Patients experiencing symptoms related to mold exposure are often caught in a cycle of inconclusive lab results, fragmented neurological evaluations, and diagnoses that fail to identify the underlying cause. As awareness of mycotoxin-related illness grows, clinicians are seeking better tools to recognize its signs and evaluate potential exposure.
In this Q&A, Racheal Onah, ND, MRN, discusses why mycotoxins can be difficult to identify, the limitations of conventional lab testing, and resources to help clinicians better understand, diagnose, and manage suspected mold-related illness.
What are mycotoxins, and how effective are current mycotoxin testing methods?
Dr. Racheal Onah: A foundational challenge is that traditional pathology isn’t designed to find mycotoxins in the first place. Standard laboratory work is built to detect the fungus itself, not the chemical toxins it produces. Because mycotoxins are small chemical compounds that are invisible under a microscope, laboratories need to move beyond visual detection entirely and use specialized assays.
The two primary methodologies used for this are enzyme-linked immunosorbent assay (ELISA) and mass spectrometry (LC-MS). The key difference in these approaches lies in what each method is looking for. Mass spectrometry looks for the exact molecular structure of a specific mycotoxin, but because many mycotoxins are structurally modified once they enter the body, this method can result in artificially low readings or false negatives. At RealTime Labs, we utilize ELISA technology because it can detect mycotoxins even when slight structural changes have occurred, making it more sensitive and less likely to produce false negatives.
Beyond the method itself, the specimen type also matters. Blood testing primarily looks for inflammatory markers or antibodies that indicate the immune system encountered mold antigens in the past. Urine panels, however, assess the active presence of mycotoxin metabolites that the body is currently processing and trying to excrete.
Why can mold-related illness be difficult to identify through standard laboratory and neurologic testing?
RO: There are several layers to this. The first being the symptoms themselves. Brain fog, fatigue, and cognitive dysfunction can closely mimic autoimmune conditions and neurological disorders. This often sends patients down a neurological workup path before anyone even considers mycotoxin exposure.
Second, mycotoxins are notoriously difficult to identify because they typically reside deep within organs, tissues, and cells rather than circulating freely in the bloodstream. Baseline urine tests, for example, often return low levels because the toxins haven’t been released yet from the tissue where they’re stored. Poor liver detoxification adds another layer of difficulty, since the body’s ability to excrete mycotoxins through urine depends on healthy liver function. This is compounded by the fact that mycotoxins can deplete glutathione, the body’s primary antioxidant. Frequently, practitioners use provoking agents like glutathione or saunas to force the excretion of these toxins into the urine so they can be detected.
From a neurological standpoint, patients often present with unremarkable MRI scans and standard neurotransmitter panels. However, if clinicians look at the patient’s organic acid profiles, they will often see elevated fungal or bacterial markers, which serves as a useful indirect signal pointing toward mycotoxicosis rather than a primary neurological disorder.
Finally, an often overlooked step is environmental assessment. Demonstrating that toxin-producing fungi are actually present in a patient’s environment can be a critical link between symptoms and mycotoxin diagnosis, and it’s a step that might be skipped if clinicians aren’t thinking along these lines to begin with.
How should clinicians interpret mycotoxin test results alongside patient symptoms and exposure history?
RO: Before running any lab panels or reviewing results, clinicians should always have the patient complete a thorough symptom assessment so they understand what symptoms are present, whether they’re localized or systemic, and whether there are multiple overlapping conditions. Different mycotoxins have entirely different effects and physiological targets in the body, and that context shapes interpretation.
For example, gliotoxin tends to accumulate in sinus cavities and is often associated with chronic sinus issues, whereas zearalenone acts as an endocrine disruptor typically seen in patients with fertility challenges or irregular menstruation cycles. For neurological symptoms, trichothecenes and ochratoxins are primary culprits that can manifest as chronic fatigue and brain fog.
From there, clinicians should analyze which specific mycotoxin groups are flagged to determine whether the exposure stems from, say, a water-damaged building or contaminated food, and then move to assessing the concentration levels. Levels being either ambiguous, mildly elevated, or significantly high informs both urgency and treatment approach.
What are the biggest misconceptions about mold toxicity testing and diagnosis?
RO: In my opinion, the most significant hurdle is the persistent disbelief among many medical practitioners regarding the validity of mycotoxin illness. I have seen instances where patients presenting with clear physiological symptoms are labeled as hypochondriacs by their primary care physicians. Even after these patients find a mold-literate practitioner, get tested, undergo treatment, and find relief, their original doctors still dismiss the illness. Ultimately, a practitioner cannot treat a condition they do not believe exists, and that skepticism causes real delays in care.
What advances are needed to improve the accuracy and clinical acceptance of mycotoxin testing?
RO: The most pressing need right now is a more comprehensive clinical education. Mycotoxin illness is simply not taught in conventional or even naturopathic medical schools. The most effective path forward is a combination of CE/CME-accredited courses and lab-led webinars and training that walk practitioners through various testing technologies, such as the nuances between ELISA versus mass spectrometry, and how to interpret results within the specific methodology being used. Practitioners who are experienced in this space should be brought in as educators. General webinars are a start, but structured, credentialed training is what will actually move the needle on clinical acceptance.
