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Ochratoxin A (OTA) is a mycotoxin—a poisonous substance produced by certain moulds—that has become one of the most concerning food and environmental contaminants worldwide. First discovered in 1965, OTA belongs to a family of three ochratoxins (A, B, and C), but OTA is by far the most toxic and widely distributed form.
The International Agency for Research on Cancer (IARC) classifies OTA as a 2B category potential human carcinogen, meaning there is evidence of cancer risk in animals, though human evidence remains limited. What makes OTA particularly problematic is its heat stability—it survives baking, roasting, and even high-pressure steam sterilisation, making it nearly impossible to completely remove from food through standard processing methods.
OTA is primarily produced by two fungal genera:
These moulds are ubiquitous in the environment and thrive in warm, humid conditions or in improperly stored grains and food products. They can contaminate crops both in the field and during storage, especially when moisture control is inadequate.
OTA contamination occurs across the food chain and is present in a surprisingly wide range of foods, including:
The widespread distribution means that low-level OTA exposure is virtually unavoidable for most people, though chronic exposure is the primary health concern. In endemic regions where Balkan endemic nephropathy (BEN) occurs, OTA levels can be significantly higher than in developed nations.
OTA’s toxic effects occur through multiple mechanisms:
Oxidative Stress: OTA triggers the production of reactive oxygen species (ROS), creating cellular damage through oxidative stress. This overwhelming of the body’s antioxidant defences is one of the primary mechanisms of OTA toxicity.
Kidney Damage: The kidneys are OTA’s primary target organ. OTA concentrates in kidney tissue through active transport mechanisms, leading to tubular cell degeneration, reduced kidney function, and impaired protein synthesis.
Gene Expression Disruption: OTA suppresses the expression of antioxidant genes, particularly those controlled by the Nrf2/KEAP1 pathway—a critical system for managing oxidative stress. This creates a vicious cycle where cells become less able to defend themselves.
Glutathione Depletion: OTA reduces cellular glutathione production, crippling one of the body’s most important detoxification and antioxidant systems. Without adequate glutathione, cells cannot properly neutralise toxins or oxidative damage.
Mitochondrial Dysfunction: OTA directly damages mitochondria, the powerhouses of cells, interfering with energy production and triggering cell death.
Intestinal Barrier Disruption: OTA damages the intestinal epithelium, increasing intestinal permeability and allowing bacterial lipopolysaccharides to enter the bloodstream, triggering inflammation.
Kidney Disease and Balkan Endemic Nephropathy: Chronic OTA exposure is strongly associated with BEN, a progressive kidney disease characterised by tubular atrophy and progressive renal failure.
Chronic Fatigue: Several clinical studies have identified OTA in the urine of individuals with chronic fatigue syndrome and a history of water-damaged building exposure. While causality requires further research, the mechanism is plausible: OTA-induced mitochondrial dysfunction and glutathione depletion would severely compromise energy production.
Gut Dysfunction and Dysbiosis: OTA damages intestinal epithelial cells, disrupts the gut microbiota composition, and reduces microbial diversity. It increases the abundance of pathogenic bacteria while decreasing beneficial species, leading to intestinal inflammation and increased intestinal permeability.
Liver Inflammation: OTA-induced changes in gut bacteria increase lipopolysaccharide (LPS) production, which triggers liver inflammation through the TLR4/MyD88 signalling pathway.
Immune Suppression: OTA depletes cellular glutathione in immune cells, impairing phagocytosis, reducing antimicrobial defences, and shifting immune responses toward inflammatory patterns.
Neurological Effects: OTA crosses the blood-brain barrier and can accumulate in brain tissue, potentially contributing to neurotoxicity.
Carcinogenicity: OTA is classified as a potential carcinogen, with evidence of upper urinary tract tumors being 90 times higher in endemic regions compared to non-endemic areas.
There is no direct pharmaceutical treatment for OTA toxicity, but several evidence-based approaches can support your body’s natural detoxification:
1. Support Glutathione Production
Since OTA’s primary mechanism involves glutathione depletion, supporting glutathione synthesis is critical. This can be achieved through:
2. Activate the Nrf2 Pathway
Since OTA suppresses Nrf2-mediated antioxidant gene expression, compounds that activate this pathway can help restore the body’s defence mechanisms:
3. Support Antioxidant Defences
4. Support Gut Microbiota
Rebalancing the gut microbiota can reduce OTA’s harmful effects:
5. Reduce Exposure
6. Support Mitochondrial Function
7. Strengthen the Intestinal Barrier
While these interventions are supported by research, OTA toxicity is complex and individual responses vary. If you suspect chronic OTA exposure or are experiencing unexplained symptoms like chronic fatigue, gut dysfunction, or kidney problems, work with a healthcare provider who understands mycotoxin exposure. Clinical laboratory tests can identify OTA in urine samples.
Be cautious of extreme interventions or unproven detoxification protocols. The evidence supports targeted nutritional support, lifestyle modifications, and exposure reduction as the primary strategies, rather than extreme dietary restrictions or unvalidated “detox” regimens.
Ochratoxin A is a genuine health concern, particularly for those with chronic exposure through contaminated food, water, or water-damaged environments. While complete avoidance is impossible, understanding the mechanisms of OTA toxicity and supporting your body’s natural detoxification systems through evidence-based nutritional and lifestyle approaches can help minimise its harmful effects.
Kozegi et al., (2016) Ochratoxin A: Molecular Interactions, Mechanisms of Toxicity and Prevention at the Molecular Level (click here)
Xia et al., (2022) Crosstalk between Mycotoxins and Intestinal Microbiota and the Alleviation Approach via Microorganisms (click here)
Li et al., (2020) Protective Effect of Astaxanthin on Ochratoxin A-Induced Kidney Injury to Mice by Regulating Oxidative Stress-Related NRF2/KEAP1 Pathway (click here)
Guilford et al., (2014) Deficient Glutathione in the Pathophysiology of Mycotoxin-Related Illness (click here)