SIBO - a deeper understanding

Many bacteria in the gut is not always beneficial

This page is for those of you who want to gain a deeper understanding of the subject of SIBO. Perhaps you have, or suspect that you have SIBO, or you work in a field where you meet people with conditions that may be linked to it.

Here we have compiled the basics about SIBO, in the hope of giving more people increased knowledge about the subject.

SIBO: When gut bacteria create health problems

Our body is in a fascinating interaction with bacteria and in our gastrointestinal tract these can play a decisive role in our health. When an imbalance occurs, this can lead to various health problems. One such imbalance that has received increased attention recently is SIBO, or "Small Intestinal Bacterial Overgrowth."

SIBO means abnormally high amounts of bacteria in the small intestine. Since the small intestine does not have the strong protective mucus layer that the large intestine has, overgrowth of bacteria can damage the wall of the small intestine and cause inflammation both in the intestine and in the rest of the body, as well as contribute to the development of chronic diseases and inflammatory conditions such as in muscles and joints.

Chronic stress is considered a major cause of SIBO. In this article, we will present what SIBO is and how health problems can arise in its wake.

The stomach's workhorses should be in the large intestine

The bacteria in our colon can be said to be real workhorses because they digest fibers from our diet that our own cells cannot use and convert these into health-promoting substances such as B and K vitamins.

Bacteria have surface structures that stabilize the outer bacterial cell wall, so-called lipopolysaccharides (LPS) and lipoteichoic acid (LTA) which contribute to maintaining the integrity of the bacteria. However, LPS and LTA are also some of the most powerful inflammation-inducing toxins we know of. Thanks to the colon's wall acting as an impenetrable barrier to LPS and LTA, these toxins cannot reach the body's immune system and cause inflammation from the colon.

This important barrier function comes from the fact that the surface of the large intestine consists of two powerful mucus layers (Figure 1) that keep the bacteria in place inside the intestine and prevent LPS and LTA from passing through the intestinal wall and into the bloodstream (1-5), but still allows salts and water to pass through the colon's two mucus layers and into the bloodstream. Absorption of water and salts into the bloodstream is one of the most important functions of the colon.

The small intestine is permeable to a variety of substances which reach the immune cells and the vascular system

The situation is completely different in the small intestine, as it does not have the same protective mucous wall as the large intestine, but only has a thin and loose superficial mucus layer (Figure 1). Since the small intestine is built to be permeable to a variety of nutrients (amino acids, fatty acids, carbohydrates, vitamins, minerals), a too thick mucus layer would have reduced this permeability. The total surface area for absorption in the small intestine is estimated to be 200 square meters, roughly the size of a tennis court, and it is this large surface area that allows a significant amount of nutrients to be transported from the inside of the gut into the bloodstream. If the small intestine would have had a mucus layer corresponding to that seen in the large intestine, the surface for adequate nutrient absorption would have had to be over 400 square meters, that is, our small intestine would then be over 12 meters instead of 6 meters long.

In the case of overgrowth of bacteria in the small intestine, the bacteria will devour and consume the amino acids, vitamins, minerals and other nutrients that should otherwise have benefitted our body. SIBO can actually be likened to a cuckoo chick that takes care of itself at the expense of others.

Figure 1. The small intestine has a superficial thin and loose mucus layer that allows nutrients to pass through the intestinal wall to the bloodstream, but the mucous is not sufficient to protect the cells of the intestinal wall in case of SIBO.

Figure 2. In the wall of the small intestine, Peyer's plaques (the arrow indicatesindicate the small lymph nodes consisting of immune cells) play an important role in tolerance to substances in our diet, but also in identifying and fighting disease-causing microbes and viruses.

Figure 2. In the wall of the small intestine, Peyer's plaques (the arrow indicate the small lymph nodes consisting of immune cells) play an important role in tolerance to substances in our diet, but also in identifying and fighting disease-causing microbes and viruses.

The immune system of the small intestine plays a central role for our health

The small intestine is an organ that contains a large accumulation of immune cells. It is estimated that up to 70% of the body's immune cells are found along the wall of the small intestine. This high concentration of immune cells is not surprising given the constant exposure to foreign substances from the 1-2 tons of food that we ingest annually; substances that our immune system must either tolerate (our diet) or react to (disease-causing microbes). The immune system in the small intestine is mainly located in small lymph nodes called Peyer's patches (Figure 2).

An example of how the immune system in the small intestine can react to unwanted bacteria is shown by the experiences from oral vaccination against the cholera bacteria. When we drink killed cholera bacteria, these end up on specialized cells in the lining of the small intestine which then transport the cholera antigen from the intestinal contents to the Peyer's plaques. After 2-4 doses of cholera vaccine, our immune system is prepared for a rapid immune response should we be infected by cholera bacteria in the future.

The example of oral vaccination shows how intimately the contents of the small intestine are linked to the immune system and that bacterial products can easily pass through the intestinal mucosa to immunocompetent cells in the wall of the small intestinal and start a reaction that results in an immune response (6).

Unlike the situation with oral vaccination where the intestinal immune cells are exposed to bacteria only on 2-4 vaccination occasions and then return to normal (calm) conditions, the situation is completely different in SIBO, where the intestinal immune cells are constantly activated by LPS and LTA from unwelcome bacteria thriving in the small intestine and thereby causing a chronic inflammation. In SIBO, the immune cells of the small intestine are overactive.

The “gut trolls”

In the oral cavity, we should not have too many unwelcome bacteria (we call them tooth trolls in Sweden) since they may cause gum inflammation due to the lack of a protective barrier. The situation in the small intestine is very similar where the wall of the small intestine also lacks protection against large amounts of bacteria. It is therefore of importance to prevent the overgrowth of unwanted bacteria in the small intestine and three mechanisms are considered relevant in this context:

  • The hydrochloric acid in our stomach, which eliminates bacteria from our food (think of all the bacteria found in, for example, a carrot pulled from the ground).
  • The intestinal peristalsis (motility), which prevents stagnation of food residues that unwelcome bacteria can start to ferment. It is through an active vagus nerve that a normal intestinal peristalsis is obtained.
  • The valve between the large intestine and the small intestine, which is kept tight under normal conditions by an active vagus nerve.

One of our body's most important check valve is sensitive to chronic stress

We can thank the ileo-cecal sphincter, as the valve between the large and small intestines is called, for preventing leakage of bacteria from the large intestine into the small intestine and, thereby, preventing SIBO. Unfortunately, this important check valve has a tendency to leak in case of chronic stress. This valve is kept closed by the vagus nerve, which is active (keeping the valve closed) when we are in a calm state. In case of stress the vagus nerve is inhibited and the valve subsequently opens and bacteria can then start to leak fecal content from the large intestine into the small intestine.

By the way, an example of where chronic stress can affect us negatively is in our workplace and according to the European Work Environment Agency one in five workers in Europe experiences work-related stress through high work demands, poor working environment and conflicts in the workplace.

Causes of SIBO

Reduced amount of hydrochloric acid in the stomach, usually via medication for "stress stomach" (gastritis/stomach inflammation) with gastric acid inhibitors (3, 5).

Impaired intestinal peristalsis can cause stagnation of food and thereby overgrowth of bacteria in the small intestine (2-5). An important cause of impaired intestinal motility is chronic stress.

Reduced closing capacity of the valve between the colon and the small intestine due to chronic stress.

Food poisoning via bacterial toxins from bacteria such as Campylobacter, Salmonella and Shigella, but also moderate alcohol consumption has been shown to contribute to SIBO (7).

How common is SIBO?

The incidence of SIBO varies depending on the population studied and the diagnostic criteria used. Surprisingly, scientific studies showed that up to 40% of healthy individuals tested positive for SIBO (8). No studies have so far investigated whether these healthy people who tested positive for SIBO developed health problems later on in life.

It's also worth mentioning that SIBO is more common in people with IBS (irritable bowel syndrome); up to 80% of people with IBS had SIBO (9). Also people on medications to treat stomach-acid issues had a higher incidence of SIBO (5). 

Symptoms of SIBO 

The symptoms of SIBO can be multifaceted and vary from person to person. Common symptoms include bloating, gas, abdominal pain, diarrhea or constipation, but also problems related to a leaky gut such as hypersensitivity to foods previously tolerated (cow's milk, eggs, grains, etc.) and low grade inflammation. These symptoms can often be confused with other gastrointestinal problems, making the diagnosis of SIBO challenging. 

It is highly important to rule out more serious causes of these symptoms such as cancer, inflammatory bowel diseases, etc.

Local symptoms (research has shown that over 80% of persons with IBS had SIBO):

  • Stomach pain or cramping
  • Bloated stomach
  • Gas and belching
  • Diarrhea
  • Constipation
  • Nausea
  • Heartburn / acid reflux

The rest of the body can also be affected in SIBO in the form of general symptoms of systemic low-grade inflammation, insulin resistance and cardiopulmonary problems (10-12).

General symptoms:

  • Fatigue
  • Joint pain
  • Muscle pain (e.g. as in fibromyalgia)
  • Food intolerance (e.g. gluten)
  • Skin inflammation / skin complaints (e.g. rosacea)
  • Depression/low mood


The gut-brain axis. The small intestine communicates with the brain via nerve fibers (vagus nerve) and via the bloodstream.

Gut bacteria and Parkinson’s disease

Parkinson's disease is thought to be caused by the protein α-synuclein clumping together
and forming toxic structures in the nerve cells. Research has previously shown that
α-synuclein occurs throughout the small intestine in people with Parkinson's disease. Previously, the cause of this accumulation of toxic α-synuclein structures has not been identified, but transport of α-synuclein via the so-called gut-brain axis has been proposed as one cause of Parkinson's disease.

Finnish researchers have recently identified an intestinal bacterium, Desulfovibrio, 
producing hydrogen sulphide, LPS and magnetite, which in close contact with the wall of the small intestine may cause this unfavorable aggregation of α-synuclein (13). From the small intestine α-synuclein could then be transported via the nerve pathways connecting the intestine to the brainstem, a region where Parkinson's disease is known to affect the dopamine neurons.

Gut bacteria and Alzheimer’s disease

Amyloid is a protein that accumulates in the brain in Alzheimer's disease. It has been shown that the bacterial toxin LPS from the intestinal bacterium Bacteroides fragilis can contribute to the deposition of amyloid in the brain and where it can clump together with amyloid in the brain in Alzheimer's disease (14, 15). In addition to the fact that LPS may increase the amount of amyloid in the brain, LPS has also been shown to cause a weakening of the cytoskeleton in nerve cells, which is typically seen in Alzheimer's disease (16, 17).

Treatment of SIBO

The treatment of SIBO usually includes a combination of antimicrobials, dietary changes and measures to improve intestinal peristalsis and management of stress. By reducing the amount of bacteria in the small intestine with antimicrobials, the symptoms can be alleviated, which in turn can contribute to reduced stress.

The most common pharmacological treatment for SIBO is using an intestinal antibiotic called rifaximin (Xifaxan®). Several studies indicate a connection between SIBO and diseases that affect the heart and vessels, endocrine organs, nervous system, kidneys, connective tissue and skin. Studies have shown that rifaximin not only reduced gastrointestinal symptoms but
also skin inflammation (rosacea) and other health problems linked to SIBO, with improved quality of life as a result (18-22).

A study showed that also botanical supplements with antibacterial properties can have equivalent effects as rifaximin (23).

Some advice 

  • Try botanical supplements with known antibacterial properties. Among others, oregano oil, magnolia bark, garlic, jatoba bark, rose root, ginger, and wormwood are considered to have these properties. SIBO supplements may also be composed of a mixture of antimicrobial botanicals.
  • Allow the small intestine to empty its contents by avoiding eating between meals. This allows the small intestine to rest and heal.
  • Mindfulness; try to do things in a calm and orderly manner.
  • Practice yoga and meditation.
  • Take deep breaths from time to time during the day. All of this can activate the beneficial vagus nerve.
  • Introduce regular and moderate exercise (e.g. walking).
  • Avoid an excessive intake of dietary fiber.
  • Intermittent fasting, with approximately 16 hours between main meals, is considered to contribute to increased intestinal motility. There also exist longer fasting programs.

In conclusion - what can we take away from this?

Unwelcome bacteria in the small intestine can cause local and systemic inflammatory conditions as well as affect the nervous system negatively.

Follow-up studies on whether healthy individuals with a positive SIBO test develop health problems have not yet been done, but regarding the nature of the small intestine, it may be considered beneficial to periodically try to reduce the occurrence of bacteria there. 

Stress reduction can both increase intestinal peristalsis and thus prevent stagnation of intestinal contents and reduce the reflux of bacteria from the large intestine to the small intestine.

In other words; the workhorses of the large intestine become “gut trolls” when they end up in the small intestine.

Gutfeeling Labs  

Gutfeeling Labs was founded by researchers in microbiology and neuroscience from Lund University, Sweden, to give the public the opportunity to increase their knowledge related to their intestinal flora and help to balance it.

Scientific references

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    1. Johansson, M. E., Sjövall, H., & Hansson, G. C. (2013). The gastrointestinal mucus system in health and disease. Nature reviews. Gastroenterology & hepatology, 10(6), 352–361.  Mag-tarmsystemets slemsystem (mucus) är den första försvarslinjen mot bakterier, men dess organisation varierar längs med tarmkanalen. Tunntarmensslemlagret transporteras fritt tillsammans med fångade bakterier mot tjocktarmen via tunnntarmens motorisk aktivitet. Tjocktarmen hanterar sin betydligt större bakteriebelastning med ett tvåskiktigt slemsystem, där det inre lagret normalt förblir ogenomträngligt för bakterier. 
    2. Vantrappen, G., Janssens, J., Hellemans, J., & Ghoos, Y. (1977). The interdigestive motor complex of normal subjects and patients with bacterial overgrowth of the small intestine. The Journal of clinical investigation, 59(6), 1158–1166. Denna studie fastställer närvaron och definierar egenskaperna hos tarmens migratoriska motorkomplex, MMC, hos människa. Det föreslås också att bakteriell överväxt kan bero på en specifik motilitetsstörning, dvs fullständig eller nästan fullständig frånvaro av det migrerande motoriska komplexet.
    3. Husebye, E., Skar, V., Høverstad, T., Iversen, T., & Melby, K. (1995). Abnormal intestinal motor patterns explain enteric colonization with gram-negative bacilli in late radiation enteropathy. Gastroenterology, 109(4), 1078–1089.  Minskad magsyra verkar vara ansvarig för kolonisering av den övre tarmen med luftvägsbakterier och förvärring av en redan etablerad gramnegativ bakterieflora i tunntarmen, medan nedsatt tarmmotilitet med största sannolikhet är en orsaksfaktor för kolonisering med gramnegativa bakterier i tunntarmen.
    4. Dukowicz, A. C., Lacy, B. E., & Levine, G. M. (2007). Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterology & hepatology, 3(2), 112–122. SIBO utvecklas när de normala homeostatiska mekanismerna som kontrollerar tunntarmens bakteriepopulationer störs. De två processer som oftast predisponerar för bakteriell överväxt är minskad magsyrasekretion och minskad motorik i tunntarmen. Bakteriell överväxt kan resultera i mikroskopisk slemhinneinflammation. Analys av tunntarmsbiopsier hos äldre patienter med bakteriell överväxt avslöjade trubbiga tarmvilli, förtunning av slemhinnans kryptor och ökade intraepiteliala lymfocyter. Antibiotikabehandling reverserade dessa slemhinnheförändringar.
    5. Jacobs, C., Coss Adame, E., Attaluri, A., Valestin, J., & Rao, S. S. (2013). Dysmotility and proton pump inhibitor use are independent risk factors for small intestinal bacterial and/or fungal overgrowth. Alimentary pharmacology & therapeutics, 37(11), 1103–1111. SIBO berodde huvudsakligen på Streptococcus, Enterococcus, Klebsiella och E. coli. SIFO berodde på Candida. 53 % hade reducerad motilitet och 43 använde protonpump-inhibitorer (PPI). PPI-användning (P = 0,0063) och dysmotilitet (P = 0,0003) var oberoende signifikanta riskfaktorer (P < 0,05) för överväxt. Symtomprofilerna var likartade mellan de med eller utan SIBO/SIFO. Reducerad tarmmotorik och användning av syranedsättande protonpump-inhibitorer var oberoende riskfaktorer för SIBO eller SIFO och fanns hos över 50 % av dessa patienter med oförklarliga gastrointestinala symtom. 
    6. Mörbe, U. M., Jørgensen, P. B., Fenton, T. M., von Burg, N., Riis, L. B., Spencer, J., & Agace, W. W. (2021). Human gut-associated lymphoid tissues (GALT); diversity, structure, and function. Mucosal immunology, 14(4), 793–802. Denna artikel beskriver GALT i relation till tarmepitelet (FAE) avseende Peyers plack och isolerad lymfoida folliklar (ILF) vilka alla spelar roll för ett immunsystem i balans.
    7. Gabbard, S. L., Lacy, B. E., Levine, G. M., & Crowell, M. D. (2014). The impact of alcohol consumption and cholecystectomy on small intestinal bacterial overgrowth. Digestive diseases and sciences, 59(3), 638–644. Av de patienter som intog en måttlig mängd alkohol hade 58 % ett positivt laktulos-utandningstest (LBT) jämfört med 38,9 % av personer som aldrig drack alkohol. De personer som tidigare fått sin gallblåsa borttagen hade signifikant lägre frekvens av positiv LBT. Studien visade att även måttlig alkoholkonsumtion är en stark riskfaktor för SIBO. Personer med borttagen gallblåsa verkade vara skyddade mot SIBO. 
    8. Ghoshal, U. C., Shukla, R., & Ghoshal, U. (2017). Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome: A Bridge between Functional Organic Dichotomy. Gut and liver, 11(2), 196–208. 1-40% av friska kontrollpersoner testade positivt för SIBO. Än så länge har inga vetenskapliga studier undersökt om dessa personer utvecklar sjukdomar vid ett senare tillfälle.
    9. Takakura, W., & Pimentel, M. (2020). Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome - An Update. Frontiers in psychiatry, 11, 664. Översiktsartikel om samband mellan SIBO och IBS.
    10. Manco, M., Putignani, L., & Bottazzo, G. F. (2010). Gut microbiota, lipopolysaccharides, and innate immunity in the pathogenesis of obesity and cardiovascular risk. Endocrine reviews, 31(6), 817–844. Systemisk exponering av LPS från det yttre membranet av gramnegativa bakterier kan orsaka ett tillstånd av "metabolisk endotoxemi" som kännetecknas av låggradig inflammation, insulinresistens och ökad kardiovaskulär risk. LPS kan framkalla en kaskad av immunsvar som slutligen resulterar i frisättning av proinflammatoriska molekyler som stör moduleringen av glukos och insulin metabolism, främjar utveckling av aterosklerotiska plack och gynnar progression av fettleversjukdom.
    11. Pussinen, P. J., Havulinna, A. S., Lehto, M., Sundvall, J., & Salomaa, V. (2011). Endotoxemia is associated with an increased risk of incident diabetes. Diabetes care, 34(2), 392–397.  Resultaten tyder på att mikrober kan spela en roll för utvecklade av diabetes. Försökspersoner med utbredd diabetes (n = 537) och de med incident diabetes (nya fall av diabetes som inträffar under studien, n = 462) hade högre endotoxinaktivitet än de icke-diabetiska individerna. Diabetes associerades med endotoxemi, vilket indikerar en koppling av metabola störningar till inflammation.
    12. Creely SJ, McTernan PG, Kusminski CM, Fisher M, Da Silva NF, Khanolkar M, Evans M, Harte AL, Kumar S 2007. Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes. Am J Physiol Endocrinol Metab 292:E740 –E747. Cirkulerande LPS från gramnegativa tarmbakterier är högre i plasma hos patienter med typ-2 diabetes jämfört med smala och friska individer. LPS aktiverade det medfödda immunförsvaret med frisättning av de proinflammatoriska mediatorerna IL-6 och TNF-alfa. Det föreslås att tarmfloran potentiellt spelar en roll för sjukdomsutvecklingen hos personer med överviktsrelaterad typ-2 diabetes via stimulering av det medfödda immunförsvaret med LPS från gramnegativa tarmbakterier.
    13. Murros, K. E., Huynh, V. A., Takala, T. M., & Saris, P. E. J. (2021). Desulfovibrio Bacteria Are Associated With Parkinson's Disease. Frontiers in cellular and infection microbiology, 11, 652617. Tarmbakterien Desulfovibrio kopplas till mekanismer som kan orsaka toxisk ansamling av ”Parkinsonproteinet” alfa-synuclein.
    14. Zhan, X., Stamova, B., & Sharp, F. R. (2018). Lipopolysaccharide Associates with Amyloid Plaques, Neurons and Oligodendrocytes in Alzheimer's Disease Brain: A Review. Frontiers in aging neuroscience, 10, 42. LPS är associerat till “Alzheimerproteinet” amyloid.
    15. Kim, H. S., Kim, S., Shin, S. J., Park, Y. H., Nam, Y., Kim, C. W., Lee, K. W., Kim, S. M., Jung, I. D., Yang, H. D., Park, Y. M., & Moon, M. (2021). Gram-negative bacteria and their lipopolysaccharides in Alzheimer's disease: pathologic roles and therapeutic implications. Translational neurodegeneration, 10(1), 49. Den patologirelaterade lokaliseringen av LPS inom CNS vid Alzheimers sjukdom antyder att LPS har en unik patologisk roll vid Alzheimers sjukdom. Dessutom är LPS direkt involverad i patologin, inklusive neuroinflammation genom mikrogliala TLR4 och induktion av neuronal celldöd via neuronal TLR4.
    16. Lukiw W. J. (2016). Bacteroides fragilis Lipopolysaccharide and Inflammatory Signaling in Alzheimer's Disease. Frontiers in microbiology, 7, 1544. LPS från tarmbakterien Bacteroides fragilis är associerat till Alzheimersjukdomen.
    17. Pogue, A. I., Jaber, V. R., Sharfman, N. M., Zhao, Y., & Lukiw, W. J. (2022). Downregulation of Neurofilament Light Chain Expression in Human Neuronal-Glial Cell Co-Cultures by a Microbiome-Derived Lipopolysaccharide-Induced miRNA-30b-5p. Frontiers in neurology, 13, 900048. LPS orsakar en svaghet i nervcellers inre skelettstruktur.
    18. Sroka, N., Rydzewska-Rosołowska, A., Kakareko, K., Rosołowski, M., Głowińska, I., & Hryszko, T. (2022). Show Me What You Have Inside-The Complex Interplay between SIBO and Multiple Medical Conditions-A Systematic Review. Nutrients, 15(1), 90. Flera studier bekräftar samband mellan SIBO och matsmältnings-, kardiovaskulära, endokrina, neurologiska, njurmedicinska, bindvävs- och dermatologiska störningar. Ytterligare forskning är dock avgörande för att verifiera de många facetterna av SIBO. Antibiotikabehandling kan minska inte bara mag-tarmsymtom utan också manifestationer av annan patologi, med förbättrad livskvalitet till följd. Detta skulle kunna skapa nya behandlingsriktningar för många välkända sjukdomar.
    19. Parodi, A., Paolino, S., Greco, A., Drago, F., Mansi, C., Rebora, A., Parodi, A., & Savarino, V. (2008). Small intestinal bacterial overgrowth in rosacea: clinical effectiveness of its eradication. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 6(7), 759–764. Prevalensen av SIBO var högre hos patienter med rosacea (52 av 113 personer) jämfört med kontrollerna (3 av 60 personer). Efter rifaximinbehandling försvann de kutana lesionerna hos 20 av de 28 personer med rosacea som blev randomiserade till antibiotikabehandling och förbättrades avsevärt hos 6 av dessa 28 personer. Denna studie visade att rosaceapatienter har en signifikant högre SIBO-prevalens än kontroller. De som förblev SIBO-negativa hade en nästan fullständig regression av deras rosacea och bibehöll detta resultat i minst 9 månader
    20. Weinstock, L. B., & Steinhoff, M. (2013). Rosacea and small intestinal bacterial overgrowth: prevalence and response to rifaximin. Journal of the American Academy of Dermatology, 68(5), 875–876. Totalt 32 av 63 patienter med rosacea hade SIBO jämfört med 7 av 30 kontrollpersoner från allmänheten och 3 av 30 helt friska kontrollpersoner. Av de 32 patienterna med SIBO behandlades 28 med rifaximin; 46 % rapporterade lindrad eller markant förbättrad rosacea, 25 % rapporterade måttligt förbättrad rosacea och 11 % rapporterade lindrigt förbättrad rosacea. Alla fyra patienter med okulär rosacea och SIBO rapporterade markant förbättring. Rosacea var oförändrad hos 18 % av patienterna.
    21. Drago, F. et al. The role of small intestinal bacterial overgrwoth in rosaca: A 3-year follow up. J. Am Acad Dermatol Sept 2016. 3-års uppföljning av patienter med rosacea och som fått rifaximin visade att 64% av patienterna fortfarande var i remission. SIBO verkar spela en roll för initiering av rosacea och 10 dagars rifaximinbehandling visade sig vara effektivt för att hålla rosacea under kontroll upp till 3 år.
    22. Drago, F., Ciccarese, G., Indemini, E., Savarino, V., & Parodi, A. (2018). Psoriasis and small intestine bacterial overgrowth. International journal of dermatology, 57(1), 112–113. Patienter med psoriasis samt rosacea kan gynnas av SIBO-behandling.
    23. Chedid, V., Dhalla, S., Clarke, J. O., Roland, B. C., Dunbar, K. B., Koh, J., Justino, E., Tomakin, E., & Mullin, G. E. (2014). Herbal therapy is equivalent to rifaximin for the treatment of small intestinal bacterial overgrowth. Global advances in health and medicine, 3(3), 16–24. Botaniska tillskott med bakteriehämmande egenskaper kan vara lika effektiva vid SIBO som rifaximin.