A Review of SIBO, IBS, and IBD Protocols from Drs. Siebecker, Sandberg-Lewis, and Kharrazian:
See dr Dinezza on prebiotics
For SIBO patients following GAPS, SCD or SCD + LOW FODMAPs and for Crohn’s patients following SCD, the bone broths must be made from meat and marrow bones only, no cartilage.
Since Crohn’s very often presents with SIBO, same rules for those patients following the SCD for their IBD, because cartilage broth contains collagen which contains soluble connective tissue fibers, and the SIBO bugs ferment the soluble fiber, create gas, bloating, distension and pain, and generally intensify symptoms (IBS-c, IBS-d, or both).
Remember that the one thing all the above diets DO have in common is the avoidance of all polyols aka sugar alcohols like mannitol, lactitol, sorbitol, erythritol, xylitol, etc. Where they differ is in the other kinds of carbs (fiber, sugars or polysaccharides) that they restrict or allow…
Sugar alcohols are highly prized since these carbs have no hormonal impact and they prevent dental carries, but SCD does not allow these sweeteners because for IBD or IBS patients they keep the gut irritated and inflamed. Often these sweeteners are touted as safe for the general population, but my understanding is that polyols can promote increased intestinal permeability in persons with no GI symptoms; so as an “ideal” sweetener for everyone, I say no for IBD and IBS patients but even for the healthy person I would still advise only occasional use if these sweeteners contribute to leaky gut in the long term.
Classic SIBO symptoms: the feeling of bloating with or without distension shortly after eating; taking fiber supps, pre-biotics or probiotics often intensifies symptoms, insoluble fiber supps increase constipation; excessive belching, chronic GERD, increased flatulence, indigestion; constipation with costive stools, alternating with occasional diarrhea or simultaneous D & C; must drink coffee in AM to go; must drink more coffee during the day to have b.m.; in most severe cases patient must use OTC laxatives, stool softeners, and so forth to have just one b.m. daily; very extreme cases patient only has 1 to 3 or 4 b.m. per week – these latter symptoms, if chronic, indicate that these are the patients that will need stimulation of the vagus nerve and brain exercises to restore motility along with some prokinetics.
SIBO can also be associated with chronic diarrhea (typically this will be associated with a positive hydrogen breath test and negative or low methane breath test since the methanogenic archaea are almost always associated with constipation). SIBO is very often a major contributor to increased intestinal permeability or leaky gut syndrome due to transcellular mechanisms.
The overgrown bacteria in SIBO can release enzymes that attack the SI epithelium or cells lining the gut. Initially this stimulates the production of mucin so we can coat the SI with mucous to protect against this attack. This interferes with good digestion and causes malabsorption of foods and nutrients.
After some time, especially when SIBO has been chronic for many months, our production of mucin becomes fatigued and the gut wall becomes exposed to the enzymes directly which leads to transcellular permeability in the SI.
Because the commensal bacteria feast on fibers, sugars and starches, they also secrete an enzyme that digests our own pancreatic and brush border saccharide-digesting-enzymes in order to rob us of the carb and fiber portions of our meals.
These bacteria can uncouple b-12 from our intrinsic factor and thus consume our dietary b-12 before we have a chance to absorb it, which long term can lead to pernicious anemia.
SIBO is also often associated with low iron levels and can lead to iron-deficiency anemia in addition to pernicious anemia!
These bacteria can also deconjugate our bile as it’s entering the duodenum which leads to malabsorption of fats and fat-soluble vitamins and long term this may cause steatorrhea or fatty stools. In this situation, since the patient cannot properly assimilate fats, SIBO may lead to deficiencies in the fat-soluble vitamins like A, D, E, and K2.
A little bit about IBD:
Crohn’s most often presents as chronic and gradually worsening constipation as the large bowel thickens over time, restricting the passage of stool. Ruling out SIBO for either IBS or Crohn’s is an important step as is, looking for the brain-based component in those clients presenting with chronic motility issues of 6 months or more…
These patients with compromised brain-gut functions will manifest with vagal dysfunctions such as asymmetrical or sluggish vibrations of the palatal arches during a tongue blade exam (say “ahhh”). It may often be revealing to have patient “pulse” their “ahhhs” by saying bursts such as “ah…ah…ah…ah…ah…ah…ah…ah” to check more closely for symmetry and amplitude.
Also depressed or very exaggerated (hypersensitive) gag reflex, using a light to light-medium touch with a tongue blade towards the back of the tongue while patient says “ahhh” again.
BTW, confirming a leaky gut requires a lactulose/mannitol challenge with a urine test; lactulose in urine confirms leaky gut and low levels of lactulose and mannitol in urine confirms malabsorption.
Or the newest test is an antibody test from Cyrex that looks for zonulin and occludin antibodies (paracellular permeability) or actimyosin antibodies (transcellular permeability).
To test for a leaky blood brain barrier which would confirm suspicion of brain-gut axis miscommunications, the patient can simply perform an oral GABA challenge with 1000 mg of pure GABA with no other precursors or brain-transportable metabolites. Relatively recently, there is, now available thru Cyrex Labs, an auto-antibody test for a leaky blood brain barrier.
GABA Challenge: Any reaction (most typically calming and sedative-like effects) to the GABA means this huge molecule made it thru the BBB which it should NOT be able to do = leaky brain! Remember this GABA challenge can also be used to confirm when the gut and brain membranes are healed and normal permeability has been restored !!
In addition, if you happen to have labs that corroborate hypochlorhydria, lack of bile, pancreatic enzymes, parasites, fungal overgrowth or other infections, this also indicates brain inflammation and possible degeneration in the autonomic areas such as the nucleus ambiguus.
These GI problems are likely the result of the lack of motility and when your food doesn’t move, it ferments…byproducts of that fermentation alter the gut chemistry and provides the right medium for more bacterial overgrowth or fungus and other opportunistic bugs…
Remember a stool test cannot confirm SIBO because that test only reflects the colon; a lactulose breath test for methane and hydrogen must be used to Dx SIBO and also the OATS urine test is not a reliable indicator of SIBO. Some practitioners say there are markers in the OATS test that correlate with SIBO, which may be true but those markers are highly unreliable….so, breath test is the way!
However, Crohn’s is typically diagnosed via the colonoscope with or without a biopsy. Both Crohn’s and UC are inflammatory bowel diseases and sometimes the inflammation can be viewed during the colonoscopy with the naked eye but if the inflammation is microscopic, then a biopsy will be needed for the Dx.
Two types of microscopic colitis can be differentiated from the biopsy, collagenous colitis (CC) and lymphocytic colitis (LC). These two conditions are more rare and mostly affect the colon and sometimes the terminal ileum; patients with unexplained diarrhea, particularly without any blood or tissue shreds, should have a biopsy to determine if they have Crohn’s, UC or one of the microscopic colitis varieties, CC or LC.
UC typically presents with bloody diarrhea and shreds of tissue, possibly fever and some may have pain and some may not whereas, Crohn’s patients often experience abdominal pain from the progressively worsening constipation; these are the typical symptoms when these two diseases present with classic textbook symptoms. However, antibiotic induced diarrhea can mimic UC, so when the symptoms point to the classic presentation of UC, a C. Diff toxin A and B test should be run to make sure this commensal bacterium is not overgrown and causing the bloody diarrhea. This bug is an anaerobe so it cannot be found by stool culture, so the toxin test is the best method to check for Clostridium Difficile when it appears UC is present.
However, the line between Crohn’s, UC and IBS are more of a continuum and these conditions can easily mimic each other, and most importantly they can occur simultaneously, for example doctors can often be confused by Crohn’s patients that also present with symptoms of IBS (which are largely identical to the classic Crohn’s symptoms: pain and cramping, loss of motility and constipation).
Particularly when SIBO is present it may be difficult to tell the difference between some of the IBS symptoms or the Crohn’s; in these cases stool testing can be used to look for a compound released by neutrophils called calprotectin. In adults, when calprotectin is >= 250 the patient is having symptoms of active IBD and should have a colonoscopy to take a look for ulcerations, but when calprotectin is < 50 the patient is having IBS.
When UC and Crohn’s present with crossover symptoms making a diagnosis unclear, then serum antibody testing can be used to differentiate the two: Crohn’s is more often associated with auto-antibodies to saccharomyces cerevisiae and UC with p-ANCA or peripheral anti-neutrophilic cytoplasmic antibodies, which are antibodies to a specific type of white blood cell.
Because the risk of colon cancer is increased up to nine times the average in patients with long term IBD, even if the IBD is in remission, folic acid supplementation should be considered. In IBD patients given > 1mg of this b-vitamin daily the occurrence of colon cancer was reduced by 86%.
Of course the best source of any vitamin is whole food but to get this therapeutic dosage supplementation should be performed with the activated form of folic acid or 5-methyltetrahydrofolate or 5-MTHF, or just plain MTHF.
To check a patient for early signs of folic acid deficiency before serum folate looks below normal even, another neutrophil test can be performed, called neutrophilic hypersegmentation index which counts the number of lobes in the nucleus of this WBC; an index > 10% means a deficiency and supplementation should be mandatory when the patient is on immunosuppressive drugs like mesalazine or sulfasalazine because these meds cause folic acid deficiency raising the patients risk for developing colon cancer in addition to their current inflammatory condition(s).
IBD is often thought as presenting when leaky gut, some genetic or even epi-genetic predisposition, and a powerful triggering event all happen together (severe gastroenteritis w/fever, vomiting, diarrhea, and cramps, for example).
These pathogens quickly release their toxic payloads, and our immune system responds by manufacturing antibodies to the various antigens which upregulates our own production of inflammatory chemicals or cytokines; however as you’ll see below, the antibodies we make to the pathogens’ CDT can also damage our own cells that control the migrating motor complex in the small intestine, leading to reduced motility and constipation.
Recent research into autoimmune reactions are suggesting it is an imbalance between various T-helper cells and when one type is dominant, this can lead to overly aggressive reactions from the immune system leading to inflammatory conditions or loss of self-tolerance and autoimmunity. In Crohn’s it is now thought that this is an exaggerated TH-1 response very often but also TH-2 or TH-17 can be involved…
Some NDs that have prescription rights may also employ low dose naltrexone (LDN) in addition to herbs like boswellia or curcumin because it works very well on modulating NF Kappa Beta and also blocks beta endorphin receptors so the patient starts making more of their own endorphins.
SIBO SUMMARY for health care providers:
It is very important to eradicate parasites or fix fungal overgrowth, and restore levels of HCL, bile and enzymes for optimal digestion. This will help with overall health and improve symptoms while treating the SIBO infection and restoring the brain-gut axis.
Remember, NOT everyone that has a cascade of GI symptoms will have a neurogenic component to their symptoms, but in chronic patients or especially failed patients that present with reduced or loss of motility (that no one has been able to fix), most likely they do because they have tried every LC diet under the sun, taken dozens of supplements, herbs, aminos, you name it, and nothing has worked…and now they’re here to see you!
For these clients you will need to treat their brain, gut, and brain-gut axis or gut-brain axis along with the typical gut healing herbs, pancreatic and brush border enzymes, HCL, and bile supps (and some LC diet of the client’s and your choosing – some may like to start the least strict and gradually eliminate other foods or groups, and some people, vice versa, they prefer going “cold turkey” on everything and gradually add foods back in…).
Brain-gut communications should be stimulated with gargling, singing, or humming exercises and motility supported with prokinetics like huperzine, galantamine, and/or Iberogast.
Diets that can be tried are low FODMAPs, SCD, GAPS or SCD with low FODMAPs, some kind of low-carb Paleo, Paleo AI and so forth, anything that eliminates fermentable starches and sugars to starve the bacterial overgrowth while treating with Rifaximin, and/or Neomycin, Berberine and/or AlliMed.
Retest with a hydrogen-methane breath test to confirm the antimicrobials were effective but if methane is not below 3 ppm or hydrogen less than 20 ppm or combined levels less than 15 ppm, do another round of the antimicrobials, mix up the meds, and/or change dosages, repeating as necessary until the SIBO is gone.
Some patients must stay on their low carb protocol to prevent relapse but some may do fine on just a low fiber maintenance diet aka the Cedars-Sinal diet originally developed by Dr. Pimental who wrote the original research in 2000 claiming most chronic idiopathic IBS is caused by SIBO. This is certainly preferable if the patient responds well because low fiber is much less restrictive and much easier to follow!
Patients on long-term PPIs or other acid blockers are much more prone to SIBO because lowered stomach HCL alters gut chemistry which encourages overgrowth and of course the antiseptic properties of gastric juice is reduced so commensal oral bacteria, or bacteria in food could contribute to the SIBO population too.
Of course low stomach acid sets up the patient for a nasty bout of gastroenteritis, stomach flu or food poisoning via pathogenic bacteria (violent cramps, vomiting and/or diarrhea). When this happens this can be the triggering event for the onset of SIBO since the common pathogens responsible for this affliction all release the same CDT toxin as our immune system responds to the invaders. Our immune system also goes after the CDT or cytolethal distending toxin and that protein is similar to the MMC motor neurons known as the interstitial cells of Cajal (ICC).
When our immune system makes antibodies to the CDT these ABs can cross react with the migrating motor complex cells (ICC) and the motor neurons are damaged by friendly fire or an autoimmune reaction. Without the MMC the SI cannot sweep debris and bacteria downstream with powerful contractions in between the times of digestion, eating, peristalsis, etc. Thus motility is compromised and food backs up, ferments and this all allows SIBO to develop.
Other causes of SIBO are post-operative if abdominal surgery left scarring that became an adhesion that constricts the bowels but also post-op patients from any surgery that are prescribed opiate pain-killers will develop severe constipation. Also patients taking pharmaceutical diuretics may also experience constipation right away from these meds.
SIBO can also be a consequence of other diseases or conditions that lead to a loss of motility, such as diabetes, hypothyroidism, and scleroderma.