Gastrointestinal Health

Exposure-Oriented Connection

Assessing mycotoxin burden that may help contextualize gut barrier dysfunction
and persistent GI symptoms. 

Evaluates mycotoxin exposure via both inhalational and dietary routes.

Mycotoxins—metabolites of molds such as Aspergillus, Fusarium, and Stachybotrys—are increasingly recognized as a contributor to chronic, treatment-resistant GI presentations, including intestinal barrier dysfunction and IBD[1,3,4]. 

The MycoTOX Profile is a urine-based LC-MS/MS assay measuring mycotoxins across the major toxigenic classes, designed to help clinicians uncover mycotoxin exposure and guide a therapeutic strategy for prevention and treatment.[1–5]

Explore the MycoTOX Profile

When to Consider MycoTOX Profile

What the MycoTOX Profile Measures

Clinical Applications & Evidence Context

How the MycoTOX Profile Supports Clinical Reasoning

How to Order the MycoTOX Profile

References

When Might Providers Consider the MycoTOX Profile?

Neurologic & Mental Health – Exposure-Oriented Connection1

IBD or Relapsing GI Presentations with Environmental Exposure History:Known or suspected mold/water-damaged building exposure in patients with Crohn’s disease, ulcerative colitis, or other relapsing GI symptoms.[3,4,5]

Dysbiosis-Pattern GI Symptoms with Environmental Exposure History: Bloating or altered bowel habits in patients with water-damaged building occupancy or high-mold-exposure food sources.[1]

Intestinal Permeability (“Leaky Gut”) Presentations: GI complaints with systemic immune or sensitivity patterns suggestive of impaired mucosal barrier integrity.[1,3,4]

GI Symptoms with Overlapping Systemic Features: GI complaints co-occurring with fatigue, cognitive changes, or mood symptoms suggestive of a broader mycotoxin burden[6].

Selected AnalytesEveryday Exposure SourcesGI Relevance
AflatoxinsPeanuts, tree nuts, corn, and other commodities with fungal contamination.[6]Primarily hepatotoxic; given close enterohepatic circulation between liver and gut, elevated aflatoxin burden may be a relevant consideration in patients with GI symptoms alongside signs of impaired detoxification capacity.[6]
Ochratoxin AGrain-based foods, coffee, dried fruits, spices; indoor mold environments.[6]The most prevalent mycotoxin in this class; primarily nephrotoxic. May add context on total mycotoxin/detoxification burden in patients with complex, multisystem GI presentations.[6]
Trichothecenes (Roridin E, Verrucarin A)Water-damaged building materials, particularly Stachybotrys-contaminated substrates; contaminated grains and cereal products more broadly across the trichothecene class.[6]Trichothecenes, including the macrocyclic forms measured on this panel, act as potent ribosome-inactivating agents; documented to disrupt intestinal tight-junction proteins and epithelial barrier integrity across the trichothecene class. Most direct mechanistic evidence for barrier dysfunction and dysbiosis-pattern GI symptoms among the analytes on this panel.[1,3,4]
ZearalenoneGrains and grain-derived products; water-damaged building environments.[6]Known primarily for endocrine-disrupting and reproductive effects; may help contextualize overlapping endocrine and GI symptom presentations during mold-related workup.[6]
Other (e.g., Enniatin B)Indoor mold environments, particularly Aspergillus, Chaetomium, and Fusarium species.[6]Enniatin B has been shown in vitro to modulate the GI toxicity of co-occurring trichothecenes on intestinal epithelial cells[2]; gliotoxin, mycophenolic acid, chaetoglobosin, sterigmatocystin, and citrinin add immunosuppressive and broader mold-burden context relevant to complex, treatment-resistant GI presentations.

ConditionClinical Encapsulation

Inflammatory Bowel Disease (Crohn’s Disease & Ulcerative Colitis)
Trichothecene mycotoxins, including the macrocyclic forms measured on this panel, have been shown in experimental and mechanistic models to impair intestinal tight-junction integrity and activate inflammatory signaling pathways, supporting a possible toxin-driven contributor in complex or relapsing IBD presentations.[3,4,5]

Intestinal Permeability (“Leaky Gut”)
Mycotoxins, including trichothecenes, have documented effects on gut epithelial barrier integrity and microbiota composition in experimental models, offering context for a toxicant-driven contributor to barrier dysfunction.[1,3,4]

Dysbiosis-Pattern GI Symptoms with Mold Exposure History
Patients with known or suspected mold exposure (water-damaged buildings, high-humidity environments, contaminated food) presenting with bloating or altered bowel habits may benefit from mycotoxin burden assessment, given documented effects on gut microbiota composition.[1]

Combined / Co-Occurring Mycotoxin Exposure
Mycotoxins frequently co-occur in food and water-damaged environments; enniatin B has been shown in vitro to modulate the gastrointestinal toxicity of co-occurring trichothecenes on intestinal epithelial cells, suggesting combined mycotoxin exposure may alter net GI toxic burden relative to single-toxin exposure.[2]

Adds Exposure Context

Adds mycotoxin data that may be considered alongside water-damaged, occupational, or dietary exposure history in patients with persistent or unexplained GI symptoms[1,6].

Mechanistic Pathway Context

Detection of specific mycotoxin classes may help contextualize biologically plausible mechanisms—including intestinal tight-junction disruption, oxidative stress, and gut microbiota dysbiosis—that are relevant to the patient’s GI symptom profile[1,3,4].

Multi-Route Exposure Assessment

MycoTOX Profile evaluates mycotoxin exposure via both inhalational (water-damaged environments) and dietary routes, broadening the clinical utility of exposure-history interpretation for GI presentations[1,6].

How to Order

Neurologic & Mental Health – Exposure-Oriented Connection1

To order the MycoTOX Profile, register for a portal account. Specimen collection kits and requisition forms are available through your account portal. For clinical support or interpretation questions, contact our clinical education team.

Order the MycoTOX Profile

Explore Other Gastrointestinal Health Lenses:

Exposure-Oriented
Connection
Metabolic
Connection
Gut-Brain
Connection
Food-Related
Connection
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This webpage is intended for licensed healthcare professionals and is for informational and educational purposes only. The test results are not intended to diagnose, treat, cure, or prevent disease. All clinical interpretation should be done by a qualified healthcare professional in the context of the individual patient. Statements regarding associations between health symptoms and conditions do not constitute diagnostic claims.

References

  1. Children’s Hospital of Philadelphia (CHOP). Autism’s Clinical Companions: Frequent Comorbidities in ASD. https://www.chop.edu/news/autism-s-clinical-companions-frequent-comorbidities-asd 
  2. Raiola A, et al. Ochratoxin A, Gut Permeability, and Tight Junction Disruption. PMC12197389. https://pmc.ncbi.nlm.nih.gov/articles/PMC12197389/ 
  3. Malík M, Tlustoš P. Ochratoxin A Neurotoxicity — Dopamine, Hippocampal Neurogenesis, and Cognitive Impairment. PMC11962726. https://pmc.ncbi.nlm.nih.gov/articles/PMC11962726/ 
  4. Ratnaseelan AM, et al. Effects of Mycotoxins on Neuropsychiatric Symptoms and Neurotransmitter Systems. LIDSEN J Neurobiol. 2018;10(1):322. https://www.lidsen.com/journals/neurobiology/neurobiology-10-01-322 
  5. Harding CF, Pytte CL, Page KG, et al. Mold inhalation causes innate immune activation, neural, cognitive and emotional dysfunction. Brain Behav Immun. 2020;87:218-228. doi:10.1016/j.bbi.2019.11.006 
  6. Iovene MR, et al. Urinary Ochratoxin A and Autism Spectrum Disorder: Italian Case-Control Study. PubMed 25597866. https://pubmed.ncbi.nlm.nih.gov/25597866/ 
  7. Lim KL, et al. Neuroinflammation, Oxidative Stress, and Mycotoxin-Mediated Glial Activation. PMC10049423. https://pmc.ncbi.nlm.nih.gov/articles/PMC10049423/ 
  8. Mycotoxin-Associated Mitochondrial Dysfunction and Electron Transport Chain Impairment. LSU HSC Faculty Publications. https://digitalscholar.lsuhsc.edu/cgi/viewcontent.cgi?article=5035&context=som_facpubs 
  9. All About ABA. Does Mold Cause Autism? Detoxification Polymorphisms (MTHFR, GST) and ASD Susceptibility. https://www.allaboutaba.com/blog/does-mold-cause-autism 
  10. Koszegi T, et al. Ochratoxin A, microRNA-132 Dysregulation, and ASD-Associated Gene Regulation (MeCP2, PTEN). PubMed 28795659. https://pubmed.ncbi.nlm.nih.gov/28795659/ 
  11. Badaeva AV, Danilov AB, Clayton P, et al. Perspectives on Neuronutrition in Prevention and Treatment of Neurological Disorders. Nutrients. 2023;15(11):2505. Published 2023 May 28. doi:10.3390/nu15112505 
  12. Mycotoxins and ASD: Systematic Review of 11 Studies (2008–2019). PMC4963856. https://pmc.ncbi.nlm.nih.gov/articles/PMC4963856/ 
  13. LC-MS/MS Pilot Study — Urinary Mycotoxins and ASD Diagnosis (n=54). PubMed 32819265. https://pubmed.ncbi.nlm.nih.gov/32819265/ 
  14. Marinov D, Eyubova S, Toneva A, et al. Linking Dietary Patterns to Autism Severity and Developmental Outcomes… Biomedicines. 2025;13(5):1178. 
  15. European Food Safety Authority (EFSA) CONTAM Panel. Deoxynivalenol in food and feed: occurrence and exposure. EFSA Journal. 2013;11(10):3379. 
  16. MoldCo. Urine Mycotoxin Test Accuracy — Result Interpretation Considerations. https://www.moldco.com/blog/urine-mycotoxin-test-accuracy-what-do-they-really-show 
  17. MosaicDX. MycoTOX Profile — Urine LC-MS/MS Test Information. https://mosaicdx.com/resource/mycotox-profile-urine/

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