Are yours as infected as his?

 

In the previous post, I talked about causes of small intestinal bacterial overgrowth (SIBO) due to compromised gastric barrier function. Today I want to talk about causes due to impaired intestinal movement or motility.

But before I do so, I need to mention that being immune compromised predisposes to SIBO. Whether it’s due to compromised gastric barrier function or impaired intestinal motility is hard to say. I would think both as compromised immunity affects all systems in the body so for that reason I can’t neatly categorize it. Nevertheless, because of the nature of these types of immune disorders, doctors and patients are usually more aware of the risk of intestinal dysbiosis and are less likely to ignore its manifestations, or at least I would hope so.

So with that as introduction, let’s dive into the second major cause of SIBO, impaired intestinal movement. This is by far the number-one cause of SIBO.

In order to move partially digested food or chyme along the entire length of your digestive tract, nerves embedded throughout your small and large intestine cause contractions that propel things along in a wave-like motion. This is called peristalsis in geek speak. Picture a very long sausage with an open end. As you repeatedly squeeze it along its length, it propels the contents forward and out. I hope that graphic didn’t permanently ruin sausages for you.

Peristalsis happens when you eat. But it also occurs between meals. In healthy subjects, these movements can occur in intervals from 20 minutes to hours. These movements are referred to as the gastrointestinal housekeeper because they keep the contents of your digestive tract from stagnating and cut the risk of pathogen attachment to the surface of the gut wall.

But just as importantly, peristalsis prevents bacteria from the colon from migrating up to the small intestine and colonizing it. A valve forms the physical barrier between the remote or distal end of the small intestine and the colon. This valve is called the ileocecal valve. It’s thought to prevent colonic contents and bacteria from refluxing back into the small intestine. However, studies in animals have failed to confirm this after resection surgery lending support to the theory that what ultimately prevents colonic bacteria from entering and colonizing the small intestine is the paristaltic movement of the small intestine.

So anything that impairs this housekeeping function in the presence or absence of chyme will also predispose you to SIBO.

Any surgical or anatomical abnormalities can interfere with these wave-like motions. Damage to nerves along the GI tract or enteric neuropathy can impede this vital function. Parkinson’s disease or damage to the vagus nerve due to diabetes are a couple of examples.

Injury due to radiation treatment and connective tissue diseases like scleroderma and Ehler-Danlos syndrome can impair peristalsis. So too hormonal diseases like low thyroid disorder and diabetic insulin resistance. Infectious diseases like Chagas and Lyme disease can affect motility as can the aftermath of viral infections like cytomegalovirus.

Chronic inflammation anywhere along the gastrointestinal wall can also impair motility due to the formation of scar tissue and inflamed nerves.

Acute fear and stress can either lead to an involuntary bowel movement as in the phrase “that literally scared the crap out of me” or stop digestion and peristalsis in its tracks as part of the fight or flight response.

Last, but not least, any drug that has opioid properties will slow or stop peristalsis. So heroin and opium predispose to SIBO. Morphine drips in hospital settings are a well-known cause of impaired small intestinal motility and constipation in patients.

So, assuming none of these causes apply to you, what other things can cause disruption of intestinal movement? Well, the culprits are likely dietary and that, dear reader, is the subject of the next two posts

 

References:

Bures J., Cyrany J., Kohoutova D., et al. (2010) Small intestinal bacterial overgrowth syndrome. World Journal of Gastroenterology, 16(24): 2978-90.

Parodi A., Lauritano E.C., Nardone G., Fontana L., Savarino V., Gasbarrini A. (2009). Small intestinal bacterial overgrowth. Digestive and Liver Disease, (3), 44-49.

Quigley E. M. M., Quera R. (2006). Small Intestinal Bacterial Overgrowth: Roles of Antibiotics, Prebiotics and Probiotics. Gastroenterology, 130: S78-S90.

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