Mold Toxins and Gut Health

Mold Toxins and Gut Health

Mold Toxins and Gut Health

There has been a lot of attention on microplastics, PFAS, pesticides such as glyphosate, and food additives, and on how they may affect human health. But one major category of exposure is often overlooked:

👉 Mycotoxins—toxic compounds produced by molds that can contaminate food.

Most people think mold exposure comes from damp homes or water-damaged buildings. However, research shows that food—especially processed and widely distributed foods—may be one of the primary sources of exposure.¹

🌾 What Is Deoxynivalenol (DON)?

One of the most common mycotoxins found in food is deoxynivalenol (DON), also known as “Vomitoxin.”

It is produced by Fusarium molds, which frequently contaminate crops like:

  • Wheat
  • Oats
  • Corn
  • Processed grain-based foods

DON and related toxins are among the most prevalent contaminants in the global food supply.¹⁷-¹⁹

🧠 Why This Matters for Gut Health

Conditions like:

  • Crohn’s disease (CD)
  • Celiac disease
  • Irritable bowel syndrome (IBS)

are complex and influenced by many factors, including genetics, diet, environment, and the gut microbiome.²-⁴

Recent research shows that people with these conditions often have:

  • Reduced beneficial bacteria
  • Increased harmful bacteria (e.g., E. coli, Shigella)
  • Increased fungal organisms (e.g., Candida)

This imbalance is known as dysbiosis.⁵-¹⁴

Interestingly, healthy individuals tend to have the opposite pattern—more bacterial diversity and less fungal overgrowth.¹⁵,¹⁶

🍄 Where Do Mycotoxins Fit In?

Some researchers are now asking:

👉 Could foodborne mold toxins be contributing to this imbalance?

Mycotoxins are not just passive contaminants—they may act as “survival tools” for fungi, helping them:

  • Compete with other microbes
  • Disrupt bacterial populations
  • Secure their place in the environment

This raises concern that chronic dietary exposure could influence the gut microbiome, especially in vulnerable individuals.¹⁷-²⁰

🔬 What Happens in the Gut?

Emerging research suggests DON may affect the gut in several important ways:

1. Weakening the Gut Barrier

DON may reduce the number of cells that produce protective mucus in the intestines.²³-²⁵

👉 This can weaken the gut’s natural defense system.

2. Increasing “Leaky Gut”

DON may disrupt tight junction proteins that hold intestinal cells together, increasing permeability.²³,²⁸

👉 This may allow:

  • Toxins
  • Bacteria
  • Food particles

to pass into the bloodstream more easily.³⁰

3. Triggering Inflammation

Once absorbed, DON may activate the immune system and increase inflammatory signals such as:

  • TNF-α
  • IL-6
  • IFN-γ

These are the same types of inflammatory pathways seen in IBD and other GI conditions.²³,³²,³³

4. Altering the Microbiome

DON exposure has been shown to change gut microbial populations, potentially worsening dysbiosis.²⁶

5. Affecting Digestion and Absorption

DON may interfere with nutrient absorption and contribute to:

  • Diarrhea
  • Malabsorption
  • GI discomfort

³⁴,³⁵

⚠️ Why Children May Be More Vulnerable

Children often consume large amounts of grain-based foods relative to their body weight.

This means they may be exposed to higher levels of DON per kilogram of body weight, sometimes exceeding recommended intake levels.³⁷

📊 Exposure Is Hard to Avoid

DON is difficult to eliminate because:

  • It can form in the field and during storage
  • It is stable under heat and processing
  • It is often invisible and undetectable without testing

This means contamination can occur from farm to table.²⁹,⁴⁰-⁴²

 

🧠 So… Is There a Connection?

At this time, we cannot say that DON directly causes diseases like Crohn’s, Celiac, or IBS.

However, the evidence suggests:

👉 DON may contribute to:

  • Gut barrier dysfunction
  • Immune activation
  • Microbial imbalance

—all of which are hallmarks of these conditions.

🌱 What Can You Do?

While exposure cannot be completely avoided, you can take steps to reduce risk:

  • Limit highly processed grain-based foods
  • Choose high-quality, tested food sources when possible
  • Store food properly (cool, dry conditions)
  • Focus on a diverse, whole-food diet

💬 Final Thoughts

Chronic, low-dose exposure to mycotoxins like DON is an emerging area of research, especially in relation to gut health.

For individuals with IBD, IBS, or Celiac disease, reducing dietary toxin exposure may be an important—and often overlooked—piece of the puzzle.

More research is needed, but the question remains:

👉 Are we fully considering what’s in our food—and how it affects our health?

 References
1. Keller NP, Turner G, Bennett JW. Fungal secondary metabolism - from biochemistry to genomics. Nat Rev Microbiol. 2005;3(12):937–947.
2. Dicksved J, Halfvarson J, Rosenquist M, et al. Molecular analysis of the gut microbiota of identical twins with Crohn's disease. ISME J. 2008;2(7):716–727.
3. Hrncirova L, Machova V, Trckova E, Krejsek J, Hrncir T. Food preservatives induce proteobacteria dysbiosis in human-microbiota associated Nod2-deficient mice. Microorganisms. 2019;7(10):10.3390/microorganisms7100383.
4. Lee D, Swan CK, Suskind D, et al. Children with crohn's disease frequently consume select food additives. Dig Dis Sci. 2018;63(10):2722–2728.
5. Chehoud C, Albenberg LG, Judge C, et al. Fungal signature in the gut microbiota of pediatric patients with inflammatory bowel disease. Inflamm Bowel Dis. 2015;21(8):1948–1956.
6. El Mouzan M, Korolev KS, Al Mofarreh MA, et al. Fungal dysbiosis predicts the diagnosis of pediatric Crohn's disease. World J Gastroenterol. 2018;24(39):4510–4516.
7. Hoarau G, Mukherjee PK, Gower-Rousseau C, et al. Bacteriome and mycobiome interactions underscore microbial dysbiosis in familial Crohn's disease. mBio. 2016;7(5):10.1128/mBio.01250–16.
8. Liguori G, Lamas B, Richard ML, et al. Fungal dysbiosis in mucosa-associated microbiota of Crohn's disease patients. J Crohns Colitis. 2016;10(3):296–305.
9. Nelson A, Stewart CJ, Kennedy NA, et al. The impact of NOD2 genetic variants on the gut mycobiota in Crohn's disease patients in remission and individuals without gastrointestinal inflammation. J Crohns Colitis. 2020.
10. Sokol H, Leducq V, Aschard H, et al. Fungal microbiota dysbiosis in IBD. Gut. 2017;66(6):1039–1048. doi: 10.1136/gutjnl-2015-310746.
11. El Mouzan M, Al-Hussaini A, Fanelli B, et al. Fungal dysbiosis in children with celiac disease. Dig Dis Sci. 2022;67(1):216–223. doi: 10.1007/s10620-021-06823-8.
12. Imhann F, Vich Vila A, Bonder MJ, et al. Interplay of host genetics and gut microbiota underlying the onset and clinical presentation of inflammatory bowel disease. Gut. 2018;67(1):108–119.
13. Mukhopadhya I, Hansen R, Meharg C, et al. The fungal microbiota of de-novo paediatric inflammatory bowel disease. Microbes Infect. 2015;17(4):304–310.
14. Tenailleau QM, Lanier C, Gower-Rousseau C, Cuny D, Deram A, Occelli F. Crohn's disease and environmental contamination: Current challenges and perspectives in exposure evaluation. Environ Pollut. 2020;263(Pt B):114599.
15. Auchtung TA, Fofanova TY, Stewart CJ, et al. Investigating colonization of the healthy adult gastrointestinal tract by fungi. mSphere. 2018;3(2):10.1128/mSphere.00092–Apr.
16. Nash AK, Auchtung TA, Wong MC, et al. The gut mycobiome of the human microbiome project healthy cohort. Microbiome. 2017;5(1):153–4.
17. Maresca M, Fantini J. Some food-associated mycotoxins as potential risk factors in humans predisposed to chronic intestinal inflammatory diseases. Toxicon. 2010;56(3):282–294.
18. Pestka JJ. Deoxynivalenol-induced proinflammatory gene expression: Mechanisms and pathological sequelae. Toxins (Basel). 2010;2(6):1300–1317.
19. Pestka JJ. Deoxynivalenol: Mechanisms of action, human exposure, and toxicological relevance. Arch Toxicol. 2010;84(9):663–679.
20. Venkatesh N, Keller NP. Mycotoxins in conversation with bacteria and fungi. Front Microbiol. 2019;10:403.
21. Food and Agriculture Organization of the United Nations, World Health Organization. Code of practice for the prevention and reduction of mycotoxin contamination in cereals. 2016:1–16.
22. Bennett JW, Klich M. Mycotoxins. Clin Microbiol Rev. 2003;16(3):497–516.
23. Bracarense AP, Lucioli J, Grenier B, et al. Chronic ingestion of deoxynivalenol and fumonisin, alone or in interaction, induces morphological and immunological changes in the intestine of piglets. Br J Nutr. 2012;107(12):1776–1786.
24. Pinton P, Graziani F, Pujol A, et al. Deoxynivalenol inhibits the expression by goblet cells of intestinal mucins through a PKR and MAP kinase dependent repression of the resistin-like molecule beta. Mol Nutr Food Res. 2015;59(6):1076–1087.
25. Robert H, Payros D, Pinton P, Theodorou V, Mercier-Bonin M, Oswald IP. Impact of mycotoxins on the intestine: Are mucus and microbiota new targets? J Toxicol Environ Health B Crit Rev. 2017;20(5):249–275.
26. Saint-Cyr MJ, Perrin-Guyomard A, Houee P, Rolland JG, Laurentie M. Evaluation of an oral subchronic exposure of deoxynivalenol on the composition of human gut microbiota in a model of human microbiota-associated rats. PLoS One. 2013;8(11):e80578.
27. Pestka JJ. Mechanisms of deoxynivalenol-induced gene expression and apoptosis. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2008;25(9):1128–1140.
28. De Walle JV, Sergent T, Piront N, Toussaint O, Schneider YJ, Larondelle Y. Deoxynivalenol affects in vitro intestinal epithelial cell barrier integrity through inhibition of protein synthesis. Toxicol Appl Pharmacol. 2010;245(3):291–298.
29. Pinton P, Tsybulskyy D, Lucioli J, et al. Toxicity of deoxynivalenol and its acetylated derivatives on the intestine: Differential effects on morphology, barrier function, tight junction proteins, and mitogen-activated protein kinases. Toxicol Sci. 2012;130(1):180–190.
30. Park SH, Kim D, Kim J, Moon Y. Effects of mycotoxins on mucosal microbial infection and related pathogenesis. Toxins (Basel). 2015;7(11):4484–4502.
31. Akbari P, Braber S, Varasteh S, Alizadeh A, Garssen J, Fink-Gremmels J. The intestinal barrier as an emerging target in the toxicological assessment of mycotoxins. Arch Toxicol. 2017;91(3):1007–1029.
32. Al-Sadi R, Boivin M, Ma T. Mechanism of cytokine modulation of epithelial tight junction barrier. Front Biosci (Landmark Ed). 2009;14:2765–2778.
33. Cano PM, Seeboth J, Meurens F, et al. Deoxynivalenol as a new factor in the persistence of intestinal inflammatory diseases: An emerging hypothesis through possible modulation of Th17-mediated response. PLoS One. 2013;8(1):e53647.
34. Grenier B, Applegate TJ. Modulation of intestinal functions following mycotoxin ingestion: Meta-analysis of published experiments in animals. Toxins (Basel). 2013;5(2):396–430.
35. Maresca M, Mahfoud R, Garmy N, Fantini J. The mycotoxin deoxynivalenol affects nutrient absorption in human intestinal epithelial cells. J Nutr. 2002;132(9):2723–2731.
36. Food and Drug Administration. Guidance for industry and FDA: Advisory levels for deoxynivalenol (DON) in finished wheat products for human consumption and grains and grain by-products used for animal feed. 2010;FDA-2013-S-0610.
37. Mishra S, Srivastava S, Dewangan J, Divakar A, Kumar Rath S. Global occurrence of deoxynivalenol in food commodities and exposure risk assessment in humans in the last decade: A survey. Crit Rev Food Sci Nutr. 2019:1–29.
38. Brotherton CS, Taylor AG, Keeling A. Fire in the belly and the professionalization of nurses: A historical analysis of Crohn disease care. Gastroenterol Nurs. 2013;36(1):21–28.
39. Hostess C. Our story. https://www.hostesscakes.com/more-to-love/. Updated 2021.
40. Food and Agriculture Organization of the United Nations, World Health Organization. Code of practice for the prevention and reduction of mycotoxin contamination in cereals (CXC 51-2003). 2016; CXC 51-2003.
41. Pestka JJ, Uzarski RL, Islam Z. Induction of apoptosis and cytokine production in the jurkat human T cells by deoxynivalenol: Role of mitogen-activated protein kinases and comparison to other 8-ketotrichothecenes. Toxicology. 2005;206(2):207–219.
42. Alshannaq A, Yu JH. Occurrence, toxicity, and analysis of major mycotoxins in food. Int J Environ Res Public Health. 2017;14(6):10.3390/ijerph14060632.