Lin HC. Uninvited guests: The impact of small intestinal bacterial overgrowth on nutritional status. Pract Gastroenterol 2003;7:27–34.
[9] Bures J, Cyrany J, Kohoutova D, et al. Small intestinal bacterial overgrowth syndrome. World J Gastroenterol. 2010;16(24):2978-2990. doi:10.3748/wjg.v16.i24.2978
[10] Pimentel M, Saad RJ, Long MD, Rao SSC. ACG Clinical Guideline: Small Intestinal Bacterial Overgrowth. Am J Gastroenterol. 2020;115(2):165-178. doi:10.14309/ajg.0000000000000501
More references!
[11] Mantis, N., Rol, N. & Corthésy, B. Secretory IgA’s complex roles in immunity and mucosal homeostasis in the gut.Mucosal Immunol 4, 603–611 (2011). https://doi.org/10.1038/mi.2011.41
[12] AFRISHAM, Reza et al.Levels of salivary immunoglobulin A under psychological stress and its relationship with rumination and five personality traits in medical students. Eur. J. Psychiat. [online]. 2016, vol.30, n.1, pp.41-53. ISSN 0213-6163.
[13] Martinsen TC, Fossmark R, Waldum HL. The Phylogeny and Biological Function of Gastric Juice-Microbiological Consequences of Removing Gastric Acid. Int J Mol Sci. 2019;20(23):6031. Published 2019 Nov 29. doi:10.3390/ijms20236031
[14] Gubergrits NB, Linevskiy YV, Lukashevich GM, Fomenko PG, Moroz TV, Mishra T. Morphological and functional alterations of small intestine in chronic pancreatitis. JOP. 2012;13(5):519-528. Published 2012 Sep 10. doi:10.6092/1590-8577/656
[15] Gunnarsdottir SA, Sadik R, Shev S, et al. Small intestinal motility disturbances and bacterial overgrowth in patients with liver cirrhosis and portal hypertension. Am J Gastroenterol. 2003;98(6):1362-1370. doi:10.1111/j.1572-0241.2003.07475.x
[16] Sikander A, Rana SV, Prasad KK. Role of serotonin in gastrointestinal motility and irritable bowel syndrome. Clin Chim Acta. 2009;403(1-2):47-55. doi:10.1016/j.cca.2009.01.028
[17] Vahora IS, Tsouklidis N, Kumar R, Soni R, Khan S. How Serotonin Level Fluctuation Affects the Effectiveness of Treatment in Irritable Bowel Syndrome [published correction appears in Cureus. 2020 Sep 1;12(9):c36]. Cureus. 2020;12(8):e9871. Published 2020 Aug 19. doi:10.7759/cureus.9871
[18] Pimentel M, Saad RJ, Long MD, Rao SSC. ACG Clinical Guideline: Small Intestinal Bacterial Overgrowth. Am J Gastroenterol. 2020;115(2):165-178. doi:10.14309/ajg.0000000000000501
[19] Chedid V, Dhalla S, Clarke JO, et al. Herbal therapy is equivalent to rifaximin for the treatment of small intestinal bacterial overgrowth. Glob Adv Health Med. 2014;3(3):16-24. doi:10.7453/gahmj.2014.019
