Don’t worry: There’ll be no talk of handcuffs or blindfolds here, just a discussion about how and why the epidemic of SIBO can show itself in so many myriad ways in young and old, male and female, from head to toe.

We often talk about small intestinal bacterial overgrowth, SIBO, as if it were an all-or-none thing—it is not.

In fact, SIBO can show itself in an impressive variety of ways. It can show as the joint and muscle pains of fibromyalgia, the skin rash of rosacea, the neurological impairment of Parkinson’s disease, or the urgent bowel movements of irritable bowel syndrome. Recall that the many ways that SIBO shows itself are due to endotoxemia, the entry of bacterial breakdown products, especially lipopolysaccharide, LPS, into the bloodstream. This explains how intestinal bacteria can be expressed on the skin, in liver, coronary arteries, or brain.

In its most basic definition, SIBO is a situation in which undesirable bowel flora species, mostly so-called Gram negative Enterobacteriaceae species (E. coli, Salmonella, Pseudomonas, and many others) as well as a limited number of Gram positive species (Staphylococcus, Streptococcus, Enterococcus), have proliferated. When these species dominate, they also suppress the numbers of  “healthy” species such as Lactobacillus, Bifidobacteria, Faecalibacteria, and some forms of Clostridia. By doing so, they also degrade the thin single-layer mucus lining of the small intestine (unlike the tougher two-layer mucus lining of the colon), reduce production of the enzyme alkaline phosphatase that would ordinarily have disabled LPS molecules, and invade the intestinal lining. There is also an increase in intestinal permeability evident by such measures as an increase in blood levels of zonulin, just as with wheat and grain consumption. In other words, the ileum, jejunum, and duodenum are not well-suited to the army of bacteria that invade in SIBO. And, of course, there are trillions of such microbes, living and dying every hour of every day, releasing their toxic byproducts, some of which enter the human bloodstream: endotoxemia.

There are many variables in SIBO that can explain why one person may experience it as irritable bowel syndrome while another experiences it as Parkinson’s disease while another experiences no symptoms at all. Among such variables are:

  • Variation in SIBO species—One person may have more Salmonella, for instance, while another may have more Enterococcus.
  • Variation in “healthy” species—Someone may have preserved more Lactobacillus species, while another may have lost all their Bifidobacteria species.
  • Variation in degree of loss of intestinal alkaline phosphatase—In addition to being a species-dependent process, this is also affected by dietary factors and genetics.
  • Differences in effects on bile acid metabolism—Various bacterial species differ in their capacity to interfere with bile acid metabolism.
  • Differences in effects in interfering with pancreatic enzymes—SIBO species that reach as high as the duodenum where pancreatic enzymes are released may or may not interfere with fat and protein digestion.
  • The presence of H. pylori in the stomach—The presence of this potential ulcer-causing species can influence SIBO species composition. This becomes a huge factor if, over time, H. pylori leads to atrophy of the stomach lining and loss of stomach acid production, providing an open door to SIBO.
  • The integrity of the mucus lining—Early in SIBO, the mucus lining may remain intact. As bacterial species increase and become increasingly dominated by aggressive SIBO species, the mucus lining can degrade considerably.
  • Loss of butyrate-producing species—Greater loss of butyrate-producing species can mean greater intestinal wall inflammation and greater degree of metabolic distortions such as high triglycerides and greater insulin resistance in the host (i.e., you).
  • How high up the gastrointestinal (GI) tract have microbes climbed? SIBO confined to 8 feet of the distal ileum will typically be milder than SIBO occupying the full 24-foot length of the small intestine. Full-length SIBO is the form best detected with breath hydrogen (H2) gas, such as that detected by the AIRE device.

You get the idea. There is potential for enormous variation in SIBO due to the many variables. The key is to therefore look for evidence of this process either by identifying tell tale signs or by measuring breath H2 gas, a process made wonderfully easier with the AIRE device.

I cannot overemphasize how varied the manifestations of SIBO can be. It could be a high triglyceride level on your cholesterol panel that refuses to drop despite following my program with wheat/grain/sugar elimination, taking omega-3 fatty acids from fish oil, and taking the other recommended nutritional supplements that improve insulin responses. Or it could be a skin rash that persists despite repeated courses of topical steroids. Or it could be a growing list of food intolerances.

And remember: This may be somewhat scary and intimidating. But burying your head in the sand about SIBO can lead to many health problems over the long-term: autoimmune diseases, fibromyalgia, ulcerative colitis, neurodegenerative diseases, diverticular disease, colon cancer and many other conditions. Recognize, then address, the 30-feet of abnormal bacterial proliferation and you can therefore drastically alter the course of your future health.