Blood Serum Mycotoxin Testing for Your Practice
Test for 14 mycotoxins with both IgG and IgE antibody detection. 28 individual results that quantify your patient's immune response to mycotoxin exposure with complimentary consultation.
Mycotoxins are among the most underdiagnosed contributors to chronic, multi-system illness. Patients present with fatigue, cognitive dysfunction, hormonal disruption, and GI symptoms that overlap with Chronic Lyme disease, Chronic Fatigue Syndrome, fibromyalgia, and autoimmune disease conditions — leading to years of misdiagnosis and ineffective treatment. MyMycoLab’s blood serum testing measures IgG and IgE antibody responses to 14 mycotoxins, giving you a quantitative immune picture that urine-based metabolite testing cannot provide. If mycotoxins aren’t part of your differential, the clinical picture may not be complete.
Test Kit Includes: a blood draw tube, a serum sample tube, a test tube mailer box, instructions and a pre-paid return envelope (U.S. patients only)
Price: $380.00 including U.S. shipping
Blood Serum Testing · 14 Mycotoxins · 28 Results · IgG + IgE Antibodies · Certified · Research Backed
Why Blood Serum Testing Matters
Most mycotoxin testing available in the U.S. relies on urine samples to detect mycotoxin metabolites. MyMycoLab tests blood serum — measuring the IgG and IgE antibodies your patient’s immune system produces in response to mycotoxin exposure. This distinction fundamentally changes what the results can tell you clinically.
Urine testing detects free mycotoxin compounds passing through the body, but low levels of mycotoxins are naturally present in common foods — cereals, coffee, nuts, wine, and others. The WHO and FAO estimate that 25% of the world’s crops are contaminated by mold. This means urine results may reflect dietary intake rather than pathological exposure. Blood serum antibody testing eliminates this variable by measuring immune reactivity, not transient metabolite presence.
Blood Serum Testing
Urine Testing (Other Labs)
What it measures
IgG and IgE antibodies: The immune system's quantified response to mycotoxin exposure
Free mycotoxin metabolites passing through the body at time of collection
What results tell you
Whether the patient has mounted a measurable immune reaction to specific mycotoxins indicating clinically meaningful exposure and current body burden
Whether mycotoxin compounds are present in urine at the time of collection
Ochratoxin A detection
Reliable. Detected through antibodies in the blood, independent of renal excretion
Unreliable. 99.8% of ochratoxin binds to albumin and is reabsorbed across all parts of the nephron by active transport and passive diffusion, making urinary excretion negligible
Dietary mycotoxin interference
Not a factor. Antibodies reflect immune response, not food intake
Significant confounder. Can detect traces from everyday foods (cereals, coffee, nuts, wine), even in healthy individuals with no pathological exposure
Exposure vs. presence
Distinguishes between immune-relevant exposure and incidental contact
Detects presence but cannot differentiate between dietary intake and environmental exposure
Antibody differentiation
Tests both IgG (toxic body burden / ongoing exposure) and IgE (allergic sensitization / mast cell reactivity) for each mycotoxin
Not applicable. Urine testing does not measure immune response
Mast cell activation relevance
IgE antibodies to mycotoxins directly indicate mast cell stimulation, relevant for MCAS assessment
No mast cell data. Unable to assess allergic or mast cell–mediated response
Number of mycotoxins tested
14 mycotoxins with both IgG and IgE delivering 28 individual results
Typically, 11–16 mycotoxins, varies by laboratory
Clinical validation
Serum antibody methodology validated in peer-reviewed research for over 20 years
Methodology varies by lab; the CDC has noted limitations of urine-based mycotoxin testing for clinical diagnosis
14 Mycotoxins.28 Results.
Our blood serum panel tests for IgG and IgE antibodies to each of the 14 mycotoxins delivering 28 quantified data points that map your patient’s immune response across the full spectrum of clinically relevant mycotoxin exposure.
Each mycotoxin has a distinct pathological profile affecting different organ systems, inflammatory pathways, and immune mechanisms. Understanding which mycotoxins are driving the immune response allows you to build a targeted treatment protocol rather than treating symptoms in isolation.
Produced by Stachybotrys (black mold), satratoxin is one of the most toxic indoor mold toxins known. It damages brain tissue, triggers widespread inflammation, and causes the death of nerve cells in the part of the brain responsible for smell. It has been found in lung fluid samples taken from infants with pulmonary hemorrhage (lung bleeding), and in those infants’ homes. Satratoxin belongs to the macrocyclic trichothecene family, which are among the most potent inhibitors of protein synthesis in humans.
Produced by Fusarium and Aspergillus molds, these toxins are among the most powerful blockers of protein production in human cells. Without proteins, cells cannot function or repair themselves. These compounds cause tremors, immune dysregulation, and inflammation, and are harmful even in very small amounts. Verrucarins have been specifically identified in Stachybotrys-contaminated indoor environments and in the sera of building occupants.
Ochratoxins come from Aspergillus and Penicillium molds and are among the most commonly detected mycotoxins in the indoor environment. Ochratoxin A (OTA) damages the kidneys, liver, brain, and immune system. Ochratoxins can cross the placental barrier. It can cause cancer and birth defects. It has been classified as a possible human carcinogen since 1993. Importantly, long-term low-level exposure to OTA can be more damaging than a single large exposure. OTA is nephrotoxic, hepatotoxic, neurotoxic, and immunotoxic. It is poorly filtered by the kidneys, which is precisely why urine testing drastically underestimates exposure and why blood serum testing is essential for this toxin. OTA builds up in breast milk, which can expose breastfed babies. Breathing in OTA has been documented to cause kidney failure within 24 hours. Emerging research links OTA to Parkinson’s disease and to autism in children
Produced by Fusarium, T-2 toxin is the only mycotoxin ever used as a biological weapon. In the early 1980s, approximately 100,000 people in Southeast Asia were killed or injured by it. It crosses from the bloodstream into the brain, causes oxidative stress (cell damage from unstable molecules), and disrupts energy production inside cells. T-2 toxin is also a potent endocrine disruptor: it lowers testosterone in both men and women and has been linked to infertility and hormonal problems.
Also called DON, vomitoxin is the most common trichothecene found indoors. In the gut, it blocks protein production, causes DNA damage, triggers inflammation, and breaks down the junctions that hold intestinal cells together, a key step in leaky gut. It crosses into the brain, directly affects neurons and support cells, and disrupts hormone signals. It can raise inflammatory markers by up to 15 times and throws off estrogen and testosterone balance.
Cladosporium is one of the most common molds in both indoor and outdoor air. Its spores are a major trigger for asthma and allergies. Beyond respiratory effects, it releases chemicals that are toxic to the nervous system. Cladosporium has been found in breast cancer tumor samples in large-scale cancer research. [13] Because Cladosporium is so ubiquitous, patients with IgE sensitization to its HSP 70 protein can experience chronic, relapsing respiratory and neurological symptoms with no obvious “moldy” environment making diagnosis particularly challenging.
These trichothecenes from Stachybotrys (black mold) affect nearly every organ system. They trigger inflammation and suppress the immune system. In the gut, they block protein production, cause oxidative stress, and can cause internal bleeding. In the nervous system, they cause tremors, headaches, seizures, sleep problems, and can damage the protective coating around nerves (myelin), leading to conditions similar to multiple sclerosis. They also disrupt hormones, lowering testosterone and raising estrogen in both men and women. In a landmark study, researchers tested blood samples from 44 people living in Stachybotrys-contaminated buildings and found trichothecene toxins in the sera of 23 of them — compared to only 1 out of 26 people from uncontaminated buildings. This was among the first studies to directly demonstrate that indoor mold exposure leads to measurable toxin levels in human blood.
Alternaria produces a toxin called alternariol that is directly toxic to cells and can damage or mutate DNA. It dysregulates immune function and triggers oxidative stress, a process where unstable molecules cause widespread cell damage. It also lowers testosterone. Alternariol is specifically genotoxic: it causes DNA strand breaks and chromosomal aberrations, meaning it does not merely damage cells but can alter the genetic instructions those cells carry forward when they divide.
This toxin from Aspergillus breaks down red blood cells and is specifically toxic to neutrophils and macrophages, two of the most important immune system’s infection-fighting cells. It dysregulates immunity broadly. The destruction of neutrophils and macrophages is particularly consequential because these are the cells the body relies on as its first line of defense against new infections. When hemolysin suppresses them, patients become vulnerable to a cascade of secondary infections that further complicate the clinical picture. Aspergillus has been found in greater amounts inside lung cancer tumors.
Produced by Aspergillus versicolor, sterigmatocystin can cause cancer and birth defects. It damages the liver and has been linked to the development of autoimmune diseases by altering how the immune system communicates and which genes get turned on or off. This epigenetic mechanism where sterigmatocystin changes gene expression without altering the DNA sequence itself may explain why some patients develop autoimmune conditions months or years after their initial mold exposure, long after the mold itself has been remediated.
This Penicillium toxin is a powerful immune dysregulator. It works by blocking the growth of immune cells (lymphocytes), broadly weakening the body’s ability to fight infections and control inflammation. Mycophenolic acid inhibits the enzyme inosine monophosphate dehydrogenase, which is critical for lymphocyte proliferation. This is the same mechanism exploited by the prescription immunosuppressant mycophenolate mofetil (CellCept), used to prevent organ transplant rejection — which underscores just how pharmacologically potent this environmental toxin is.
Produced by Aspergillus fumigatus, gliotoxin dysregulates the immune system, damages nerves, and harms DNA. Studies show it causes demyelination of nerves. Research has linked it to multiple sclerosis. It can kill immune cells even at extremely low concentrations. Gliotoxin is active at picomolar concentrations — quantities so small they are nearly undetectable by standard laboratory methods. It induces apoptosis (programmed cell death) in immune cells, effectively disarming the body’s defenses from the inside.
Fumonisins come from Fusarium mold. They block a critical process in fat metabolism, which has been linked to depression that does not respond to standard antidepressants. Specifically, fumonisins inhibit ceramide synthase, disrupting sphingolipid metabolism — a pathway essential for cell membrane integrity and brain signaling. This disruption of brain lipid chemistry may explain why affected patients experience depression that is biologically resistant to conventional serotonin-based treatments. Disrupting sphingolipid metabolism can lead to Alzheimer’s and Parkinson’s disease. Fumonisin contamination of corn along the Texas–Mexico border has been connected to higher rates of neural tube defects in newborns. Fumonisin B1 is classified as a possible human carcinogen. These toxins also damage the mitochondria (the energy-producing parts of cells) and harm the liver and kidneys.
Produced by Fusarium, zearalenone (ZEA) mimics estrogen in the body. It latches onto estrogen receptors and disrupts the hormonal balance. In women, it lowers the chances of a successful pregnancy and reduces milk production. In young girls, it can trigger early puberty. In men, it reduces testosterone and lowers sperm production. ZEA is classified as a non-steroidal estrogen: it is structurally similar enough to human estrogen to bind estrogen receptors, but its effects are disruptive rather than physiological. A recent study found elevated ZEA in blood samples from stillborn and newborn babies with physical malformations and developmental problems. It is classified as a possible carcinogen by IARC.
Ordering Mycotoxin Test is Simple
Register your practice, order test kits, and receive comprehensive results with complimentary consultation, all through our practitioner portal.
01
Register Your Practice
Create a practitioner account through our portal. Registration is free and gives you immediate access to order tests, manage patients, and view results.
02
Order Test Kits
Order serum collection kits directly through the portal. Kits can be shipped to your clinic for on-site blood draws or sent directly to your patient's home. $380 per panel. Fee-for-service, no insurance billing required.
03
Patient Blood Draw
Your patient visits any phlebotomist for a standard blood draw using the provided collection kit. No fasting required. Patients should discontinue immunosuppressive drugs, including corticosteroids and chemotherapeutic agents, 6 to 8 weeks prior to testing. Other medications and supplements do not affect antibody testing.
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Results in 14 Business Days
Once we receive the serum, testing begins within 24 hours. Results are delivered to your practitioner portal within 14 business days. Each report includes quantified IgG and IgE antibody levels for all 14 mycotoxins, 28 individual data points showing your patient's immune response to mycotoxin exposure.
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Clinical Support from Our Medical Advisors
New practitioners receive onboarding support from our medical advisory team to help you interpret your first results and understand IgG and IgE antibody patterns. As you continue ordering, our advisors remain available whenever clinical questions arise.
The Only Blood Serum Mycotoxin Lab in the U.S.
MyMycoLab is the only laboratory testing blood serum for 14 mycotoxins with both IgG and IgE antibody detection, diagnostic specificity unavailable through urine-based testing.
20+ Years of Published Research
MyMycoLab’s blood serum methodology is validated by peer-reviewed studies in medical journals spanning over two decades of clinical research.
Trusted by 2,500+ Practitioners
Healthcare providers across the country rely on MyMycoLab’s blood serum testing to help identify mycotoxin exposure in their patients.
Frequently Asked Questions
Registration is free through our practitioner portal. Once registered, you can immediately begin ordering test kits, managing patients, and viewing results.
Urine testing detects mycotoxin metabolites, which can reflect dietary intake from everyday foods rather than pathological exposure. MyMycoLab tests blood serum for IgG and IgE antibodies — measuring your patient's immune response to mycotoxin exposure. This is especially critical for mycotoxins like ochratoxin A, where 99.8% binds to albumin and is reabsorbed by the kidneys, making urinary detection unreliable.
No fasting is required. Patients should discontinue immunosuppressive drugs, including corticosteroids and chemotherapeutic agents, 6 to 8 weeks prior to testing. Other medications and supplements do not affect antibody testing.
Results are typically available within 14 business days after our lab receives the serum sample. You'll be notified through the practitioner portal when results are ready.
Results show quantified IgG and IgE antibody levels for each of the 14 mycotoxins tested, 28 individual data points. IgG levels indicate the body's current toxic burden from mycotoxin exposure, while elevated IgE levels indicate that the patient is currently being exposed to mycotoxins and may point to mast cell reactivity.
New practitioners receive onboarding support from our medical advisory team to help interpret initial results and understand antibody patterns. Our advisors remain available for clinical questions on an ongoing basis.
A patient who has tested positive for mycotoxins should be retested 6 months after starting treatment to evaluate progress.
The panel of 28 antibody results is $380 per test. MyMycoLab is a fee-for-service laboratory and does not bill insurance providers, including Medicare. International return shipping is not included in the price.
Mycotoxin testing is available for individuals aged 2 years and older.
Our Learning Center features peer-reviewed research, clinical case studies, on-demand webinars, practitioner guides, and detailed FAQs — all designed to help you confidently integrate mycotoxin testing into your practice. [Visit the Learning Center →]
See What Others Miss
Add blood serum mycotoxin testing to your practice. 14 mycotoxins. 28 results. IgG + IgE antibodies. Clinical support when you need it.
Backed by Peer-Reviewed Research
MyMycoLab’s approach to mycotoxin testing is grounded in over two decades of published clinical research. Our medical advisory team has contributed to peer-reviewed studies spanning the neurological, immunological, and gastrointestinal effects of mycotoxin exposure — research that directly informs the methodology and clinical framework behind our testing.
Detection of Trichothecene Mycotoxins in Sera from Individuals Exposed to Stachybotrys chartarum in Indoor Environments. Archives of Environmental Health. 2004;59(6):317-323.
Neural Autoantibodies and Neurophysiologic Abnormalities in Patients Exposed to Molds in Water-Damaged Buildings. Archives of Environmental Health. 2003;58(8):464-474.
Antibodies to Molds and Satratoxin in Individuals Exposed in Water-Damaged Buildings. Archives of Environmental Health. 2003;58(7):421-432.
Antibodies against Molds and Mycotoxins Following Exposure to Toxigenic Fungi in a Water-Damaged Building. Archives of Environmental Health. 2003;58(6):324-336.
Mold and Mycotoxins: Effects on the Neurological and Immune Systems in Humans. Advances in Applied Microbiology. 2004;55:375-406.
Combination of High-Dose Intravenous Immunoglobulins and Itraconozole in Treating Chronic Mycotic Demyelinating Optic Neuritis. The Scientific World Journal. 2003;3:640-646.
Neurophysiological Effects of Chronic Indoor Environmental Toxic Mold Exposure on Children. The Scientific World Journal. 2003;3:281-290.
Metabolism of Mycotoxins, Intracellular Functions of Vitamin B12, and Neurological Manifestations in Patients with Chronic Toxigenic Mold Exposures. The Scientific World Journal. 2004;4:736-745.
Lyme Disease and Mycotoxicosis: How to Differentiate Between the Two. Alternative Therapies in Health and Medicine. 2019;25(4):8-11.
Mold, Mycotoxins, and their Effects in Children. Alternative Therapies in Health and Medicine. 2021;27(1):8-10.
The Brain and Mycotoxins. Alternative Therapies in Health and Medicine. 2020;26(6):8-11.
Molds, Mycotoxins, the Brain, the Gut and Misconceptions. Alternative Therapies in Health and Medicine. 2022;28(3):8-12.
The Great Masquerader: Mycotoxins. Alternative Therapies in Health and Medicine. 2023;29(8):6-10.
Molds and Mycotoxins: A Brief Review. Alternative Therapies in Health and Medicine. 2016;22(3):8-11.