Mould Illness and SIBO: The Hidden Connection Your Doctor Is Missing
If you've been through the rounds — treated for SIBO, seen some improvement, but keep relapsing — there's a question I find myself asking more and more in clinic: have you been exposed to mould?
Over the years, working with complex gut cases, I've noticed a striking pattern. People with a history of living or working in water-damaged buildings, or who test positive for mycotoxins, often have stubborn, recurrent gut problems — bloating, distension, altered motility, food intolerances — that don't fully resolve until the mould exposure is addressed. When I dig into the research, it turns out this connection is not just clinical intuition. There's a growing body of evidence suggesting that mycotoxins — the toxic compounds produced by moulds — may be a significant, under-appreciated driver of SIBO.
In this article, I want to walk you through the biology of why that might be.
First, what is SIBO?
SIBO stands for Small Intestinal Bacterial Overgrowth. Your small intestine is supposed to be a relatively low-bacteria environment — its job is to absorb nutrients, and a large bacterial population interferes with that. In health, several defence mechanisms keep the small intestine clean: stomach acid, bile, pancreatic enzymes, and crucially, a wave-like muscular cleaning action called the migrating motor complex (MMC). If these mechanisms fail — including gastric acid, bile, and pancreatic enzymes — the likelihood of developing SIBO increases.
When bacteria overpopulate the small intestine, the result is fermentation of carbohydrates where it shouldn't be happening, producing gases like hydrogen and methane. The hallmark symptoms are bloating, distension (often worse as the day goes on), belching, altered bowel habits, and nutrient malabsorption. SIBO is strongly linked to IBS, and the two conditions significantly overlap.
What are mycotoxins, and where do they come from?
Mycotoxins are toxic secondary metabolites produced by moulds. You can be exposed to them in two main ways: through contaminated food (particularly grains, nuts, coffee, dried fruits, and corn) and through inhalation in water-damaged buildings.
The most clinically significant mycotoxins include:
Aflatoxin
Ochratoxin A (OTA)
Zearalenone
Gliotoxin
Citrinin
Trichothecenes
The Gut as Ground Zero for Mycotoxin Damage
The gastrointestinal tract is the first place mycotoxins land when you ingest contaminated food, and the last place they land before elimination when you’ve been breathing them in, in a water damaged building. The gut bears the brunt of their effects. Mycotoxins are not passive passengers passing through your gut — they actively disrupt its structure and function in several key ways.
1. Mycotoxins Damage the Gut Lining
The intestinal lining is your body's primary barrier against pathogens and foreign molecules. Every gut cell is joined to its neighbour by tight junctions — molecular "zips" that seal the gaps between cells. An impairment of the barrier function of the epithelial lining cells and the sealing tight junction proteins has been noted, as this could result in an increased translocation of luminal antigens and pathogens and an excessive activation of the immune system.
Research has demonstrated that trichothecenes, fumonisins, and aflatoxins interfere with the proteins that link epithelial cells together. These effects increase intestinal permeability, causing leaky gut and rendering the gut vulnerable to infection.
When the gut lining is compromised in this way, bacteria that should stay in the colon can migrate upward. The immune system becomes chronically activated. The environment inside the small intestine shifts in ways that favour bacterial overgrowth.
2. Mycotoxins Drive Dysbiosis
A healthy gut microbiome is one of your best defences against mycotoxin toxicity — certain beneficial bacteria can actually break down and neutralise mycotoxins. But here's the vicious cycle: mycotoxins simultaneously destroy the very microbiome you need to deal with them.
Mycotoxins contribute to dysbiosis by suppressing beneficial bacteria such as Lactobacillus and Bifidobacterium while promoting the overgrowth of inflammatory species like Escherichia coli and Clostridium perfringens.
Mycotoxin exposure also impairs the production of short-chain fatty acids (SCFAs), notably butyrate, acetate, and propionate, by altering the activity of fermentative microbial communities. Reduced SCFA availability can compromise epithelial energy supply, disrupt mucosal repair mechanisms, and diminish anti-inflammatory signalling.
This dysbiosis creates a permissive environment for the wrong bacteria to colonise the wrong part of the gut. SIBO is, at its core, a problem of bacteria being where they shouldn't be — and mycotoxin-driven dysbiosis helps set the stage.
3. Mycotoxins Interfere with Gut Motility and the MMC
This is one of the mechanisms I find most compelling clinically.
As I mentioned above, your small intestine has a self-cleaning mechanism called the migrating motor complex — a wave of muscular contractions that sweeps bacteria and food debris from the small intestine into the colon during the fasting state (between meals). The MMC serves to transport bacteria from the small intestine to the large intestine and to inhibit the migration of colonic bacteria into the terminal ileum; an impairment to the MMC typically results in small intestinal bacterial overgrowth.
Available data allow the conclusion to be drawn that impaired intestinal motility, as evidenced by attenuated migrating motor complex activity, results in bacterial overgrowth.
So what do mycotoxins have to do with the MMC? This is where things get particularly interesting. Research has found that DON (deoxynivalenol) directly disrupts gut motor activity through its effects on serotonin signalling. Deoxynivalenol inhibits gastric emptying by inducing intestinal migrating motor complexes through a peripheral action at the serotonin-3 receptors. In other words, DON effectively hijacks the neurochemistry that controls gut motility.
Serotonin is not just a mood chemical — approximately 90% of the body's serotonin is made in the gut, and it plays a central role in coordinating peristalsis and MMC activity. When mycotoxins dysregulate serotonin pathways in the enteric nervous system, the self-cleaning mechanism of the small intestine becomes impaired. Bacteria accumulate. SIBO develops or persists.
Furthermore, some studies have indicated that mycotoxins may affect the morphology and neurochemical character of the enteric neurons. The enteric nervous system — sometimes called the "second brain" — is the nerve network embedded in the gut wall. If mycotoxins damage enteric neurons, the consequences for motility could be long-lasting.
Mould and mycotoxins are specifically recognised as potential causes of MMC impairment within expert SIBO literature, sitting alongside other known disruptors such as VIP dysregulation, mast cell activation, and autonomic nervous system dysfunction.
The Bile Connection: A Central Piece of the Puzzle
Of all the mechanisms linking mycotoxins to SIBO, I believe the bile axis is the most underappreciated — and potentially the most important.
Bile is produced in the liver and stored in the gallbladder. When you eat fat, bile is released into the small intestine, where it emulsifies fats to allow absorption. But bile does far more than digest fat. Bile acid pool size and composition regulate gut microbial ecology by exerting direct antimicrobial effects on intestinal microbes via their detergent properties and indirect effects by inducing the production of antimicrobial peptides and regulating host immunity. The antimicrobial activity of bile acids is demonstrated in rodent models of biliary obstruction and liver injury, which results in small intestinal bacterial overgrowth that can be reversed by administration of bile acids.
Read that again: reducing bile flow can directly cause SIBO, and restoring bile flow reverses it. This is a fundamental but widely overlooked mechanism.
Now here is the connection to mould: mycotoxins are highly lipophilic (fat-soluble) toxins. They are processed primarily through the liver, via the same phase I and phase II detoxification pathways that handle other environmental toxins. Phase III liver detoxification involves the transport and elimination of conjugated toxins out of hepatocytes, primarily into the bile or urine for excretion, ensuring their removal from the body.
In other words, bile is a key excretion route for mycotoxins. When your body is dealing with a significant mycotoxin burden, it is actively using bile to remove these toxins. The research is clear on this:
Hepatocytes synthesise bile acids, and bile acids can degrade endotoxin, combine with mycotoxins (mycotoxins have lipophilicity), improve the ability of enzymes to degrade toxins, and convert endotoxin and mycotoxins into non-toxic substances, which will be excreted with the faeces.
Furthermore, bile acid activates FXR, and the activated FXR promotes the decomposition of T-2 toxin under the detoxification effect of the liver.
Here is where the problem compounds: mycotoxins themselves are known to impair liver function and alter bile acid metabolism. Mycotoxins interfere with bile acid metabolism, shifting the balance between primary and secondary bile acids, which further influences microbial composition, nutrient absorption, and intestinal barrier stability.
Mycotoxins can lead to bile acid synthesis and excretion disorder, detoxification dysfunction, free radical metabolism and immune disorders, oxidative stress and inflammatory response.
So mycotoxins impair the liver's ability to produce and process bile; reduced bile output means reduced antimicrobial protection in the small intestine; and the same bacteria that should be cleared can now proliferate. You end up with a perfect storm: mycotoxins compromise the bile system that is supposed to both detoxify mycotoxins and protect against SIBO.
This is a mechanism I see playing out repeatedly in clinical practice.
Mycotoxins and the Immune System: Fuelling the Fire
One more mechanism worth understanding is the relationship between mycotoxins, immune dysfunction, and the gut environment.
Mycotoxin exposure may directly increase susceptibility to bacterial, viral, and parasitic gut infections by decreasing intestinal immunity.
Mycotoxins affect the immune system and promote intestinal inflammation. This chronic inflammatory state in the gut contributes to altered motility, disrupted barrier function, and — ultimately — conditions that favour bacterial overgrowth.
There is also an important bidirectional relationship here. Patients with pre-existing gut issues such as irritable bowel syndrome (IBS) and SIBO may be more severely impacted by mycotoxin exposure than people with a healthy gut microbiota, due to changes in their gut bacteria that reduce their detoxification capacity.
This means the relationship between mould illness and SIBO is not simply a one-way street. Poor gut health makes you more vulnerable to mycotoxin damage; mycotoxin exposure makes your gut health worse. Each amplifies the other.
Putting It All Together: The Mould-SIBO Connection
Let me draw the threads together.
If you've been exposed to mycotoxins — whether through a water-damaged building or chronic dietary exposure — here is how the cascade toward SIBO may unfold:
Mycotoxins enter the gut → damage tight junctions and the gut lining → drive dysbiosis and suppress beneficial bacteria → impair enteric nervous system function and serotonin signalling → disrupt the MMC, allowing bacteria to accumulate in the small intestine → simultaneously burden the liver and impair bile production and secretion → reduce bile's natural antimicrobial protection in the small intestine → SIBO develops or becomes resistant to treatment.
This is not a theoretical model — each step in this chain is supported by peer-reviewed research. What is still needed are large-scale human clinical trials directly documenting the mycotoxin → SIBO pathway, and this remains an important gap in the literature. But from a mechanistic and clinical standpoint, the connection is compelling, and the pattern I see in practice is consistent with what the research predicts.
Could Mould Be the Reason Your SIBO Keeps Coming Back?
If you find that:
Your SIBO symptoms improve with treatment but keep returning
You have a history of living or working in a water-damaged building
You have unexplained fatigue, brain fog, and chemical sensitivities alongside your gut symptoms
You have a sluggish liver, poor fat digestion, or a history of gallbladder problems
Your gut symptoms are accompanied by hormonal or immune dysfunction
…then it's worth asking whether mould illness could be part of your picture.
🧪 Think You Might Have SIBO? Get Tested.
The only way to know whether SIBO is contributing to your symptoms is to test for it. A breath test measures the gases produced by bacteria in the small intestine — hydrogen and methane — and is the gold-standard non-invasive diagnostic tool for SIBO.
Order the Healthpath SIBO Breath Test here.
Testing gives you and your practitioner the information needed to understand what you're actually dealing with — because treating symptoms without a clear diagnosis is guesswork.
Want to Go Deeper?
If you suspect both mould illness and SIBO are part of your story, this is exactly the kind of complex, overlapping presentation we work with every day. Understanding how these two conditions reinforce each other — and addressing both systematically — is essential for lasting recovery.
Want to learn more. Explore The Mould Mastery Programme.
References
Knez E, Kadac-Czapska K, Grembecka M. The importance of food quality, gut motility, and microbiome in SIBO development and treatment. Nutrition. 2024;124:112464.
Scarpellini E, et al. Small Intestinal Bacterial Overgrowth (SIBO) and Twelve Groups of Related Diseases — Current State of Knowledge. International Journal of Molecular Sciences. 2024. PMC11117733.
Ridlon JM, et al. Bile acids as modulators of gut microbiota composition and function. Gut Microbes. 2023;15(1):2172671.
Deloose E, et al. The migrating motor complex: control mechanisms and its role in health and disease. Nature Reviews Gastroenterology & Hepatology. 2012;9:271–285.
Fung TC, et al. Gastrointestinal motility disorders and bacterial overgrowth. Gastroenterology. 1995. PMID: 7714466.
Trabelsi H, et al. Mycotoxins and the Enteric Nervous System. International Journal of Molecular Sciences. 2020. PMC7404981.
Dong F, et al. Microbiome–mycotoxin interactions and probiotic strategies: implications for gut health and cancer. Frontiers in Nutrition. 2026. PMC12975935.
Pinton P, Oswald IP. The intestinal barrier as an emerging target in the toxicological assessment of mycotoxins. Archives of Toxicology. 2016. PMID: 27417439.
Wan MLY, et al. Mycotoxin: Its Impact on Gut Health and Microbiota. Frontiers in Cellular and Infection Microbiology. 2018. PMC5834427.
Pestka JJ, et al. The mycotoxin deoxynivalenol delays gastric emptying through serotonin-3 receptors in rodents. European Journal of Pharmacology. 1993. PMID: 8371135.
Doi K. Neurotoxicological effects of mycotoxins on humans and methods of neuroprotection. Toxins. 2025;17(1):24.
He S. Study on accelerating the decomposition of mycotoxins: bile acids and mycotoxin detoxification. Huazhong Agricultural University / AllAboutFeed. 2023.
Bail A, et al. Bile acids: minimising mycotoxin damage in poultry diets. All About Feed. 2023.
Mosaic Diagnostics. The Liver: Its Important Role in Detoxification. 2024. mosaicdx.com.
Janik E, et al. Mycotoxin and Gut Microbiota Interactions. Toxins. 2020. PMC7761905.
Kashyap PC, et al. Critical appraisal of the SIBO hypothesis and breath testing: A clinical practice update. Neurogastroenterology & Motility. 2024;36:e14817.
