Why SIBO Matters
Why does a proper diagnosis for SIBO matter?
Small intestinal bacterial overgrowth (SIBO) is a condition in which there is increase in bacteria in the small intestine, it is also associated with motility problems. Prognosis is poor, dependent upon the underlying condition that led to SIBO.
The pathogenesis of irritable bowel syndrome (IBS), once thought to be psychogenic in origin, is now thought to be caused by multi factors. One of the reasons for this paradigm shift is the realization that gut dysbiosis, including small intestinal bacterial overgrowth (SIBO), causes IBS symptoms. Between 4% and 78% of patients with IBS and 1% and 40% of controls have SIBO and such wide variations might result from methods to diagnose SIBO.
SIBO has many underlying, overlapping and co conditions, many of which are serious including various immune deﬁciency syndromes, severe malnutrition disorders, liver failure and cancer.
SIBO results in the production of many toxins such as H2S, ammonia and other dangerous metabolites.
SIBO is also associated with a range of other diseases including obesity, diabetes and heart disease making SIBO a very costly condition. SIBO affecting both infants and the elderly disproportionately leads to even higher age associated inherent health care costs.
The medicines used to treat IBS and numerous other gut conditions might actually lead to SIBO making diagnostic tools a crucial investment.
H2S SIBO may be the most dangerous form of SIBO.
Hydrogen Sulﬁde (H2S) is a colorless gas that, owing to its sulfur content, smells like rotten eggs and is referred to as “sewer gas.”H2S affects the gut, liver, immune system, nerves, heart, and brain simultaneously. H2S is highly poisonous.
The small intestine are much less eﬃcient at detoxifying this gas
Bacteria, fungi, and actinomycetes release hydrogen sulﬁde during the decomposition of sulfur-containing proteins and by the direct reduction of sulfate. Humans may be exposed to hydrogen sulﬁde from both its endogenous production and exogenous sources. Most endogenous production results from the metabolism of sulfhydryl-containing amino acids (e.g., cysteine) by bacteria present in both the intestinal tract and the mouth.
In the body, H2S must be detoxiﬁed by oxidation. While H2S can be produced in large quantities by sulfate reducing bacteria in the colon, it is normally rapidly metabolized by a specialized detoxiﬁcation system in the colonic mucosa.
More proximal sites of the gastrointestinal tract including the small intestine are much less eﬃcient at detoxifying this gas.
H2S then enters the liver
If the detoxiﬁcation system is overwhelmed, H2S would escape the gut to enter the portal vein. In the portal vein, a small amount of H2S is detoxiﬁed by oxygen bound to hemoglobin. The majority then enters the liver. Inﬂammatory bowel disease is a chronic inﬂammatory disease caused by the generation and persistence of CD4+ effector and memory T cells that react to antigens of commensal bacteria.
A dysfunctional autophagic mechanism leads to chronic intestinal inﬂammation in IBD. The pathogenesis of the liver manifestation of IBD is related to gut inﬂammation that results in inﬂamed portal tracts of the enterohepatic circulation of lymphocytes from the gut to the liver.
H2S is pro inﬂammatory
H2S affects the gastrointestinal smooth muscle cells and has a pro inﬂammatory effect.
Donation of H2S contributes to chloride secretion, which aggravates certain types of gastritis.
An increase in the steady state H2S levels is thought to play a role in the etiology of inﬂammatory bowel disease and related cancers.
H2S is also a byproduct of dietary sulfate metabolism by gut bacteria. Inﬂammatory bowel diseases such as ulcerative colitis are associated with an increase in the colonization by sulfate reducing bacteria along with an increase in H2S production.
H2S as a gasotransmitter producing oxidative stress
H2S is associated with the regulation of homeostasis as a vital gaso-transmitter. Its role is important because cardiovascular and cerebrovascular diseases as well as gastrointestinal cancers are among the top causes of human mortality. Gastrointestinal contractility shows sensitivity to H2S, which affects the gastrointestinal smooth muscle cells as well as the neurons in the enteric nervous system. The concentration of H2S is enhanced when abdominal sepsis or endotoxemia occurs. H2S leads to exacerbation of these conditions, mainly because of its pro-inﬂammatory effect. H2S-induced inﬂammation has a relationship with the NF-κB signaling pathway. H2S has long been regarded as a strong toxin that inhibits mitochondrial respiration by combining the cytochrome c oxidase copper and/or heme iron site, resembling hydrogen cyanide, a wellknown lethal toxin. H2S generates a state of oxidative stress.
H2S is also reported to have a speciﬁc relationship with NO. They both have a synergistic effect on vasodilation as well as an inhibitory effect on the twitching of the ileum stimulated by electricity. H2S causes blockage of electron transfer within the mitochondria which in turn could lead to respiratory arrest at high enough concentrations
H2S is continually produced by luminal sulfate-reducing commensal bacteria in the colon. Excess H2S could contribute to unwanted T cell activation toward commensal H2S-producing bacteria. Combined with the novel physiological signaling function for H2S as a costimulator of T cell activation and proliferation, these ﬁndings establish H2S as an endogenous and exogenous co-regulatory signal for T cells.
H2S can paralyze nerves and has an inhibitory effect on the ileum
H2s can cause immediate paralysis of olfactory nerves above safe levels and/or with chronic low level exposure. H2S can lead to demyelination of nerve ﬁbers of the central nervous system and cause respiratory tract injury. It can also lead to Endotoxin-induced cardiovascular collapse and apoptosis of human aorta smooth muscle cells.
The multiple labels given various gut conditions may be outdated but H2S SIBO may be one condition where an effective test for an early diagnosis is long overdue.
New H2S SIBO Test Coming Soon
What can you do to prevent H2S SIBO?
There are several intrinsic and extrinsic factors that prevent overgrowth of bacteria in the small intestine.
Intrinsic factors include:
1. Secretion of gastric juice and bile, which have antibacterial effect.
2. Peristaltic movement preventing adherence of bacteria into the intestinal mucosa.
3. Normal gut defense including humoral and cellular mechanisms.
4. Mucin production by intestinal mucosal epithelial cell inhibiting pathogenic bacteria.
5. Gut antibacterial peptides such as defensins
6. Ileocecal valve preventing retrograde translocation of bacteria from colon to the small intestine.
Extrinsic factors include:
1. Diet and drugs modulating gut ﬂora pre and probiotics
2. Infants who are not breastfed are at an early stage with SRB (and with methane-forming bacteria).
3. Gastric acid suppressants such as proton pump inhibitors (PPIs), H 2 blockers, and antibiotics and drugs altering motility (anticholinergics, and opioids).
When it is not SIBO dysbiosis
Dysbiosis may contribute to development of symptoms in a subset of IBS patients. Though SIBO is a form of quantitative alteration of small bowel microbes, altered microbiota (dysbiosis) does not necessarily mean SIBO only.
These gases may also be produced in the colon among patients without SIBO in presence of carbohydrate malabsorption.
A Healthy Microbiome Is Necessary To Prevent SIBO
Other Risk Factors
• Normal gut ﬂora may provide several beneﬁcial effects to the host. These include fermentation of un-digested dietary residue and endogenous mucus producing short chain fatty acids, which are nutrients to the colonic epithelial cells and conservation of energy, absorption of NaCl and water, particularly from the right colon, synthesis of vitamin K, control of epithelial cell proliferation, protection against pathogens by a barrier effect and training of the immune system.
• Secondary deﬁciency of disaccharidases (e.g., lactase) is well known in patients with SIBO. Lactase deﬁciency is an immune deﬁciency. This results in maldigestion of carbohydrates such as lactulose, sucrose and sorbitol. Fermentation of carbohydrates leads to formation of short chain fatty acids like acetic acid, propionic acid and butyric acid.
• Other causes include immunodeﬁciency conditions, such as common variable immunodeﬁciency, IgA deﬁciency, and hypogammaglobulinemia.
• E. coli, shown in this electron micrograph, is commonly isolated in patients with bacterial overgrowth. Certain species of bacteria are more commonly found in aspirates of the jejunum taken from patients with bacterial overgrowth.