While it may seem like the trendy diagnosis of the moment amongst the gut focused, functional medicine community (present company included), the existence and troubling ramifications of SIBO (Small Intestinal Bacterial Overgrowth) make it an issue to be investigated and if discovered, imperative to address in order to continue on the journey towards optimal health.
SIBO is, as the name describes, an overgrowth of bacteria in the small intestine. When we think of “good,” gut friendly bacteria, flora, or probiotics, we are generally referring to the beneficial variety that mainly populate the large intestine, and to a much lesser degree the distal small intestine. The large intestine or colon is the area of your gastrointestinal tract that is distal to, & shorter in distance, but larger in diameter (hence the name) than the small intestine. The large intestine is compromised of the ascending, transverse, descending, and sigmoid colon, concluding with the rectum.
In comparison, the small intestine exists more proximal, or further up anatomically and sequentially along the digestive tract. It is substantially longer in total distance, but smaller in diameter. It consists of the duodenum, jejunum, and ileum and is site where the mass majority of nutrient and mineral absorption takes place. After food travels down the esophagus, and concludes its HCl acid bath in the stomach, it empties into a portion of the small intestine called the duodenum.
Ideally there should be relatively low amounts of bacteria here, as this is a hub for digestion consisting of digestive enzymes and connections to other important digestive machinery like the pancreas, liver, and gall bladder. As such, with the exception of varying amounts of strep, staph, lactobacillus, acidophilus, and a few others, very few bacteria should be in the small intestine; particularly this far from their ideal home in the large intestine.
However, for a variety of reasons an overgrowth of bacteria can occur in the small intestine. Potential facilitators of this process include, but are not limited to:
Dysfunction of the MMC (Migrating Motor Complex) resulting in decreased motility or necessary movement through the gut. This can result in bacteria or other pathogens being provided more time to gain a foothold and colonize. It also makes it easier for bacteria residing in the large intestine to translocate or move upstream into the small intestine, especially if the next facilitator is concurrently present.
Dysfunction of the Ileocecal Valve, which is a sphincter muscle valve that separates the distal small intestine (the ileum) from the proximal large intestine (in the lower, right abdominal quadrant, near the appendix). Just like we don’t want our esophageal sphincter (valve separating our esophagus and acid rich stomach) inappropriately open leading to a reflux of acid, dysfunction at the ileocecal valve can literally leave the door open for our friendly large intestinal bacteria to migrate into our small intestine. This structure and whether it is open or closed can be seen with a colonoscopy and can lead to ileocecal reflux, contributing to, or causing SIBO.
Before continuing on with other potential SIBO facilitators, let’s take a step back to the importance of gut motility and the aforementioned MMC. There are many things that negatively effect this, so let’s start there:
OPIOID USE: negatively affects the MMC, as seen with the well documented occurrence of opioid induced constipation.
STRESS, HIGH CORTISOL & ADRENAL DYSFUNCTION: stops the MMC
(Conversely, arguably the polar opposite of high stress and cortisol is sleep and melatonin. As such, we have yet another reason to enhance sleep quantity and quality as it fires up that MMC, specifically in the small intestine.)
Counterintuitively, eating actually inhibits a component of the MMC called peristalsis, which is the waves of smooth muscle contraction that shuffles food (and unwanted, freeloading bacteria) through the gut. So we also see a seldom referred to potential benefit of another currently popular and highly effective trend, intermittent fasting or time restricted eating.
More on intermittent fasting:
In addition to simply giving your gut a break to heal and optimize, periods of not eating also turns on that small intestinal portion of the MMC.
HEARTBURN, ANTACIDS & PPIs:
As we discussed in a previous talks:
Bridging a gap between heartburn and SIBO, the use of antacids or proton pump inhibitors can also facilitate SIBO. In addition to needing our stomach acid to digest food, absorb vitamins and minerals, and utilize food for energy, adequate stomach acid also helps to neutralize the bacteria or other pathogens inevitably coming in via the oral route. Acid reflux should no doubt be investigated and addressed, but to do so in such a myopic manner as to simply block your body’s production of imperative stomach acid completely disregards and disrupts all other function in the body; including the neutralization of exogenous bacteria and thus can facilitate SIBO.
DO YOU ALREADY DEMONSTRATE/SUSPECT AUTOIMMUNITY ?:
Obviously, the presence of certain bacteria can provoke an immune response in the form of inflammation, and subsequent formations of antibodies to fight the bacteria. Certain strains of bacteria, especially those encountered via food (and alcohol) poisoning (aka gastroenteritis), can lead to an attack (either through hyper immune reactivity and/or molecular mimicry) on what are called the ICK (Interstitial Cells of Kahal). These cells serve as the pacemaker for the MMC. Damage to the ICK via antibodies produced by our own immune system can thus inhibit the MMC and be another facilitator of SIBO.
(Polyautoimmunity or the presence of an immune attack on numerous tissues in the body is not only common, but to be expected if factors that cause immune reactivity remain or mount. We noted in previous posts and discussions that even though there may not be a name or specific disease label for it, no tissue is immune to an autoimmune attack. We bring this up here because the parietal cells of the stomach that produce stomach acid are also fair game for antibody damage. As such autoimmunity could very well play a duel role in SIBO by ultimately decreasing stomach acid due to destruction of the stomach acid producing parietal cells congruent with damage to the ICK, altering the function of the MMC.
These multiple explanations and descriptions of mechanisms are not to overwhelm, but to let you know what you may be up against. This is not a one size fits all approach, and often times we find it to be a confluence of factors that must be addressed to rectify the issue. Being aware of the potential contributors and investigating whether they are present and require addressing is the first layer to be peeled in the process.)
CARBS CARBS CARBS:
We couldn’t wrap up this portion of the discussion without taking a well deserved shot at another trendy target: the carbohydrate. Specifically we are speaking of excess carbs. Just like many cancer cells, the preferred fuel source for bacteria is the breakdown of your carbohydrate or sugar in the form of glucose.
If there exists an inappropriate level or strain of bacteria in the proximal small intestine (duodenum), they will also look to feed on protein found on the tip of structures that line the intestinal wall, called microvilli. The tips of microvilli house enzymes (i.e. sucrase, maltase, etc,) necessary for digestion of various carbs. Many of the digestive enzymes being depleted are responsible for breaking down those “healthy” foods that all of the sudden, due to malabsorption and SIBO, we no longer tolerate, and worse over, paradoxically react negatively to.
When we have less of these enzymes, we are less able to digest carbs, leading to increased carbohydrate malabsorption; which in turn leaves more fuel for the SIBO to multiply. It also means more digestion and fermentation by the bacteria, which translates to hydrogen (H2), methane (CH4), and/or hydrogen sulfide (H2S) gas driven bloating, distention and gas for you and those fortunate to be around you. And all you were attempting do was provide room and board to some bacterial drifters. It ain’t right.
We’ll wrap this SIBO discussion up here, but stay tuned as we proceed beyond potential causes into additional diagnostic clues that may warrant a deeper consideration into the possibility of SIBO.