Today we have another educational installment from Karl Seddon, founder of the British biotech manufacturing firm that produces Elixa Probiotic.
Years back, I recall hearing almost daily about Adrenal Fatigue and it struck me as one of those things with a list of symptoms so numerous, vague, and broadly defined that it was as though it could be argued that both every condition is Adrenal Fatigue and no condition is Adrenal Fatigue, all at the same time.
Does SIBO constitute a similar vein of catch-all-and-none? Well, let’s see.
The road to self-diagnosis is paved with wishful thinking
If you’re currently on a quest to correct some aspect of your health, then likely you’ll be able to associate with that feeling of excitement when you come across a theory that you’d not heard of before and everything… suddenly… just…. clicks!
‘Yes, this makes perfect sense! All my symptoms fit, and the logic on paper is infallible!’
A part of this euphoria and ones willingness to progress to a state of excitation comes from desperation. Nothing wrong, or surprising, about that. I’ve felt this same thing many times. Just like the inventor who has been mulling over a sticking point in her design and has a spark of what the solution may be…or a physicist who suddenly has some potential breakthrough in his theory while laying in bed, staring at the ceiling.
Unfortunately, quite often what follows is the actual test of the theory as per the guidelines of whichever resource you are reading. This is where people get sorely let down and waste a lot of time and money. Different people have different thresholds of when and under what circumstances they can look at the matter objectively and realise it just ain’t working.
By all means, test everything that has logic to it. Just don’t waste time by not being objective with your analysis of the results or baselessly believing that weeks or months must pass before progress is visible. There may be some reason why results can be delayed by weeks and then suddenly arise. But at least have some mechanism explaining that delay.
Playing devil’s advocate against yourself is an invaluable trait.
In this article, I shall share my thoughts on one of the most commonly self-diagnosed conditions: SIBO. I shall list the two most common observations that people make to arrive at their self-diagnosis. We’ll have a look at the typical conclusion that most people make.
Then I’ll present an alternative conclusion for both observations; changing the implications entirely.
SIBO – Small Intestinal Bacterial Overgrowth
My product, Elixa, is an ultra high strength probiotic, and so I mainly get questions related to gut health. And one of the most common conditions that people ask me about is SIBO. This stands for Small Intestinal Bacterial Overgrowth. In essence, it’s an excess of bacteria throughout all or part of the duodenum, jejunum, and ileum, the three sections comprising the small intestine.
SIBO is not the mere presence of bacteria in the small intestine because the small intestine in a healthy state is far from sterile. In fact, it’s only relatively sterile when compared with the large intestine—its downstream neighbour.
Bacterial excess in the small intestine can be defined directly—by a certain number of bacterial cells per millilitre of intestinal fluid—or indirectly—as some empirically arrived-at score on a diagnostic test, such as a hydrogen or methane breath test.
Let’s briefly recap the layout of the digestive tract between the stomach and the large intestine.
Imagine you take an uninflated balloon and insert a funnel into its opening. You pour a cup of water into the balloon and add some chewed up food. Then, put a little air into it and tie up the end. Imagine using both hands to slowly massage the food and fluid back and forth. This is essentially what the stomach does when you eat food. The food plops down into the hydrochloric acid and digestive enzymes. The stomach massages it back and forth, occasionally opening the pyloric sphincter—leading into the small intestine—to squirt a bit of this mush onwards when it’s deemed ready.
The main difference between how this works and how some may imagine it to work is (1) the massaging action, and (2) the extremely developed control of different food substances being retained or being moved on by the stomach via the pyloric sphincter. Rather than the fixed, bucket-like stomach seen in diagrams—with its always-open entrance and an always-open exit—the stomach is more like an accordion being extended and contracted slowly and with an exit valve that can release partially-digested food matter based on chemical and physical signals.
The Small Intestine
The small intestine begins directly after the stomach. It’s divided into three sections along its 23-ft length (the length of 4 average height men). The first section is the duodenum, then the jejunum and last is the ileum.
The last two sections—jejunum and ileum—comprise the majority of the length of the small intestine, because their main function is the absorption of nutrients. Absorption requires a large surface area, which is in part facilitated by its length and principally by the whole villi and microvilli array. In fact, the first section—the duodenum—is less than one ft long. However, a lot happens there.
Several unique actions occur in the duodenum, but if you want to remember just one, then view it as a buffer zone between the pH of the stomach and that of the small intestine. The gastrointestinal tract flows from stomach to small intestine continuously, so there must be a mechanism by which to convert the acidic contents of the stomach into an alkaline slurry downstream because the small intestine is the primary site of carbohydrate enzyme activity, which requires an alkaline pH.
This is done in the duodenum by the release of bicarbonate from the pancreas into the duodenum and from the lining of the duodenum itself.
If you’re struggling to envisage this, then imagine having an acidic river, where at some position you constantly unload dumper trucks of baking soda (sodium bicarbonate—an alkali) into it: mixing and churning together, such that the flow downstream of this dumping point is now alkaline.
After the partially broken-down, fully broken-down, and enzyme-resistant food passes through the duodenum, it enters the jejunum and ileum. This is where nutrient absorption occurs. Both micronutrients (vitamins & minerals) and the enzymatically fragmented sub-units of macronutrients (carbs/fats/proteins) are absorbed along this section.
Directly after the Ileum is the Cecum, which is the beginning of the large intestine. So, we’ll stop at this point along the gastrointestinal tract and re-focus on the small intestine.
As could be expected, the bacterial concentrations slowly increase as we move from the duodenum (neighbouring the harsh, acidic environment of the stomach) along to the Ileum (which harbors the bacterial fleet—the large intestine).
SIBO (Small Intestinal Bacterial Overgrowth) is the condition of overgrowth somewhere in the region between the exit of the stomach and the entrance to the large intestine.
People contact me asking whether Elixa can resolve their SIBO. Very few stop to ask whether I think they have the condition in the first place. Some even get back to me a few weeks later saying that Elixa did dramatically reduce their bloating, pain, etc., and conclude that their SIBO hunch must have been correct after all—ignoring the fact that bloat does not automatically equal SIBO and that a probiotic is far more likely to have eradicated bloating via its action in the large intestine than in the small intestine.
Why you think you have SIBO
Here are the two most common reasons many people believe they have an overgrowth of bacteria in their small intestine, as opposed to a dysbiosis of their large intestine. The conclusion to the first observation, in particular, appears to be logical. Nevertheless, I have provided alternative conclusions for both points.
1. Time until bloat
- You eat a meal and within about 1 hour your belly is distended, and you feel uncomfortably tight and bloated.
- This may even occur immediately after consuming the meal.
- Bloating is not the only effect that may occur. There may also be pain, diarrhoea, and a feeling of mental fog.
Conclusion: The food can’t possibly have reached the large intestine in that time, and so it must be related to the small intestine.
2. Symptoms’ lists
- abdominal pain
Conclusion: You suffer from many of these symptoms, so it seems like a perfect fit.
Alternative conclusion to Observation #1
Rapid onset of bloating and other symptoms after eating is a compelling reason to believe it is SIBO, but there is an alternative explanation. When we consume food, it triggers a domino effect along the gastrointestinal tract.
This Mexican wave effect begins when food enters the stomach and can reach measurable (myoelectrical) levels within just 15 minutes and possibly earlier, depending on your gastroenterological state, including your visceral sensitivity and neurotransmitter levels related to gastric motility. The gastrocolic reflex is the upregulation in peristaltic action, thus shifting all the matter in your intestinal tract further along. Its magnitude varies along the tract but, generally speaking, all the food is pushed forward along the entire GI tract.
It ought to be apparent from everyday observation: the urge to take a bathroom break after eating a large meal. It’s obviously not the food you’ve just eaten that needs to be evacuated, but the meal was certainly the trigger. ‘Making room’ for the incoming food is the common-sense explanation for why we have evolved this response.
…As an aside, let’s play around with the implications of this for a minute. If we eat less frequently, we could assume that food is moved through our digestive tracts more slowly (or at least more slowly through certain sections). That may at first seem odd because surely there is some required amount of time that food must be in contact with the small intestinal wall to allow complete absorption of nutrients. And, this would imply that eating more frequently would ‘cut short’ the time that the previous meal[s] get to spend in the caress of the small intestinal microvilli.
Well, this ‘cutting short’ might be completely sensical. Because, when the body has the option of making room for a fresh, undigested bolus of food versus continuing to dredge out the last morsels from the previous meal, it would obviously opt for the incoming meal. When a hunter-gatherer had food in abundance and was eating and not storing it, why would the body put up resistance to taking in that next meal only so as to not ‘waste’ some of what was previously ate?
The longer the food remains in the small intestine, the less time-efficient the nutrient extraction would be. Better to keep the energy-packed food coming while the coming is good. The alternative would be that the hunter-gatherer is repelled by further intake of food or vomits the meal back up until complete small intestinal digestion of the previous meal is complete. There’s no other option: either make room for it or don’t consume it. Clearly, making room is the best way to take advantage of what’s on offer.
Back on point
So, if the consumption of a meal can trigger a gastrocolic reflex, it means that it can (a) cause fermentable components of the diet (FODMAPs et al.) to move along the GI tract. It can also (b) shift lumenal fermentation byproducts (SCFAs, ethanol, acetaldehyde, unconjugated compounds, pockets of gas, etc.) from one place in the large intestine along to another place in the large intestine. To put simply: It can (a) move bacterial food along, and (b) move the byproducts of bacterial feeding along.
Looking at (a), moving bacterial food along, we zoom in on the Ileum. The Ileum is the final part of the small intestine, directly before the Cecum.
I view the Cecum as a bacterial fermentation melting pot. I believe this area is the most critical portion of the large intestinal microbiota if you had to pick an area.
- It’s where the fermentable components first arrive.
- It’s shaped in a pouch-like manner, which implies to me that this is an intended point of temporary accumulation and mixing of substrates and bacteria. If you watch a colonoscope filming food passing from the ileum into the cecum, then you’ll get my point.
- It is upstream of the remainder of the large intestine—thus being a huge determinant of what byproducts, substrates, and microorganisms are carried downstream to the later sections: the ascending, transverse, descending, and sigmoid portions of the large intestine.
- The appendix connects directly to the cecum. The appendix is designed to restore a gut microbiota that has been dramatically ravaged by an acute gastrointestinal infection. Think: Hunter-gatherer ate a chunk of diseased meat and had explosive diarrhoea for three days straight. So it would make evolutionary sense that the appendix would be positioned at the most critical point required for reinoculation of the large intestine.
The (a) point is the movement of the fermentable substrate, the residue of your meal which has not been absorbed in the small intestine and that can be broken down by microbes.
If there was some fermentable substrate hanging around the Ileum and then the gastrocolic reflex kicks in and shunts it through the ileocecal valve into the bacterial cauldron aka cecum, then this would cause it to begin immediately breaking down into the various byproducts. If these byproducts were gaseous, they would lead to bloating. If they were something like ethanol or acetaldehyde, then they could result in mental effects. If they were some pain-inducing metabolite, then they may lead to that sharp stabbing pain, right there in the bottom right of your abdomen—that dreaded IBS pain.
Nota bene: do not assume that gas produced in the large intestine only leads to flatulence and that gas in the small intestine is what leads to bloating. Gas can be trapped in the large intestine for a long period before making its way over to the exit 1.5 slow-moving metres away. And until it exits, is absorbed, or degraded, it will be experienced in the form of abdominal bloat.
Pause for a moment to recall the overarching point we’re making: the alternative conclusion to Observation # 1, above, ‘Time until bloat,’ so we don’t lose the thread of what we are exploring here.
The (b) point is the movement of the gas and other metabolites. If the gastrocolic reflex shunts them along from one point to another in the large intestine, there’s an opportunity for different concentrations of these metabolites to be exposed to different portions of the large intestinal wall, thus making their effects more or less pronounced based on the visceral sensitivity of that area of the GI tract.
Let’s make it clearer by considering an example: If you had a pocket of gas that was building up along the transverse section of the large intestine, the gastrocolic effect might kick it along to the flexure between the transverse portion and the descending portion. Maybe there’s already a pocket of gas accumulated there (these are common areas of accumulation), and so now, this flexure is feeling increased stretch from the gas pressure and a more pronounced bloating sensation.
Considering other metabolites, we can hypothesise that some of them building within a bolus of matter in the lumen of the intestine may now be rearranged by the peristaltic Mexican wave and release volumes of the metabolite closer to the intestinal wall, thus allowing them to have their effect via diffusion into the bloodstream or otherwise (e.g. localised pain).
Both these mechanisms can explain why your symptoms follow rapidly after consuming a meal, yet neither are related to fermentation in the small intestine.
The alternative conclusion to Observation #2 is far briefer: There are almost NO symptoms on the SIBO symptoms’ lists (at least the ones I have seen circulated online) which are not identical to that of a large intestinal dysbiosis. The few symptoms that would be exclusively indicative of an issue within the small intestine would be those stemming from malnutrition or small intestinal hyperpermeability because these conditions can relate to abnormalities of the brush border of the small intestine.
So if you’re basing your SIBO self-diagnosis on bloating, flatulence, brain fog, diarrhoea, abdominal distension, and abdominal pain, then consider that none of these exclusively indicate the site of action within the small intestine.
Unless there was a confirmed motor problem or anatomical defect in the small intestine, I believe it is far more likely for problems to stem from the large intestine. And there is also potential for problems localised in the small intestine to be instigated by large intestinal problems anyway. Just in the same way that another membrane (the skin) is hugely affected by the flora of our large intestine.
Two questions remain:
- What if I really do have SIBO – What caused it and how can I resolve it?
- What are these malnutrition and intestinal hyper-permeability consequences of genuine SIBO?
I’ll share my thoughts on those in Part 2.
No matter how you slice it, in my experience of a long time now with Elixa, with so many readers trying it, sending Karl and I hundreds of testimonials, repeat product orders, and lots of comments on the blog, it seems to improve the lives of most that have frequent or chronic digestive problems—whether they believe it’s SIBO or not.
I must say I find that most ‘hypesters’ of SIBO tend to be generally or fervently promoters of various forms of low-carbohydrate, anti-carbohydrate, anti-fiber-carbohydrate, nothing-but-big-meat-and-big-fat kinda folk. And FODMAP is a pejorative term.
To put it plainly: one must seriously consider that their proposed “cure” for all of these self-diagnosed and assumed “SIBO problems” is in fact—Occam’s Razor syle—the very cause of their problems by means of a starving large intestine.