The antibiotic approach to SIBO...
A reasonable approach to Small Intestinal Bacterial Overgrowth (SIBO) treatment? Perhaps. Effective long term? Probably not.
So the question is not “should I take Rifaximin or Neomycin/Rifaximin or plant antimicrobials?” Which I go into detail on this blog post . The question is what should I do after I take them? Because we all know of the infamous likelihood of a SIBO relapse.
Too dive into this question we should look at the factors that lead to SIBO:
Intrinsic factors that prevent bacterial overgrowth (Ghoshal, Shukla, & Ghoshal, 2017):
1. Secretion of gastric juice and bile which have antibacterial effects. Basically proper stomach acid and gallbladder function.
2. Peristaltic movement preventing adherence into the intestinal mucosa. Basically regular bowel movement.
3. Normal gut defense including humoral and cellular mechanisms. Basically adequate immune defenses in the gut such as proper Secretory IgA levels
4. Mucin production by intestinal mucosal epithelial cell inhibiting pathogenic bacterial. Basically an intact gut lining.
5. Gut anti-bacterial peptides such as defenses.
6. A patent ileocecal valve preventing retrograde translocation of bacteria from the colon to the small intestine.
7. A well-functioning migrating motor complex (this runs during the interdigestive/fasting period between meals) every 90 or so minutes.
Your clinician should be able to hunt down which of the risk factors you have for SIBO and plan to work on reversing them or supporting these areas after the antimicrobial phase of treatment.
How SIBO causes problems?
Short Chain Fatty acids which are created by the fermentation of certain carbohydrates and starches by colonic bacteria provide nutrients for the colonocytes, conservation of energy and absorption of water and electrolytes. However in the small bowel this should not really be taking place in the large amounts that we see in SIBO.
So in the small bowel, short chain fatty acids production:
1. Inhibit nutrient absorption
2. Inhibits Jejunal motility (via the ileal break) via the liberation of Peptide YY, neurotensin, glucagon peptide-1 which promotes SIBO . Basically this means the middle part of the small intestine gets sluggish and bacterial builds up instead of moving through.
3. Cell wall breakdown (ie. Lipopolysaccharides derived from Gram negative bacteria hanging out in the gastrointestinal tract may also affect motility.
4. Bacterial derived metabolites may effect colonic motility i.e.; Formyl-methionyl-leucyl-pheynalanine may affect the enteric nervous system. This is the nervous system of the gut that may be disrupted by the biproducts of bacteria hanging out in large amounts where they shouldn't be.
(Ghoshal et al., 2017)
Bacterial overgrowth produces a lot of toxic compounds
1. Peptidoglycans
2. D-lactate
3. Serum amyloid A
(Ghoshal et al., 2017)
All of these may promote inflammation, damage the brush border of the enterocytes (gut cells) and increase small intestinal permeability. Oh, and effect moods like creating lowered moods, anxiety, or brain fog.
The net result is some people have no digestive symptoms with SIBO and yet feel achy and depressed. But most have bloating, gas, constipation and/or diarrhea and also mood changes.
An adequate SIBO treatment should address brain/gut repair and address the underlying cause and mechanism of the SIBO process.
I am in particularly interested in diving into the connection of sleep disruption/circadian rhythm disruption and grazing behavior and the development of SIBO which as you can see is the first area I look at in my treatment cycle below.
Adam Rinde, ND
Bellevue, WA
Dr. Rinde has been treating and lecturing about SIBO since 2007 after reading The New IBS Solution by Dr. Mark Pimentel. This book changed his practice to addressing functional digestive disorders.Dr. Rinde's first lecture was at Grand Rounds at Bastyr University in 2007 and since has lectured and taught continuing education on the subject. He is available for interviews, consults, and lectures.
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