Time to stop treating SIBO like an infection and more like an injury

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

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

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

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.

Conclusion

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.

 

4 thoughts on “Time to stop treating SIBO like an infection and more like an injury

  1. johncoltparis says:

    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.

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