Naturally Immune For Life

The dangers of hydrogen sulfide (H2S SIBO) 

Dr. Henry Lin is an expert in H2S SIBO. H2S SIBO is likely the most dangerous form of SIBO which has since been confirmed by research today. Research that also confirms SIBO links to liver damage, metabolic syndrome, obesity, heart disease, autoimmune conditions, demyelination of nerves, fibrosis and immune system exhaustion.

H2S affects the gut, liver, immune system, nerves, heart, and brain simultaneously. 
H2S is highly poisonous—when inhaled, it has a level of toxicity similar to that of cyanide.
The small intestine is inefficient in detoxifying this gas.

Hydrogen Sulfide (H2S) is a colorless gas that, owing to its sulfur content, smells like rotten eggs. Frequently referred to as “sewer gas,” 

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.

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.

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 affects the gastrointestinal smooth muscle cells and has a pro inflammatory effect

H2S is associated with the regulation of homeostasis.  H2S as a vital endogenous gaso-transmitter. Its role is important because cardiovascular and cerebrovascular diseases as well as gastrointestinal cancers are among the top causes of human mortality. Patients with Down syndrome overproduce H2S because their urinary excretion of thiosulfate. H2S-releasing bacteria in the intestine are a major source of endogenous H2S. Donation of H2S contributes to chloride secretion, which aggravates certain types of gastritis. 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 well-known lethal toxin. Studies suggest that H2S also binds and reduces ferric heme in microsomal cytochrome P450, generating 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 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 of the intestine by sulfate reducing bacteria along with an increase in H2S production. Inflammatory bowel disease is a chronic inflammatory disease caused by the generation and persistence of colitogenic CD4+ effector and memory T cells that react to antigens of commensal bacteria. H2S is continually produced by luminal sulfate-reducing commensal bacteria in the colon and is normally detoxified by rhodanese in the surrounding mucosal cells to thiosulfate. An increase in the steady state H2S levels is thought to play a role in the etiology of inflammatory bowel disease and related cancers. Data provides a logical link between reports that the 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 co-stimulator 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 threshold levels and/or with chronic low level exposure.

H2S and Cancer
What do rotten eggs and colon cancer have in common?
Researchers have discovered that hydrogen sulfide — the pungent-smelling gas produced by rotten eggs — is a key player in colon cancer metabolism, and a potential target for therapies for the disease.

University of Texas Medical Branch at Galveston researchers have discovered that hydrogen sulfide — the pungent-smelling gas produced by rotten eggs — is a key player in colon cancer metabolism, and a potential target for therapies for the disease.

In a paper appearing online this week in the Proceedings of the National Academy of Sciences, the UTMB scientists describe cell-culture and mouse experiments demonstrating that colon cancer cells produce large amounts of hydrogen sulfide, and depend on the compound for survival and growth.

“They love it and they need it,” said UTMB professor Csaba Szabo, an author on the paper. “Colon cancer cells thrive on this stuff — our data show that they use it to make energy, to divide, to grow and to invade the host.”

Antidotes

Until recently there has been little in the way of antidote for animals or humans suffering from hydrogen sulfide poisoning. Oxygen is usually given to workers overcome by the gas in attempts to revive them and is usually successful as a treatment in most cases. Now researchers have discovered that high doses of a natural form of Vitamin B12 may be the answer as an effective antidote.

Lack of B vitamin production affects fermentation in a negative manner, especially of fructose, and leads to excess H2S production.
Humans cannot synthesize vitamin B12, and, thus must obtain it from organisms that can.

Lactic Acid Bacteria And The Production Of B12

Lactic acid bacteria are capable of producing B Complex Vitamins Lactobacillus rossiae is an obligately hetero-fermentative lactic acid bacterium, which can be isolated from a broad range of environments including sourdoughs, vegetables, fermented meat and flour, as well as the gastrointestinal tract of both humans and animals. This strain in fact represents one of a small number of bacteria known to encode a complete de novo biosynthetic pathway of vitamin B12 (in addition to other B vitamins such as folate and riboflavin). In addition, it possesses the capacity to utilize an extensive set of carbon sources, a characteristic that may contribute to environmental adaptation, perhaps enabling the strain’s ability to populate different niches.

Probiotics like bifido and many others that utilize lactose (whole fat mammal milk) as an energy source greatly reduce the production of H2S.

Peppermint is effective at sweeping H2S out of the small intestine and works 75% of the time for IBS. Peppermint is a natural prokinetic.

SIBO Recipe SIBO recipe does not cause high PH in the stomach despite containing small amounts of baking soda, MoM does not induce effects until it reaches the small intestine which is naturally more alkaline than the stomach. SIBO recipe containing MoM, zinc and baking soda creates a slow dissolve oxygen that quickly neutralizes H2S. Zinc also neutralizes H2S and other odor causing bacteria.
Bifido Strains of probiotics 
Vinegar Acidifies the stomach, kills bacterial overgrowth there, and aids digestion.

Daily FAST diet

Autophagy or 13 hour daily fasts can quickly help digest Bacteria, fungi, and actinomycetes that release hydrogen sulfide during  decomposition.

Diet will not have a curative effect on SIBO. Diet is not the cause of SIBO. Diet tips like preparing well cooked easy to digest food and reducing fiber are for symptom control. A liquid or elemental diet can be dangerous and is used only for extreme conditions. Common gluten free diets that utilize other starches for bread replacement actually produce more H2S. Vitamin B (pantothenic acid) depleted yeast produces more H2s and leads to aberrant fermentation of fructose.

Risk factors:

Normal gut flora may provide several beneficial effects to the host. 

There are several intrinsic and extrinsic factors that prevent overgrowth of bacteria in the small intestine.

Intrinsic factors include:

Infants who are not breastfed are at an early stage with SRB (and with methane-forming bacteria).

Extrinsic factors include:

Diet and drugs modulating gut flora pre and probiotics (FOS and some other prebiotics are thought to be contraindicated in SIBO)(HFCS is contraindicated in SIBO)(maldigestion might lead to unnecessary SIBO diagnosis)
gastric acid suppressants such as proton pump inhibitors (PPIs), H 2 blockers, and antibiotics and drugs altering motility (anticholinergics, and opioids)

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. Though short chain fatty acids are useful for colon by providing nutrients to the colonocytes, conservation of energy and absorption of water and electrolytes, in the small bowel, it inhibits nutrient absorption and inhibits jejunal motility (ileal brake) through liberation of peptide YY, neurotensin and glucagon like peptide-1, which promotes SIBO. Lipopolysaccharides derived from Gram negative bacteria may also affect the GI motility. Bacterial derived metabolites may affect colonic motility.

Fibromyalgia, a condition associated with IBS, is also associated with SIBO. A study showed that all 42 patients with fibromyalgia had positive breath test. This percentage was significantly higher than the control population. These data might suggest that somatic hypersensitivity is also influenced by altered gut flora.

Disorders of the immune system can cause bacterial overgrowth. Chronic pancreatitis, or inflammation of the pancreas can cause bacterial overgrowth through mechanisms linked to this. The use of immunosuppressant medications to treat other conditions can cause this.

Other causes include inherited 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.

The most common isolates are:

 Escherichia coli
 Streptococcus
 Lactobacillus
 Bacteroides
 Enterococcus species

Many patients with chronic diarrhea have bacterial overgrowth as a cause or a contributor to their symptoms. While the consensus definition of chronic diarrhea varies, in general it is considered to be an alteration in stool consistency or increased frequency, that occurs for over three weeks. Various mechanisms are involved in the development of diarrhea in bacterial overgrowth. First, the excessive bacterial concentrations can cause direct inflammation of the small bowel cells, leading to an inflammatory diarrhea. SIBO can similarly sometimes be triggered by an acute gastrointestinal infection.

One current hypothesis of the cause of SIBO is an acute bout of food poisoning, which had never been properly treated.

When it is not SIBO dysbiosis

Though the pathophysiology of IBS remains largely enigmatic, evidence from recent studies does show that dysbiosis may contribute to development of symptoms, at least in a subset of patients.

Though SIBO is a form of quantitative alteration of small bowel microbes, altered microbiota (dysbiosis) does not necessarily mean SIBO only.

Dysbiosis includes qualitative alteration of gut flora (most authors reported on fecal microbiota) but also its quantitative change (SIBO). In the recent review, importance of dysbiosis including that of SIBO has been recognized by several experts. In SIBO, bacterial fermentation of diet in the lumen produces hydrogen, methane and carbon dioxide gases, which may contribute to symptoms like distension, flatulence, abdominal pain, and bloating. Methane is known to slow gut transit resulting in constipation.

These gases, however, may also be produced in the colon among patients without SIBO in presence of carbohydrate malabsorption.

SIBO is more often associated with diarrhea than constipation-predominant IBS. Mechanism of diarrhea in patients with SIBO include de-conjugation of bile salts, enterotoxic effect of bacterial metabolites, increased small intestinal permeability, deficiency of vitamin B 12 and low grade inflammation resulting from immune activation in the small intestinal mucosa.

SIBO is often misdiagnosed and generally under diagnosed. Clinical symptoms might be non-specific (dyspepsia, bloating, abdominal discomfort). Nevertheless, SIBO can cause severe malabsorption, serious malnutrition and deficiency syndromes. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.

Bifido maternal strains protect babies from SIBO
Infants who are not breastfed are at an early stage with SRB (and with methane-forming bacteria) settled (Baquero et al, 1988;. Hudson, Roberts, 1993).
Infants fed formula are also more likely to develop necrotizing enterocolitis. Lactose does not cause NEC even in premature infants.

Surprisingly components of the human microflora were found to inhibit the growth of SRB (sulfate reducing bacteria) and their H 2 S production efficiently, B. bifidobacteria. Desulfovibrio and Bifidobacterium are physiologically and metabolically so different that such an inhibitory effect was not expected, but rather the reverse would have been expected, inhibition of bifidobacteria by H 2 S.

Use of viable anaerobic bacteria for the preparation of a medicament for inhibiting the growth of sulphate reducing bacteria

H 2 S is detoxified by methylation (THF and Vit.-B12-dependent), by reaction with cysteine, by mercaptan formation (short-chain fatty acids, aldehydes) and oxidation to sulfate in the liver in the host body. These reactions may be due to the enormous excess consumption of serine, cysteine and methionine exhaust (methyl metabolism) which can no longer control of the degenerate mucosa, so that H 2 S accumulates. Due to the strong infiltration with macrophages at the site of inflammation and the additional exposure to NO and hydrogen peroxide is formed an uncontrolled reaction mixture. This has the consequence that H 2 S is chemically re-oxidized to thiosulfate or even sulfite. Both compounds are reduced by SRB again to H 2 S, so that a vicious circle is created with low available sulfate. Last but not least is the reaction with glutathione to glutathione-persulfide a dramatic deterioration of physiological redox potential occurs with numerous side effects. The reduction of protein sulfhydryl and DNA repair capacity found in IBD patients (Markowitz et al., 1988), is probably the basis for possible degeneration with direction to colon cancer. Thus, it was found that by means of activity of certain anaerobic viable bacteria such as bifidobacteria, sulfate reduction of sulfate-reducing bacteria can be inhibited, for example, by inhibiting the growth of these bacteria thus IBD or any related conditions can be tackled effectively.

Dec 16, 2014 – Cedars-Sinai Medical Center

SIBO-caused conditions include:

• irritable bowel syndrome
• fibromyalgia
• chronic pelvic pain syndrome
• chronic fatigue syndrome
• depression
• impaired mentation
• impaired memory
• halitosis
• tinnitus
• sugar craving
• autism
• attention deficit/hyperactivity disorder
• drug sensitivity
• an autoimmune disease, for example MS or SLE Lupus
• and Crohn’s disease.

For any infectious or parasitic disease to start, it is always a requisite that the host suffer IMMUNODEFICIENCY. At the same time, infectious and parasitic diseases themselves cause additional IMMUNE SUPPRESSION and more MALNUTRITION. This immune suppression is SECONDARY to the accumulation of free radicals, especially oxidizing species, that occurs during and after infectious and parasitic diseases.

Clinical Aspects of Immunology and Biochem J.