During the lightning round in the recent interview I did with Graeme Jones, CEO and clinical physiologist from Nordic Clinics in Stockholm, his response when I said, “SIBO” was, “Migrating motor complex”. That people with small intestinal bacterial overgrowth, or SIBO, have an impaired migrating motor complex(MMC) isn’t exactly revolutionary thinking, we’ve known this for several years. However, many people may not realize the genius behind this comment. It clearly illustrates that the way most people think about and treat SIBO is wrong. (To check out that interview, click here)
What I mean by this is that if we look at an impaired migrating motor complex as a cause of SIBO, then we can’t really address SIBO as an infection, we need to address it as an injury. Why address it this way? There’s ample evidence as to many of the causes of impaired motility, and they are behavioral, not infectious.
Think about it…SIBO is an overgrowth of commensal bacteria in the small intestine. It’s not that you were infected by something, it’s that something that’s supposed to be there overgrew when or where it shouldn’t have. Under normal operating conditions, the mucosal defense system prevents this overgrowth from happening.
In addition to an impaired migrating motor complex, antimicrobial peptide secretion would have to be impaired as would the loose mucus layer in the small intestine. These factors help prevent bacteria from contacting the intestinal barrier, trap excess bacteria in the mucus, and sweep them out of the small intestine and in to the colon. If this doesn’t work, the system must be impaired and the data suggests that this is probably due to an injury and not your commensal bacteria impairing your motility.
So why, then, is the primary way of addressing this problem in the conventional medicine world a round of antibiotics? That’s not to say that antibiotics can’t be part of the approach. But if you break your arm you can’t expect it to get better just by taking antibiotics. You need to cast it, not use it for a period, give it time to heal, and then use physical therapy to rebuild strength and coordination in the limb.
Unfortunately, you can’t cast the gut. But what you can do is address things you’re probably doing that are causing more damage and preventing existing damage from healing. This includes avoiding foods that cause inflammation, avoiding hyperglycemia and alcohol, and optimizing circadian rhythms.
Avoiding inflammatory foods
I do believe some people end up addressing this factor by avoiding foods that cause inflammation or GI discomfort. Unfortunately I feel they spend far too much time restricting these foods. Make no mistake about it, food sensitivity is a symptom, not a cause.
If foods give you excessive bloating when you eat them, they’re probably feeding the overgrowth. If they’re causing excessive inflammation you just aren’t breaking them down properly. This could be due to impaired enzyme secretion or an insufficient mucus layer. Either way, best to stop doing either until the injury heals.
However, I believe both of these issues will correct by addressing the other factors mentioned: hyperglycemia, alcohol, and circadian disruption. And it’s important to do just that so that your food list doesn’t dwindle until it becomes a handful of foods.
Hyperglycemia has clear detrimental effects on the gut from the esophagus to the colon. People with Type 2 diabetes have impaired esophageal motility, delayed gastric emptying and abnormal small intestinal motility. In general, the migrating motor complex in Type 2 diabetics is abnormal when compared to healthy controls.
The reason for impaired motility in Type 2 diabetics is believed to be multifactorial, with impaired vagus function being a leading cause. While it’s important to point out that there are stark differences between people with Type 2 diabetes and healthy controls, there is evidence in human trials that hyperglycemia, even in healthy individuals, impairs the MMC.
In 2 separate studies, the infusion of glucose to induce hyperglycemia in healthy people caused a dysfunctional MMC. In the first study, they found that hyperglycemia induced a shortening of the MMC via a decrease in phase 2 contractions, which function similarly to the way an agitator works in a washing machine. They also found that hyperglycemia decreased spontaneous bile release, which functions as a detergent to help wash away bacteria. This effect was due to impaired vagus nerve function, something they referred to as equivocal to a medical vagotomy.
The second study had a similar layout but dug a little deeper. They found similar effects on phase 2 contractions during hyperglycemia in healthy men and women between the ages of 23-34. However, they also found that phase 2 was lower even in the jejunum. Furthermore, phase 3 contractions, which are meant to move food towards the colon, were impaired during hyperglycemia.
In fact, late phase 3 contractions in the area of the duodenum adjacent to the stomach moved food back towards the mouth, something believed to be a major contributor to gastroesophageal reflux disease(GERD). Thus, hyperglycemia, even in individuals without overt Type 2 diabetes, impairs the migrating motor complex at least in part through damage to the vagus nerve.
The question on most peoples’ mind is can they get to this level of hyperglycemia via normal feeding? I do believe it’s possible, but that depends to a large extent on the lifestyle of the individual . Put it this way, I don’t believe it’s inconceivable for someone who is sedentary that indulges frequently in large meals with highly palatable, processed foods to get there.
Based on the data from another study, postprandial blood glucose levels around 175mg/dL seem to impair the MMC, but how much they impair it is likely dependent on how long it stays at that level. I’d say most people do that every weekend, and eating too frequently, late at night, or even just being sedentary can get most people there regularly. The question is, how frequently do you need to do that before you get in to trouble?
Alcohol consumption is another factor that can mess with your migrating motor complex. In addition to damaging the vagus nerve as hyperglycemia does, alcohol causes damage to the upper part of the GI tract, specifically the stomach and duodenum. Alcohol also has calories, so it’ll typically shut the migrating motor complex down if consumed between meals or for a prolonged period of time.
Unfortunately, it seems that most of the negative effects of alcohol are occurring through damage to the vagus nerve. In a study looking at the effects of alcohol on motility, researchers found that the negative effects on GI motility from alcohol persisted even after blood alcohol was low, and that the primary effect was lowered motility during the day and increased motility during the night.
In essence, alcohol abolished the circadian variation in motility. Since we consume most of our calories during the day, this could set us up for SIBO by allowing food to stick around in the gut longer than it should during our primary feeding window. It’s also a natural segue in to our next topic: circadian disruption.
Circadian rhythms are variations in physiological processes that occur over a roughly 24 hour period. The gut is under heavy circadian control, and this regulates everything in the gut from digestive enzyme secretion to motility to intestinal permeability to the repair of damaged tissues. Under circadian disruption, secondary insults to the gut such as alcohol cause more damage and lead to greater intestinal permeability.
The reason for this is two-fold…Actually, it’s probably fifty-fold, but in the interest of brevity I’ll just cover 2 of those reasons. First, circadian rhythms prepare our gut for the approaching onslaught of food. The gut is best prepared for digestion and absorption at the beginning of our active period, which also just so happens to be the end of our fasting period. This makes sense, nothing should have been in it for quite some time so enzymes, antimicrobial peptides, and energy in the form of ATP have time to build up.
Secondly, but not separately from this phenomenon, our gut is typically repaired during our fasting period. Nutrient sensing pathways in the gut cause repair processes to be segregated from metabolic processes that generate energy. This is because both use NAD+, but in different ways. Under circadian disruption, digestion and motility are poorer and the damage we accumulate won’t be repaired adequately enough. Over time, this can allow damage to accumulate to the point where it can’t be repaired, and pathology will ensue.
It’s interesting to point out that circadian disruption decreases cardiac vagal tone. In other words, it causes heart rate and blood pressure to increase by decreasing the ability of the vagus nerve to keep heart rate and blood pressure in a healthy range. While this doesn’t necessarily mean it affects vagal tone in the gut, circadian rhythms regulate physiology via the autonomic nervous system which partially regulates gut function via the vagus nerve. So, it would be a bit surprising if circadian disruption didn’t impair the ability of the vagus to regulate the gut as well.
It’s easy to confuse SIBO with an infection because bacteria are involved. The problem is, the bacteria are supposed to be there and an antibiotic effective against a commensal bacteria may not necessarily be a great idea against something you don’t want to remove entirely. Under normal conditions an overgrowth is prevented, but when gut function is impaired these mechanisms also become impaired and normally helpful bacteria become problematic.
The current paradigm ignores this fact and treats SIBO as an infection, with a restrictive diet and oral antibiotics to chase the bugger away. The problem is, it’s not truly an infection, it’s an injury. And failure to address the injury even while addressing the overgrowth with an antibiotic will only give temporary relief. In order to prevent relapse, the injury that allowed the overgrowth to happen in the first place needs to be addressed as well.
No matter the initial cause of the injury, there are several factors that happen regularly enough in most people to warrant attention. Not only to repair the current overgrowth, but to prevent another one from happening later down the road. These factors include prevention of hyperglycemia, consuming alcohol intelligently, and optimizing circadian rhythms.
Avoiding foods that cause inflammation or bloating is also a good idea in the short-term, but prolonged restrictive dieting probably has as many negative effects as positive. I suspect that this is only a symptom of the problem for most people, and something that should correct by addressing all of the former.
Wondering how to prevent hyperglycemia or optimize your circadian rhythms? Want to know what intelligent alcohol consumption is and things you can do to mitigate the damage? If you’re a member of the Circadian Retraining Program you get these details and more in a Facebook Live coming out this Wednesday.
Not a member? You can find the details here.
12 thoughts on “Time to stop treating SIBO like an infection and more like an injury”
Excellent informative article!
Thanks, and thanks for reading!
If antibiotics + diet aren’t the solution, what do you suggest to do?
I’m struggling with SIBO-C, where fats (which is what I should eat to be healthy) cause bloating and are poorly absorbed, and carbs cause the same problems they cause in mostly people, primarily hypoglycemia, inflammation, and further GI discomfort.
Search the blog for stuff on bile and circadian rhythms. We need bile to absorb fats properly and bile is heavily circadian .
Great article. Very true. Admire your work on circadian importance as it’s something I’ve discovered personally to be very important
Thanks! Glad you enjoy the info.
As hyperglycemia slows down gut motility, I do think the same is with hypoglycemia which kind of shuts down the system due to stress. So I think it’s about balance.
I wonder about restrictive diets and food sensitivities. I heard a lot of people could tolerate lactose after treating gut infections. And good organic raw dairy is a very nutrient rich product. When it comes to gluten though, our ancestors seem to have digested it well and didn’t have the chronic disease epidemic. However, research now shows that everyone is sensitive to gluten at some level, it’s about the capacity of restoration. I think we are so overburdened with other stressors that things like gluten seem to affect us more nowadays.
Wondering if not eating gluten for multiple years, would be called “restrictive” ? or it’s better to eat it once in a while to let your gut & bugs adapt to it and create more like a hormetic effect in the gut ?
Thanks. Great post by the way !
Hey Dovydas, I do think restricting anything for a prolonged period can make people sensitive to it, but it’s not guaranteed. I think certain things require some assistance from our microbiome, and when we remove it long term, the microbes that assist can dwindle and we can have a harder time with it.
I don’t think it’s accurate to say everyone has a problem with gluten. I am aware of the study that people use to make this claim but it’s not a good representation of what happens in a living human. They took tissue samples of the small intestine and exposed them to gluten. Yes, all tissues had some level of permeability, but this isn’t a good model for a living human eating gluten. Since that study was published, we’ve identified at least a couple of dozen members of our microbiome that break down gluten. Many of them live in our mouth and get to work while we chew.
I was a part of the anti-gluten brigade until I read Gluten Freedom by Dr. Alessio Fasano. He’s the guy who identified gluten a the trigger for celiac disease. Even he says gluten is fine for most, and he certainly knows more about it than anyone else.
Stuff like that is why I created the blog. There are a lot of things people say regarding the gut and diet that are either poor interpretations of the data or wrong. I am opposed to needless restriction as it brings people into more and more restrictive diets.
Thanks for reading!
Is it really hyperglycaemia that is the issue, or just maybe occult Thiamine deficiency…?
If those with high blood sugar are also found to have Gastroparesis & SIBO, then it’s easy to assume the hyperglycaemia is the issue. Could occult Thiamine deficiency even be behind the poor glucose metabolism? Could the amount of Thiamine-guzzling food in our modern diet be driving the Thiamine deficiency & poor glucose metabolism?
Unfortunately our modern highly refined, nutrient-stripped wheat & sugar-laden diet forces the body to use waaaay more Thiamine (& other nutrients) than it supplies. Also, many commonly & often over-imbibed or consumed substances, such as tea, coffee, chocolate & alcohol, & certain drugs & medications can also block or inhibit its uptake.
So heavily involved in both the generation of energy (ATP) from food (particularly carbohydrates) & the entire nervous system, any lack can seriously impede any area of the body that is controlled by the nerves (which is pretty much all of it). Muscles, brain, reflexes, digestion, breathing, etc, etc, all or any of them may be affected.
Beriberi – acute Thiamine deficiency – or the symptoms of it, was first investigated in the 1880’s, when it was realised that white polished rice caused the symptoms whilst unpolished brown rice didn’t. It created a range of neurological issues & severe energy deprivation. These days it is thought to have been largely eliminated by food fortification, however modern Beriberi is very much alive & kicking in our modern society, & the fortification is just enough to prevent the old severe textbook symptoms but not enough to prevent isolated (& usually misdiagnosed) ones, such as neuropathies, heart & CVS issues, digestive problems, vision issues, energy deprivation issues, etc, etc.
Because it rarely resembles the original textbook symptoms – now being more a chronic issue rather than an acute one – because our diet is very different to the Indonesian diet in the 1800’s, the symptoms get categorised & treated as anything but Thiamine deficiency. Whilst for them rice was the staple food & made up the bulk of people’s diets, we live in a very different world & lifestyle.
However, as Dr. Derrick Lonsdale, who co-authored the book ‘Thiamine Deficiency Disease, Dysautonomia & High-Calorie Malnutrition’, coins it, we do indeed live in an era of highly processed & refined, high-calorie, ‘empty calorie’ food (of which new ‘products’ spew out of the factories by the second & stores are groaning under the weight of), that takes away far more than it ever gives. Rather than being calorie-restricted & undernourished as they were back then, today’s diets are often very much calorie-rich but nutrition-poor, and modern Thiamine deficiency behaves in a very different way compared to the 1800’s.
Because of the need for Thiamine for gut function & motility, & that it is rarely, if ever connected to aberrant gut function including the Migrating Motor complex – which is of course driven by the Autonomic Nervous System, thousands of people are potentially suffering needlessly.
Personally, Thiamine (I use Benfotiamine) has been amazing for my gut function, which continues to improve week by week. I also take the other B vitamins in a good B-50 complex, extra B12 (as sublingual drops with both active forms, Methylcobalamin & Adenosylcobalamin, plus I ensure I get plenty of Magnesium & Potassium as Thiamine uses them as it works in the body.
Thiamine is unlikely to be the primary driving factor. It may play some minor role, but given how type 2 diabetes works, taking more thiamine is a band-aid approach.
Type 2 diabetes occurs when we accumulate fat in the liver and pancreas, and this impairs both organs. It causes hyperglycemia, which causes us to dump thiamine. Thiamine May play some minor role in the neuropathy caused by hyperglycemia, but if it does, it simply routes excess glucose from glycolysis to create reducing equivalents to fix the damage caused by hyperglycemia.
The fix is to eliminate hyperglycemia, not replace the excess thiamine you’re peeing out.