Comprehensive guide to Hydrogen Sulfide SIBO and LIBO {2021}

Hydrogen Sulfide SIBO (Small Intestinal Bacterial Overgrowth) and the related large intestinal bacterial overgrowth are both particularly challenging to treat forms of dysbiosis. This article provides you with a comprehensive overview of the causes, symptoms, diagnosis and natural treatment approach.

Jump to:

• What SIBO and LIBO are
• All about the H2S gas
• How H2S is produced
• The role of H2S in the body
• Proposed negative effects of excess H2S
• Negative effects of excess H2S on the gut
• Negative effects and symptoms of excess H2S on general health
• Why Hydrogen Sulfide SIBO and LIBO occurs
• The mechanisms behind why H2S can be toxic to health
• Diagnosing Hydrogen Sulfide SIBO and LIBO
• Proposed treatment
• Work with Me
• References

What SIBO and LIBO are

SIBO is Small Intestinal Bacterial Overgrowth, an inappropriate overgrowth of the bacteria normally found in healthy amounts in the large intestine. In SIBO, there are too many bacteria in the small intestine which should have much lower numbers than the large intestine. I have written more in depth about SIBO here. You can also read about my treatment approach to SIBO.

All about the H₂S gas

Hydrogen sulfide (H₂S) is a gasotransmitter found normally in the human body including in the gut. It’s produced by our own body, but also by the bacteria found in the gut. Dysfunction in either of those two areas can create negative health effects.

H2S SIBO is the third type of SIBO, alongside hydrogen SIBO and methane SIBO (which has recently been renamed to IMO since methanogens are not bacteria). Along with SIBO, LIBO is another possibility which is where there is an overgrowth of bacteria in the large intestine which may be due to slow transit of waste material. Hydrogen sulfide excess can be an issue in both the small intestine and the large intestine. 

H2S usually plays a largely protective and essential role to our health, but in some cases it can become a significant problem if too much is produced. As with the other gasotransmitters, Nitric Oxide and Carbon Monoxide, H₂S is favourable to health at lower concentrations and hazardous at higher concentrations.

How H₂S is produced

Hydrogen sulfide is produced by our own cells but also by the bacteria found in our gut microbiome. Our cells produce H₂S via the enzymes cystathionine-β-synthase (CBS), cystathionine-γ-lyase (CSE), 3-mercaptopyruvate sulfurtransferase (3-MST) and D-aminoOxidase (DAO). In addition to the activity of those enzymes, Sulfate-Reducing Bacteria (SRB) found in the gut also produce H₂S via a dissimilatory sulfate reduction (DSR) pathway. These are in the Proteobacteria phylum and use the fermentation product hydrogen as a substrate along with sulfate which mostly comes from food. Some bacteria that are not in the SRB category can also produce H₂S.

Methanogens, Acetogens and SRB compete for hydrogen - often, one of these hydrogen-consuming bacterial classes predominates in the gut. We are supposed to have low amounts of hydrogen produced by the bacteria in the small intestine and higher amounts in the large intestine.

The most predominant genus in the SRB category is Desulfovibrio, which utilise lactate and hydrogen as substrate. Other genera being Desulfobacter, Desulfomonas, Desulfobulbus, and Desulfotomaculum.

Bacterial species belonging to different genera, such as Streptococcus, Fusobacterium, Salmonella, Enterobacter, and Helicobacter also produce H₂S from the amino acid L-cysteine. Klebsiella, Staph Aureus, some Firmicutes species and Fusobacterium can also produce H2S.

The two main species we investigate for H₂S issues are Bilophila wadsworthia and Desulfovibrio piger.

The role of H₂S in the body

H₂S is an essential gasotransmitter or gaseous signalling molecule that exerts its effect on different systems, such as gastrointestinal, neuronal, cardiovascular, respiratory, renal, and hepatic systems. H₂S is considered the third gasotransmitter, in addition to nitric oxide (NO) and carbon monoxide (CO), and is involved in inflammation, gut motility, oxidative stress, ulcer healing, vascular tone, neuromodulation, cryoprotection, memory formation, hormone secretion, apoptosis and many other vital biologic functions.

In the gut, H₂S regulates functions such as inflammation, ischemia/reperfusion injury and motility.

H₂S plays an essential role in our health, but an excess level has negative health effects often on the same physiological functions. There are currently novel therapies being developed which aim to either suppress H₂S or enhance its availability. This is a perfect example of how H₂S is essential to health, but can be a problem in excess.

Proposed negative effects of excess H₂S

The suspected negative effects caused by excess H₂S are found in both the digestive tract but also systemically, around the body. This is because H₂S, as a gasotransmitter, can travel around the body and be produced in various cells of the body.

The evidence for the negative effects of H₂S comes via a combination of sources: associations made between disease states and microbiome composition in humans, clinical observations that marry our understanding of the activity of H₂S with reported symptoms and, lastly, animal models which often test hypotheses more directly than can be done in humans. As is the case with all topics in science, we don’t have all the answers just yet and, in some cases, an individual’s symptoms may be caused by something else. This is why differential diagnosis is so important. 

The current science linking H₂S to disease is inconclusive and it’s unclear whether an overgrowth of H₂S producing bacteria are simply part of these conditions or if they are actually a driving force behind them. Hopefully, there will be more conclusive evidence discovered in future that can be utilised in treatment. So, it is important to find a balance whereby the link between H₂S and disease is not overstated, but we recognise it is a possible culprit in the mix when it comes to specific diseases and symptoms.

Negative effects of excess H₂S on the gut

H₂S derived from gut microbes has been found to be associated with gastrointestinal disorders such as ulcerative colitis, Crohn’s disease and irritable bowel syndrome. H₂S also inhibits oxidation of butyrate, contributing to a lack of energy for the gut lining which may lead to increased intestinal permeability (leaky gut). The bacteria can also degrade mucin, effectively breaking down the protective mucus layer and exposing the colon lining to harmful metabolites that may eventually lead to colon cancer.

The link to colorectal cancer

Genomic analysis of the colorectal carcinomas revealed the expansion of Fusobacterium on the mucosal surface of these cancers.

E. coli, another H₂S-producing enteric bacteria, has also been found to be associated with CD and colorectal cancer.

Gut Inflammation

The connection between H2S-producing gut bacteria and inflammation was further supported by the finding that Bilophila wadsworthia, a sulfite-reducing bacteria that generates H₂S similar to Desulfovibrio was higher in concentration in mice fed with high fat diet and this was associated with proinflammatory responses in genetically susceptible mice

SRB and H₂S were also found to be much higher in Pouchitis [66]. 

SRB were found in greater number in constipation-predominant IBS patients compared to controls.

The link to IBD

Research has uncovered many pertinent associations between IBD and SRB:

• A high number of SRB have been found in patients with ulcerative colitis (UC)
• SRB was also observed in higher number in feces of IBD Crohn’s Disease (CD and UC) patients
• Fecal H₂S levels were reported to be greater in UC compared to controls 
• The consumption of meat and high sulfur or sulfate containing diet that could promote the production of H2S was associated with an increased likelihood of relapse for UC patients further suggesting a role of these microbes in the pathogenesis of UC
• A medication commonly prescribed for UC is actually known to reduce levels of SRB which may explain partly how it works. 

Negative effects and symptoms of excess H₂S on general health

SRB were also found to be associated with other inflammatory conditions such periodontitis and increased levels of H₂S have also been detected in periodontal pockets. 

We know that H₂S is essential to so many different body systems, which means that an excess level can also potentially affect all the body systems with a wide variety of potential symptoms.

Some of the potential signs and symptoms of excess H₂S:

• Fatigue
• Brain fog
• Obesity
• Smelly stool, flatulence, and/or breath (halitosis)
• Compromised barrier function (due to inhibition of butyrate oxidation) - leaky gut, immune dysfunction
• Cramping pain in the gut
• Intolerance to high sulfur foods eg. eggs, kale, red meat, garlic, onions
• Sulfur burps (often associated with H.pylori)
• Diarrhoea (usually if the H2S is coming from the small intestine)
• Can also cause constipation (usually if the H2S is coming from the large intestine)
• IBD, mostly Ulcerative Colitis
• Colorectal cancer
• Panic attacks
• Bladder symptoms such as bladder pain, painful urination or irritation
• Headache
• Cardiovascular symptoms – eg. low blood pressure, low heart rate, palpitations, arrhythmias
• Orthostatic intolerance
• Paresthesias – numbness, heat, tingling
• Alcohol intolerance even with small amounts
• Night sweats
• Dermatitis or eczema
• Body/joint pain

The above list is a combination of signs and symptoms observed by clinicians such as Dr Greg Nigh and Nirala Jacobi along with associations reported in the scientific literature.

Why Hydrogen Sulfide SIBO and LIBO occurs

There are a number of theories as to why H₂S can become an issue:

The first theory revolves around a classic SIBO and/or LIBO picture whereby hydrogen is converted to H₂S in excessive amounts in either or both of the small intestine or large intestine. This is somewhat of a typical dysbiosis picture, with high levels of pro-inflammatory Proteobacteria that includes the SRB and other H₂S producers and lower levels of protective bacteria and metabolites such as butyrate. This particular theory has been covered really well by people like Jason Hawrelak, PhD, Nirala Jacobi ND. This theory’s main point is that specific dietary patterns predispose to excess levels of H₂S, specifically high levels of meat and/or dairy, and not enough plant foods. These foods provide sulfur and also saturated fat which we know the SRB thrive on. Problematic saturated fats also include coconut and palm oils, so it’s not exclusively a problem related to saturated fats from meat and dairy.

The second theory has been proposed by Greg Nigh, ND, based on clinical observations and his discussions with Dr Stephanie Seneff, PhD. This theory proposes that excess SRB and H₂S production is an adaptive response to a deficiency in usable sulfur (sulfate or SO₄), which you can learn more about on this podcast episode and this article. Hydrogen sulfide is a substrate (ingredient) for the production of SO₄ and there are numerous reasons proposed as to why an individual may have difficulty in producing sufficient SO₄ - such as lack of sun exposure (so common these days due to fear of the sun), glyphosate use on crops and heavy metal exposure which can interfere with the action of the SUOX enzyme that converts sulfite to sulfate.

The interesting thing about his observations is that he noted his clients were more sensitive to plant sources of sulfur such as garlic and kale whereas Dr Jacobi noted in her case it was more about the animal sources of sulfur such as eggs, red meat and dairy.

Another interesting fact is that SRB play a role in the biotransformation of arsenic. So, perhaps in some people it could be a protective response if they have high arsenic levels OR it could be a cause of increased H₂S. There are particular foods in the food supply known to have high levels of arsenic such as brown rice.

Diet is a big influence - the sulfur containing amino acids are a potent generator of H₂S. This includes cysteine, methionine and taurine.

Antibiotic use can promote the growth of SRB because these species are resistant to broad-spectrum antibiotics and H₂S is produced as a defense mechanism when antibiotics are used. Taking antibiotics will also reduce the levels of bacteria that can keep the SRB levels balanced by helping hydrogen gas to go down a different pathway than to H₂S production.

SIBO H₂S in particular can be an issue because the small intestine and stomach both have a lower capacity of the mucosa to metabolise H₂S compared to the large intestine. So, an overgrowth of H₂S producing species in the small intestine could be a much bigger issue than a comparable overgrowth in the large intestine.

Low FODMAP diet or a typical SIBO-type diet may worsen H₂S sulfur due to an increase in animal foods. Also, Paleo and Primal style diets include a high intake of the animal proteins, saturated fats and coconut oil that are associated with H₂S production. Interestingly, an increased consumption of brassicas, such as broccoli, was associated with a decrease in SRB, so it appears that plant sources of sulfur foods are not as big an issue compared to animal foods.

The mechanisms behind why H₂S can be toxic to health

A high level of H₂S induces DNA damage, inhibits cytochrome c oxidase, and inhibits butyrate oxidation, reduces oxygen consumption, alters response to oxidative stress, and leads to decreased/increased cell proliferation - the latter is related to colorectal cancer.

H₂S is also metabolised in the presence of oxidative stress and inflammation to a substance called tetrathionate which can promote the growth of pathogens such as Salmonella. So, this is a downstream, secondary negative effect of H₂S. Salmonella also produces H₂S, so it’s a nasty vicious cycle.

Depending on the individual, an overgrowth of H₂S producing species also means a high level of pro-inflammatory LPS (endotoxin) which has its own negative health effects. Health-promoting and ant-inflammatory short chain fatty acid butyrate is often low in people with chronic gut issues - this can come about due to low intake of prebiotic fibres from plant foods and antibiotic overuse (itself a risk factor for H₂S overgrowth). So, H₂S excess is usually not found in isolation in people who are unwell - there is always more to the story.

Diagnosing Hydrogen Sulfide SIBO and LIBO

There are some pathology options available to us which should always be interpreted with signs and symptoms before making any conclusions.

In terms of stool testing, we can look for the proportion of H₂S producing bacteria against what we currently believe to be the optimal range. Stool testing is reflective of the large intestine only, and even then there are different species and levels of bacteria through the length of the large intestine. The two main species we investigate for H₂S issues are Bilophila wadsworthia and Desulfovibrio piger so it’s important to choose a test that measures these.

SIBO breath testing can give more of an indication of H₂S status in the small intestine. There is currently the TrioSmart test available in the US which measures all 3 gases - hydrogen, methane and hydrogen sulfide, however it only uses lactulose and glucose as test sugars. Fructose isn’t available - Jason Hawrelak has recently mentioned that he believes fructose testing for SIBO is very important. So, in countries where the TrioSmart is not available and for fructose breath tests, H₂S SIBO (and possibly LIBO) may be indicated where there is a “flat line” of gas production for both hydrogen and methane. We expect to see an increase in hydrogen in the large intestine for everyone (so, the 3rd hour of the breath test), so if this doesn’t occur - and methane also hasn’t increased - it is especially suspicious. 

Proposed treatment

• Diet changes - short term elimination of animal based foods (especially red meat, dairy, eggs) and temporary elimination of high sulfur plant foods. Switch to more of a plant based diet including soy foods (the isoflavones help with H₂S). Many people with H₂S SIBO do worse on a low FODMAP diet, which is contrary to standard SIBO cases.
• It may be important to minimise food sources of arsenic such as brown rice
• Specific prebiotic fibres and colonic foods to acidify the colon via short chain fatty acid production (including butyrate)
• H₂S binders
• Specific herbal medicines - there are numerous herbs that can be used for H₂S SIBO and LIBO using an individualised protocol known to reduce H₂S
• Rifaxamin can be used for H₂S SIBO according to SIBO expert Dr Mark Pimentel. For my clients using rifaximin I always add extra supplements as adjuncts that are shown to help it work better
• A probiotic used in research L. plantarum P-8 has been shown to reduce levels of Desulfovibrio. This strain isn’t available commercially so other strains of Lactobacillus plantarum are worth trying.
• Support sulfur pathways in the body with specific nutrients

Work with Me

Struggling with chronic digestive symptoms? Have a tough case of SIBO? Relapsed after treatment? I'm here to help you. Find out more about how I treat SIBO as a Naturopath and Nutritionist.

I have completed Advanced SIBO training with The SIBO Doctor and have also undertaken courses presented by Jason Hawrelak, PhD. I also have personal experience successfully treating hydrogen and methane SIBO in myself.

Ready to book in? Make a booking.

References

Buret, A.G., Allain, T., Motta, J-P., and Wallace, J.L. (2021). Effects of Hydrogen Sulfide on the Microbiome: From Toxicity to Therapy. Antioxidants & Redox Signaling. ahead of print
http://doi.org/10.1089/ars.2021.0004

Carbonero, F. et al (2012) Microbial pathways in colonic sulfur metabolism and links with health and disease. Front. Physiol., 28 November 2012 | https://doi.org/10.3389/fphys.2012.00448

G.R. Gibson, J.H. Cummings, G.T. Macfarlane, Growth and activities of sulphate-reducing bacteria in gut contents of healthy subjects and patients with ulcerative colitis, FEMS Microbiology Ecology, Volume 9, Issue 2, December 1991, Pages 103–111, https://doi.org/10.1111/j.1574-6941.1991.tb01742.x

Jowett SL, Seal CJ, Pearce MS, Phillips E, Gregory W, Barton JR, Welfare MR. Influence of dietary factors on the clinical course of ulcerative colitis: a prospective cohort study. Gut. 2004 Oct;53(10):1479-84. doi: 10.1136/gut.2003.024828. PMID: 15361498; PMCID: PMC1774231.

Noortje Ijssennagger et al (2015) Gut microbiota facilitates dietary heme-induced epithelial hyperproliferation by opening the mucus barrier in colon. PNAS August 11, 2015 112 (32) 10038-10043; first published July 27, 2015; https://doi.org/10.1073/pnas.1507645112

Levine J, Ellis CJ, Furne JK, Springfield J, Levitt MD. Fecal hydrogen sulfide production in ulcerative colitis. Am J Gastroenterol. 1998 Jan;93(1):83-7. doi: 10.1111/j.1572-0241.1998.083_c.x. PMID: 9448181.

Loubinoux J, Bronowicki JP, Pereira IA, Mougenel JL, Faou AE. Sulfate-reducing bacteria in human feces and their association with inflammatory bowel diseases. FEMS Microbiol Ecol. 2002 May 1;40(2):107-12. doi: 10.1111/j.1574-6941.2002.tb00942.x. PMID: 19709217.

Elizabeth A Magee, Caroline J Richardson, Róisín Hughes, John H Cummings, Contribution of dietary protein to sulfide production in the large intestine: an in vitro and a controlled feeding study in humans, The American Journal of Clinical Nutrition, Volume 72, Issue 6, December 2000, Pages 1488–1494, https://doi.org/10.1093/ajcn/72.6.1488

Oliphant, K., Allen-Vercoe, E. (2019) Macronutrient metabolism by the human gut microbiome: major fermentation by-products and their impact on host health. Microbiome 7, 91
https://doi.org/10.1186/s40168-019-0704-8

Podcast: https://www.thesibodoctor.com/2017/12/20/sibo-and-hydrogen-sulfide/#dr-greg-nigh

https://ndnr.com/gastrointestinal/sibo-as-an-adaptation-a-proposed-role-for-hydrogen-sulfide/

Singh, S. B., & Lin, H. C. (2015). Hydrogen Sulfide in Physiology and Diseases of the Digestive Tract. Microorganisms, 3(4), 866–889. https://doi.org/10.3390/microorganisms3040866

Wang L, Zhang J, Guo Z, Kwok L, Ma C, Zhang W, Lv Q, Huang W, Zhang H. Effect of oral consumption of probiotic Lactobacillus planatarum P-8 on fecal microbiota, SIgA, SCFAs, and TBAs of adults of different ages. Nutrition. 2014 Jul-Aug;30(7-8):776-83.e1. doi: 10.1016/j.nut.2013.11.018. Epub 2013 Dec 4. PMID: 24984992.