Mycotoxins from mold can massively effect human health and decrease Vitamin D in 4 ways

Mycotoxins restrict Vitamin D in intestine, liver, kidney, and cells
Mycotoxins and Their Impact on Human Health
Mycotoxins and Alzheimer's Disease: Exploring the Toxic Connection
VitaminDWiki - End of Alzheimer's videos, transcripts and many studies
Research concludes vitamin D may treat or prevent allergy to common mold – Sept 2010
Vitamin D and Mold Allergies - Mercola 2010

Mycotoxins restrict Vitamin D in intestine, liver, kidney, and cells

The Complex Relationship Between Mycotoxins and Vitamin D Metabolism
Perplexity AI - Deep Research April 2025
Mycotoxins, secondary metabolites produced by various fungi, have profound effects on animal and human health, particularly through their interference with essential metabolic processes. Among these, the disruption of vitamin D metabolism represents a significant concern with far-reaching implications for calcium homeostasis, bone health, and immune function. This report examines the multifaceted relationship between mycotoxins and vitamin D, highlighting mechanisms of interference, clinical manifestations, and potential mitigation strategies.

Disruption of Vitamin D Metabolism Pathways

Vitamin D plays a crucial role in calcium homeostasis and bone metabolism. Its conversion from inactive to active forms occurs through a two-step process involving the liver and kidneys. Mycotoxins interfere with this vital process at multiple points, compromising vitamin D functionality.

Impaired Absorption and Activation

Mycotoxins, particularly aflatoxins, directly impair the intestinal absorption of vitamin D3 (cholecalciferol), the inactive dietary form of vitamin D 2. This represents the first obstacle in vitamin D utilization. The normal metabolic pathway involves conversion of vitamin D3 to its active form through two hydroxylation steps: first in the liver to create 25-hydroxycholecalciferol, then in the kidneys to produce 1,25-dihydroxycholecalciferol (calcitriol), the biologically active form essential for calcium and phosphorus absorption 2.
Mycotoxins disrupt both of these critical activation steps. Liver damage caused by aflatoxins, T-2 toxin, and ochratoxin A prevents the first activation step of cholecalciferol 2. Studies with rats have shown that administration of deoxynivalenol (DON), T-2 toxin, or aflatoxin B1 decreased the activity of the enzyme 25-hydroxylase in hepatic tissue by 28-58%, significantly hampering this initial conversion 2. Similarly, kidney damage from aflatoxins and ochratoxin A interferes with the second activation step while simultaneously increasing urinary calcium elimination and reducing plasma calcium levels 2.

Vitamin D Receptor Interference

Beyond disrupting vitamin D metabolism, mycotoxins—particularly aflatoxin B1 (AFB1)—directly target vitamin D receptors (VDRs), which are essential for mediating vitamin D's biological effects. Research demonstrates that AFB1 exposure significantly down-modulates VDR expression in osteosarcoma cell line SAOS-2 4 [|PDF] Toxicity of aflatoxin B1 towards the vitamin D receptor (VDR) - CORE 5. Experimental data indicate a dose-dependent relationship, with 58% decreased VDR expression at 5 ng/mL of AFB1 and 86% reduction at 50 ng/mL 4 5.
This toxicity toward VDRs suggests that AFB1 interferes with vitamin D's actions on calcium-binding gene expression in the kidney and intestine 4. Interestingly, the chemical structures of vitamin D and AFB1 are partially overlapping in their poly-aromatic systems, which could explain the mycotoxin's interference with VDR function [|PDF] Toxicity of aflatoxin B1 towards the vitamin D receptor (VDR) - CORE 5.

Impact on Calcium Homeostasis and Bone Health

The disturbance of vitamin D metabolism by mycotoxins cascades into broader implications for calcium homeostasis and skeletal integrity.

Altered Mineral Metabolism

As vitamin D is crucial for calcium, phosphorus, and magnesium absorption, mycotoxin-induced disruption of vitamin D metabolism leads to mineral imbalances. Mycotoxins create a metabolic situation that reduces circulating calcium and phosphorus levels in the blood, ultimately diminishing bone strength 10. This effect is particularly pronounced with aflatoxins, which have been shown to significantly decrease bone mineralization parameters, including tibia breaking strength and the percentages of calcium and phosphorus in the tibia 10.
Multiple mycotoxins, including AFB1, ochratoxin A, T-2 toxin, and fumonisin B1, can adversely affect bone growth strength and cause bone fragility 10. These effects may be mediated through disruption of parathyroid hormone (PTH) and 1,25-dihydroxycholecalciferol balance, which are essential regulators of calcium metabolism 10 11.

Clinical Manifestations in Animals and Humans

In poultry, vitamin D deficiency resulting from mycotoxin exposure leads to declining eggshell quality within days, with increasing occurrences of thin-shelled, mottled, cracked, and broken eggs 2. The laying rate typically decreases within two to three weeks, and severe cases may present with skeletal problems and feather picking 2.
In humans, particularly children, the implications can be severe. Research suggests that exposure to AFB1 during early life, combined with certain vitamin D receptor genetic variants (specifically the F allele), increases the risk of developing rickets in African children 4 5.
This indicates that mycotoxin exposure may be an unrecognized contributor to the high prevalence of rickets in regions with endemic aflatoxin contamination of food supplies.

Mycotoxins and Immune Function: The Vitamin D Connection

Beyond bone health, the relationship between mycotoxins and vitamin D has significant implications for immune function, creating a complex interplay that can exacerbate health risks.

Immunomodulatory Effects

Vitamin D plays a crucial role in immune regulation, and its deficiency can impair immune function. Mycotoxins are known to have immunomodulatory effects, often suppressing immune responses 3. The combination of mycotoxin-induced immunosuppression and vitamin D deficiency creates a concerning scenario where both factors may synergistically weaken host defense mechanisms 8 11.
Research indicates that mycotoxin exposure may be particularly detrimental in individuals with pre-existing immune dysregulation, potentially exacerbating underlying pathophysiology, including allergic and non-allergic chronic inflammatory diseases and autoimmune disorders 3. This suggests that populations with compromised immune systems may be especially vulnerable to the adverse effects of mycotoxins on vitamin D metabolism.

Microbiome Interactions

Mycotoxins can also influence the gastrointestinal microbiota, potentially leading to dysbiosis 3. The gut microbiome plays a significant role in regulating intestinal homeostasis and is an important component of the mucosal immune system 3. Mycotoxin-induced alterations in gut microbiota composition may further complicate vitamin D metabolism and absorption, creating a cascade of effects that extend beyond direct interference with vitamin D pathways 3.

Clinical Recognition and Intervention Strategies

Understanding the relationship between mycotoxins and vitamin D has important implications for clinical practice and intervention strategies.

Diagnostic Considerations

Persistent low 25-OH vitamin D levels despite adequate supplementation may be indicative of mycotoxin exposure, particularly in cases of mold exposure from water-damaged buildings 6. Additionally, elevated 1,25-vitamin D levels in conjunction with low glutathione status may serve as markers for mycotoxicosis 6. These patterns suggest that vitamin D laboratory parameters should be interpreted with consideration for potential mycotoxin exposure, especially in treatment-resistant cases.

Mitigation Approaches (want 60-90 ng/mL of vitamin D)

Several strategies may help mitigate the effects of mycotoxins on vitamin D metabolism. In clinical settings, practitioners may need to use higher-than-maintenance doses of vitamin D to overcome receptor blockade, aiming to achieve 25-OH vitamin D levels between 60-90 ng/mL for at least three months 6. Emulsified forms of vitamin D appear to be better tolerated by patients with mold exposure 6.
In animal husbandry, particularly poultry farming, supplementation with already activated forms of vitamin D (1,25-dihydroxy-vitamin D3) may bypass the impaired metabolism, as this form doesn't require conversion in the liver and kidneys 11. This approach allows direct binding to vitamin D receptors, potentially counteracting the effects of mycotoxins on calcium absorption and immunity 11.
Mycotoxin binders are commonly used to reduce mycotoxin impact, though care must be taken in their selection. Studies show that while many binders have minimal effect on vitamin D bioavailability, they may significantly adsorb other fat-soluble vitamins like vitamin E 9. Specifically, vitamin D was only substantially adsorbed by yeast cell wall binders (20.2%) when tested in isolation 9.

Conclusion

The relationship between mycotoxins and vitamin D represents a complex interaction with significant implications for human and animal health. Mycotoxins disrupt vitamin D metabolism at multiple levels—impairing intestinal absorption, interfering with hepatic and renal activation steps, and directly targeting vitamin D receptors. These effects cascade into broader disturbances in calcium homeostasis, bone health, and immune function.
The recognition of this relationship opens new perspectives for understanding persistent vitamin D deficiency and related conditions such as rickets, particularly in regions with endemic mycotoxin contamination of food supplies. It also highlights the importance of considering mycotoxin exposure in cases of treatment-resistant vitamin D deficiency.
Future research directions should focus on developing more effective strategies to mitigate mycotoxin effects on vitamin D metabolism, particularly in vulnerable populations. Additionally, greater attention to mycotoxin contamination as a public health concern may be warranted, especially in regions with high prevalence of vitamin D-related disorders.

Citations:

Mycotoxins and Their Impact on Human Health

Perplexity AI - Deep Research April 2025
Mycotoxins are toxic secondary metabolites produced by various fungi that contaminate agricultural crops, food products, and buildings worldwide. These compounds pose a significant threat to human health, causing effects ranging from acute poisoning to chronic diseases including cancer, immune suppression, and neurological disorders. According to the Food and Agriculture Organization (FAO), approximately 25% of the world's agricultural products are contaminated with mycotoxins 15. Despite decades of research, the full impact of widespread mycotoxin exposure on human health remains incompletely understood, though evidence increasingly points to their role in various serious health conditions across multiple organ systems.

Origins and Types of Mycotoxins

Mycotoxins are produced by certain molds, primarily species of Aspergillus, Fusarium, and Penicillium 7 11. These fungi can grow on various food crops before harvest, during the harvesting process, or after harvest during storage, especially in hot and humid conditions 2 15. Several hundred mycotoxins have been identified, but about a dozen have gained the most attention due to their severe effects on human health and their occurrence in food 1.
The most significant mycotoxins include:

Aflatoxins: Produced by Aspergillus species (particularly A. flavus and A. parasiticus), considered the most potent and carcinogenic 2 15
Ochratoxins: Produced by Aspergillus and Penicillium species, with nephrotoxic properties 3
Trichothecenes: Including T-2 toxin and deoxynivalenol (DON), produced by Fusarium species 7
Fumonisins: Produced by Fusarium species, linked to neural tube defects and possibly esophageal cancer 6 [|PDF] Mycotoxins and human health - 13
Zearalenone: Produced by Fusarium species, with estrogenic properties 7
Patulin: Produced by Penicillium and Aspergillus species 8

The World Health Organization has classified aflatoxins as human carcinogens (Group 1), ochratoxins and fumonisins as possible human carcinogens (Group 2B), while trichothecenes and zearalenone are not recognized as human carcinogens (Group 3) 15.

Exposure Routes and Global Prevalence

Humans are exposed to mycotoxins through three primary routes:

Ingestion of contaminated food and beverages such as cereals, nuts, dried fruits, coffee, wine, beer, and spices 3 7
Inhalation of fungal spores and mycotoxins, particularly in water-damaged buildings 3 14
Dermal absorption through skin contact 10 15

The prevalence of mycotoxin contamination varies globally but is generally higher in regions with hot and humid climates that provide optimal conditions for fungal growth and toxin production 2. Food contamination is particularly problematic in developing nations with less stringent food safety regulations 15.

Acute Toxicity and Poisoning

Acute mycotoxicosis results from high-dose exposure and can cause severe illness and death. Several documented outbreaks include:

Turkey X disease in 1960 caused by aflatoxins, resulting in hepatic necrosis 15
Aflatoxicosis outbreaks in Kenya in 1981, 2001, 2004, and 2005, with the 2004 outbreak resulting in 123 deaths 15
Mycotoxin outbreaks in Taiwan and Malaysia (1967 and 1988) where people died after consuming contaminated moldy rice and Chinese noodles 4

Symptoms of acute poisoning vary depending on the mycotoxin but commonly include vomiting, diarrhea, abdominal pain, dizziness, and in severe cases, liver failure characterized by bleeding, edema, altered digestion, and mental changes or coma 2 7.

Chronic Health Effects by Organ System

Hepatotoxicity and Kidney Damage

The liver is the primary target organ for many mycotoxins, particularly aflatoxins:

Aflatoxins can cause acute hepatic necrosis, cirrhosis, and hepatocellular carcinoma 2 [|PDF] 13
Chronic exposure increases the risk of developing liver and gallbladder cancer through mutations in the p53 gene 2
Ochratoxin A is primarily nephrotoxic, causing kidney disease in both animals and humans, and has been linked to focal segmental glomerulosclerosis 3
Multiple mycotoxins have been documented to cause kidney diseases in both humans and livestock 3 4

Neurotoxic Effects

Research increasingly reveals significant neurotoxic effects of mycotoxins:

Several mycotoxins including T-2 toxin, macrocyclic trichothecenes, fumonisin B1, and ochratoxin A can cross the blood-brain barrier and accumulate in the brain 6 12
Exposure has been associated with cognitive impairments, learning difficulties, behavioral abnormalities, and neurological disorders, particularly in children 9
Mechanisms of neurotoxicity include disruption of neuronal signaling pathways, DNA damage, oxidative stress, mitochondrial dysfunction, and neuroinflammation 9 12
Studies have linked mycotoxin exposure to decreased frontal cortex activity, and some mycotoxins are suspected triggers of autism spectrum disorders 12
Ochratoxin A can cause acute depletion of striatal dopamine and its metabolites, with evidence of neuronal cell apoptosis in the substantia nigra, striatum, and hippocampus 6
Fumonisins can induce neuronal degeneration in the cerebral cortex by disrupting ceramide synthesis 6

Immunosuppression and Immune Dysregulation

Mycotoxins significantly impact the immune system, increasing susceptibility to infectious diseases:

Mycotoxin-induced immunosuppression manifests as depressed T or B lymphocyte activity, suppressed immunoglobulin and antibody production, reduced complement or interferon activity, and impaired macrophage function 5
Different mycotoxins affect the immune system in specific ways: aflatoxins suppress macrophage function and T-cell activation 11, while gliotoxin inhibits neutrophil recruitment 14
The vulnerability of the immune system to mycotoxins stems from the continual proliferation and differentiation of cells participating in immune-mediated activities 5
Individuals with pre-existing immune dysregulation are particularly vulnerable, as mycotoxins can exacerbate allergic and non-allergic chronic inflammatory diseases, autoimmune disorders, and even HIV disease progression 8
Studies have shown positive correlations between elevated aflatoxin levels and increased HIV viral burden in HIV-positive individuals 8

Carcinogenic Properties

Several mycotoxins have established or suspected carcinogenic properties:

Aflatoxins are established carcinogens for liver cancer, with elevated risk in people chronically infected with hepatitis B virus 2 [|PDF] Mycotoxins and human health - IARC Publications 13
Aflatoxin metabolites intercalate into DNA and alkylate bases through their epoxide moiety, causing mutations in the p53 tumor suppressor gene 2
Fumonisins may play a role in esophageal cancer, particularly in Africa and parts of China 4 [|PDF] Mycotoxins and human health - 13
Ochratoxin A is classified as a possible human carcinogen (Group 2B) by the WHO 15

Other Health Effects

Additional health impacts documented in research include:

Stunted growth and delayed development in children exposed to aflatoxins 2 [|PDF] Mycotoxins and human health - 13
Potential role of fumonisins in neural tube defects [|PDF] Mycotoxins and human health - 13
Reproductive toxicity and endocrine disruption from certain mycotoxins like zearalenone 7 12
Compromise of epithelial barriers in the intestines and respiratory tract, facilitating further toxin absorption and microbial invasion 8

Specific Mycotoxins and Their Health Impacts

Aflatoxins

Aflatoxins, particularly aflatoxin B1, are considered the most toxic and well-studied mycotoxins:

No animal species is immune to their acute toxic effects, with children particularly vulnerable 2
Effects include liver cancer, acute liver failure, immune suppression, and increased viral load in HIV-positive individuals 2
Chronic exposure increases the risk of liver and gallbladder cancer through p53 gene mutations 2
Dietary factors may mitigate effects; consumption of apiaceous vegetables (carrots, parsnips, celery, parsley) may reduce carcinogenic effects 2
Treatment for aflatoxicosis is primarily supportive, including intravenous fluids with dextrose, vitamin K, B vitamins, and a restricted but high-quality protein diet 2

Ochratoxin A (kidney)

Ochratoxin A (OTA) is primarily associated with kidney diseases:

Produced by species of Aspergillus and Penicillium, OTA can contaminate a wide range of foods 3
Associated with nephrotoxicity and potential links to focal segmental glomerulosclerosis 3
Demonstrates neurotoxic effects including depletion of striatal dopamine and neuronal apoptosis 6
Treatment approaches include cholestyramine, a bile-acid-binding resin used to reduce enterohepatic recirculation of OTA 3
Chronic exposure may contribute to immunosuppression through inhibition of autophagy and upregulation of p-Akt1 8

Trichothecenes (brain)

This group includes T-2 toxin and deoxynivalenol (DON):

T-2 toxin can induce neuronal cell apoptosis in both fetal and adult brain tissue 6
DON has been associated with vomiting syndromes in humans, with outbreaks documented in multiple countries 7
Acute poisoning symptoms include chills, nausea, vomiting, abdominal pain, and diarrhea 7
Mechanisms of toxicity include inhibition of protein synthesis through ribosome targeting and disruption of mitochondrial function 8
Can cause immunosuppression in lymphocytes, increasing susceptibility to infections 8

Fumonisins

Fumonisins exhibit various toxic effects:

Can induce neuronal degeneration in the cerebral cortex by disrupting ceramide synthesis 6
Potentially linked to esophageal cancer in high-exposure regions of Africa and China 4 [|PDF] Mycotoxins and human health - 13
May play a role in neural tube defects during fetal development 13
Primarily affects the brain, liver, and lungs in experimental animal studies 12
Shown to preferentially affect glial cells rather than neurons in some studies, potentially contributing to neurodegenerative diseases 12

Vulnerable Populations

Certain populations are particularly susceptible to mycotoxin effects:

Children: More vulnerable to aflatoxin exposure, which can lead to stunted growth, delayed development, and cognitive impairments 2 9 [|PDF] Mycotoxins and human health - 13
Individuals with chronic hepatitis B infection: Face significantly higher risk of liver cancer when exposed to aflatoxins [|PDF] Mycotoxins and human health - 13
People with pre-existing immune dysregulation: Including those with allergic conditions, autoimmune disorders, and HIV 8
Individuals with compromised barrier function: Those with asthma, inflammatory bowel disease, or multiple sclerosis may be more susceptible due to impaired epithelial or blood-brain barriers 8
Residents of developing nations or regions with hot, humid climates: Face higher exposure risk due to favorable conditions for fungal growth and potentially less stringent food safety regulations 2 15

Prevention and Treatment Strategies

Given the widespread nature of mycotoxin contamination, prevention remains the primary approach:

Food safety measures and regulations to monitor and control mycotoxin levels in food and feed 4
Physical, chemical, or biological detoxification strategies for contaminated food 15
Proper food storage practices to minimize fungal growth and mycotoxin production 15
Remediation of water-damaged buildings to reduce inhalational exposure 3 14
Dietary interventions including binding agents that can reduce mycotoxin absorption 2 3
Treatment for mycotoxicosis is primarily supportive and symptom-based, as there are no specific antidotes for most mycotoxins 2
For certain mycotoxins like OTA, sequestering agents such as cholestyramine can reduce enterohepatic recirculation 3

Conclusion

Mycotoxins represent a significant global health challenge affecting multiple organ systems and causing a spectrum of adverse health effects. While the acute and chronic impacts of some mycotoxins (particularly aflatoxins) are well-established, the full health implications of many others require further research. The liver, kidneys, immune system, and nervous system appear particularly vulnerable to mycotoxin damage, with effects ranging from acute poisoning to chronic diseases including cancer, immune suppression, and neurological disorders.
The evidence reviewed demonstrates that mycotoxins are not merely contaminants of concern in agricultural settings but represent genuine public health hazards deserving greater attention. As climate change potentially increases fungal growth and mycotoxin production globally, understanding and mitigating these health impacts becomes increasingly urgent. Future research should focus on refining detection methods, establishing better biomarkers of exposure, developing effective treatments, and implementing stronger preventive measures to protect human health worldwide.

Citations:

Mycotoxins and Alzheimer's Disease: Exploring the Toxic Connection

Perplexity AI - Deep Research April 2025
Emerging research has revealed compelling evidence that mycotoxins, which are toxic compounds produced by various fungi and molds, may play a significant role in the development and progression of certain forms of Alzheimer's disease. This connection involves complex pathways of neuroinflammation, blood-brain barrier disruption, and direct neurotoxic effects that can potentially trigger or accelerate neurodegenerative processes. Recent studies have identified a specific subtype called "Toxic Alzheimer's Disease" linked to environmental exposures, suggesting new avenues for prevention and treatment.

Understanding Mycotoxins and Their Sources

Mycotoxins are secondary metabolites produced by various fungi, particularly molds that grow in damp environments and on certain foods. These toxic compounds can enter the human body through multiple routes and potentially affect neurological function.

Types and Sources of Mycotoxins

Mycotoxins comprise several classes of fungal toxins with varying chemical structures and biological effects. Common mycotoxins implicated in neurological health include:

Aflatoxins: Produced primarily by Aspergillus species and found in contaminated nuts, grains, and dried fruits
Ochratoxin A (OTA): Produced by Aspergillus and Penicillium species, commonly found in cereals, coffee, dried fruits, and wine
Trichothecenes: Produced by Stachybotrys (black mold) and found in water-damaged buildings
Fumonisins: Primarily produced by Fusarium species in corn and corn products
Gliotoxins: Produced by several mold species including Aspergillus 1 6

Humans are exposed to these mycotoxins through three primary routes: ingestion of contaminated food, inhalation of airborne mold spores and fragments in water-damaged buildings, and direct skin contact 7. A 2021 study noted that these exposures are widespread, with mycotoxins such as OTA "present in almost every Canadian daily diet" despite regulations 13.

Neurotoxic Properties of Mycotoxins

Mycotoxins possess several properties that enable them to affect the central nervous system. Studies have shown they can:

Disrupt neurotransmitter synthesis and signaling
Deplete the body's antioxidant reserves
Impair blood-brain barrier integrity
Induce neuronal apoptosis (cell death)
Promote inflammation in neural tissues
Interfere with protein synthesis and cellular metabolism 1 6 9

A study published in 2021 emphasized that "growing evidence suggests a link between these fungal metabolites and neurodegenerative diseases," though research has been constrained by limited access to human patients and suitable model systems 2.

Toxic Alzheimer's Disease: A Distinct Subtype

Recent research has identified what appears to be a distinct form of Alzheimer's disease associated with environmental toxin exposure, particularly mycotoxins.

Dr. Bredesen's Classification (type 3 due to toxins)

Dr. Dale Bredesen, a neurologist researching Alzheimer's disease, has proposed that Alzheimer's is not a single condition but rather a syndrome with multiple subtypes. He has identified three main types:

Type 1: Inflammatory (associated with systemic inflammation)
Type 2: Atrophic (associated with reduced trophic support)
Type 3: Toxic (associated with exposure to specific environmental toxins) 6 12

According to the Amos Institute, "Toxic Alzheimer's is the third subtype of Alzheimer's disease that is characterized by an exposure to toxic molds, heavy metals, or other environmental contaminants along with hormonal irregularities." This form typically produces symptoms earlier than other subtypes and can be more difficult to diagnose 1.

Connection to Chronic Inflammatory Response Syndrome

Toxic Alzheimer's disease appears to be closely related to Chronic Inflammatory Response Syndrome (CIRS), a condition resulting from exposure to biotoxins—particularly mycotoxins. Dr. Shoemaker and colleagues have demonstrated that biotoxins like mycotoxins are associated with a broad range of symptoms, including cognitive decline 6.
The relationship between CIRS and toxic Alzheimer's is so strong that some researchers consider type 3 Alzheimer's to be "a phenotypic manifestation of CIRS" 6. Both conditions present with cognitive decline beyond just memory problems, often including executive dysfunction, depression, stress hypersensitivity, and HPA axis dysfunction 6.

Evidence Linking Mycotoxins to Alzheimer's Disease

Multiple lines of evidence suggest a relationship between mycotoxin exposure and Alzheimer's disease, though the strength of this evidence varies across studies.

Fungi and Fungal Material in AD Brains

One of the most direct pieces of evidence comes from studies detecting fungal presence in brain tissue of Alzheimer's patients. A Spanish research team analyzed brain tissue from 11 deceased AD patients and found "several fungal species" in all cases, while finding no evidence of fungi in 10 control subjects 10.
The researchers concluded: "Collectively, our findings provide compelling evidence for the existence of fungal infection in the CNS from AD patients, but not in control individuals" 10. Their work showed that fungal material was present in different brain regions, including the frontal cortex, cerebellar hemisphere, and hippocampus 10.
Supporting this connection, elevated chitinase levels (enzymes that break down chitin, a component of fungal cell walls) have been found in the blood and cerebrospinal fluid of Alzheimer's patients 10.

Neuroinflammatory and Oxidative Processes

A 2025 study published in a major journal reported that "mycotoxins penetrate the central nervous system via a compromised blood-brain barrier, which may cause oxidative stress and neuroinflammation, these can also contribute to amyloid-beta (Aβ) plaque accumulation, Tau protein hyperphosphorylation, and neurofibrillary tangle formation" 5.
These findings suggest mycotoxins could directly influence the primary pathological processes seen in Alzheimer's disease. The study further noted that "mycotoxins also activate microglia, cause neuronal apoptosis, and disrupt central nervous system function" 5.

The Candida Connection

Researchers at Baylor College of Medicine discovered a specific mechanism by which the fungus Candida albicans can trigger Alzheimer's-related processes. Their 2023 study found that this common fungus "uses enzymes to penetrate the blood-brain barrier and trigger brain cells to both clear the infection and produce amyloid beta peptides" 8.
This finding is particularly significant because it demonstrates a direct causal pathway between fungal infection and the production of amyloid beta, a hallmark of Alzheimer's disease pathology 8.

Epidemiological Observations

While large-scale epidemiological studies specifically examining mycotoxin exposure and Alzheimer's risk remain limited, some geographical correlations have been noted. The Alzheimer's Drug Discovery Foundation report mentions that "Finland has the highest mortality rate from dementia in the world, and its cold, humid climate, which facilitates mold growth in heated buildings, has been suggested to contribute to the elevated mortality risk" 11

Mechanisms of Mycotoxin Neurotoxicity

Scientists have identified several mechanisms through which mycotoxins may contribute to neurodegeneration and Alzheimer's disease pathology.

Blood-Brain Barrier Disruption (can be compromised by mycotoxins)

The blood-brain barrier (BBB) is a crucial protective interface that regulates what substances can enter the brain from the bloodstream. Mycotoxins can compromise this barrier, allowing themselves and other potentially harmful substances to access brain tissue 5 6.
Once the BBB is compromised, mycotoxins can directly affect neural function and trigger inflammatory responses within the central nervous system 5. This disruption represents a fundamental mechanism through which environmental toxins can influence brain health.

Oxidative Stress and Mitochondrial Dysfunction

Mycotoxins induce oxidative stress in neural tissues, damaging cellular components through the production of reactive oxygen species. A study in rats showed that "chronic low-dose aflatoxin B1 exposure led to a decrease in brain antioxidants coupled with an increase in lipid peroxidation and protein carbonylation in the brain" 11
Additionally, mycotoxins can directly impair mitochondrial function. Studies in neuronal cell cultures have shown that fumonisin B1 "inhibits mitochondrial complex I and leads to a dysregulation of calcium homeostasis and signaling" 11 Since neurons have high energy demands, mitochondrial dysfunction can severely impact their survival and function.

Amyloid-Beta and Tau Protein Effects

The hallmark pathological features of Alzheimer's disease are amyloid-beta plaques and neurofibrillary tangles composed of hyperphosphorylated tau protein. Evidence suggests mycotoxins may influence both of these processes.
The study involving Candida albicans demonstrated that this fungus triggers brain cells to produce amyloid-beta peptides as part of an immune response 8. This finding supports the emerging hypothesis that amyloid-beta may serve as an antimicrobial peptide, with its accumulation representing the brain's attempt to combat infection 11
Regarding tau pathology, the 2025 study noted that mycotoxin exposure can contribute to "Tau protein hyperphosphorylation and neurofibrillary tangle formation" 5, potentially through pathways involving neuroinflammation and oxidative stress.

Neurotransmitter Disruption and Excitotoxicity

Several mycotoxins interfere with neurotransmitter systems critical for cognitive function. For example, research on ochratoxin A (OTA) found that it "reduces the membrane expression of GLAST and GLC-1 proteins, and thus, suppresses the glutamate absorption and glutamine synthetase, resulting in excessive glutamate in human bodies" 13.
This glutamate dysregulation is particularly concerning because excessive glutamate can cause excitotoxicity—a process where neurons are damaged or killed by overactivation of glutamate receptors. The researchers propose that "OTA is likely to cause long-term potentiation of neurons, leading to amyloid β peptide aggregation or Tau deposit which interferes with normal neuronal function and induces the Alzheimer's disease" 13.

Additional Metabolic Mechanisms

Other metabolic pathways affected by mycotoxins that may contribute to neurodegeneration include:

Vitamin B12 metabolism: Mycotoxin exposure is associated with vitamin B12 deficiency unrelated to diet, which can affect cognitive function 11
Lipid metabolism: Lipophilic mycotoxins can bind to lipoproteins and interfere with cholesterol metabolism, potentially contributing to both cardiovascular issues and neurodegeneration 11
Sphingolipid metabolism: Some mycotoxins disrupt sphingolipid synthesis, affecting cell membrane structure and signaling in the brain 11

Diagnosis and Genetic Susceptibility

Identifying toxic Alzheimer's disease presents unique challenges, particularly since many healthcare providers are unfamiliar with this subtype.

Genetic Susceptibility Factors

Research has identified specific genetic factors that may increase vulnerability to mycotoxin-related cognitive decline. Certain HLA-DR/DQ haplotypes are associated with heightened sensitivity to biotoxins and susceptibility to CIRS 6 11
Dr. Bredesen has hypothesized "that there may be a particular set of HLA-DR/DQ haplotypes which are especially vulnerable to mycotoxin-induced dementia, possibly due to an altered or excessive neuroimmune response to the mycotoxin antigens" 11 This genetic susceptibility helps explain why not everyone exposed to mycotoxins develops neurological symptoms.

Biomarkers and Laboratory Testing

Several laboratory abnormalities may help identify patients with toxic Alzheimer's disease:

Elevated TGF-β1 (a marker of inflammation)
Elevated C4a (a component of the complement system)
Presence of MARCoNS (Multiple Antibiotic Resistant Coagulase Negative Staphylococci) in the nasal cavity
Compromised visual contrast sensitivity
Detection of mycotoxins in urine or blood samples 6 11

A case study described in the research literature mentioned a patient with cognitive decline who had the HLA-DR/DQ haplotype 12-3-52B, "which is uncommon (less than 5% of the population) and strongly associated with hyper-sensitivity to biotoxins." The patient also showed elevated TGF-β1 and C4a levels, along with MARCoNS colonization 6.

Clinical Presentation

Symptoms that may suggest toxic Alzheimer's disease include:

Earlier onset of cognitive symptoms compared to typical Alzheimer's
Cognitive decline temporally associated with exposure to water-damaged buildings
Poor response to conventional Alzheimer's treatments
Presence of other symptoms typical of CIRS, such as fatigue, respiratory issues, and gastrointestinal disturbances 1 6 11

Dr. Bredesen notes that one distinguishing feature is that the "projected mold-related cognitive impairment does not respond to the drugs traditionally used for AD" 11 , suggesting a different underlying pathology.

Treatment Approaches for Mycotoxin-Related Cognitive Decline

Unlike conventional Alzheimer's disease, for which treatment options remain limited, toxic Alzheimer's disease may respond to interventions targeting the underlying mycotoxin exposure.

The Shoemaker Protocol

Dr. Ritchie Shoemaker developed a multi-step protocol for treating CIRS that has shown promise for patients with toxic Alzheimer's disease. This comprehensive approach includes:

Toxin binding using cholestyramine to prevent reabsorption of mycotoxins in the gastrointestinal tract
Treatment of MARCoNS with BEG (Bactroban, EDTA, and gentamicin) nasal spray
Administration of intranasal vasoactive intestinal peptide (VIP) to help regulate inflammatory responses
Removal of the toxin source through environmental remediation
Addressing hormonal, gastrointestinal, and biochemical abnormalities
Regular follow-up testing to monitor progress 6

Case reports indicate that some patients have shown significant improvement with this protocol. One case described in the research literature involved a patient who "began to show subjective improvement in cognition after several weeks" of treatment with the Shoemaker Protocol 6.

Environmental Remediation

A critical component of treatment is identifying and addressing sources of mold and mycotoxin exposure:

Professional assessment of home and workplace for water damage and mold
Proper remediation of contaminated environments
Use of air filtration systems to reduce airborne mold spores and mycotoxins
Attention to food sources of mycotoxins, particularly grains, nuts, and coffee 7 11

As one researcher noted, "In searching for potential toxic etiologies, both mycotoxins and mercury were identified as candidates," highlighting the importance of comprehensive environmental assessment 6.

Supportive Measures

Additional approaches that may support recovery include:

Anti-inflammatory diet to reduce systemic inflammation
Antioxidant supplementation to combat oxidative stress
Cognitive rehabilitation exercises
Stress management techniques, as stress can exacerbate symptoms 6 11

Prevention Strategies

Given the potential neurological impacts of mycotoxin exposure, prevention represents a critical strategy for reducing risk.

Indoor Environment Quality

Since water-damaged buildings are a primary source of harmful mycotoxin exposure, maintaining healthy indoor environments is essential:

Prompt repair of water leaks and damage
Maintaining proper ventilation and humidity control
Regular inspections for mold growth, especially in hidden areas
Professional remediation of identified mold problems 7

A proactive approach to indoor environment quality may be particularly important for individuals with genetic susceptibility to mycotoxin sensitivity 11 .

Food Safety Practices

To minimize dietary exposure to mycotoxins:

Proper storage of susceptible foods (grains, nuts, coffee, dried fruits)
Discarding visibly moldy foods
Supporting regulatory limits on mycotoxins in the food supply
Considering testing of foods in high-risk situations 11

The Alzheimer's Drug Discovery Foundation notes that "since there are no effective treatments after exposure, prevention is paramount" 11

Conclusion: Future Directions and Implications

The emerging connection between mycotoxins and Alzheimer's disease represents an important frontier in neurodegenerative disease research with significant implications for prevention, diagnosis, and treatment.
The identification of toxic Alzheimer's disease as a distinct subtype offers new hope for a subset of patients whose cognitive decline may be addressable through targeted interventions. Unlike conventional Alzheimer's disease, which has proven resistant to treatment, mycotoxin-related cognitive decline may be reversible if identified early and addressed comprehensively 6 12.
Future research directions should include larger epidemiological studies, identification of more specific biomarkers, optimization of treatment protocols, and development of preventive strategies. The potential to identify modifiable environmental risk factors for what has long been considered an inevitable age-related condition could transform our approach to Alzheimer's disease.
For clinicians, these findings underscore the importance of considering environmental factors—including mold exposure—when evaluating patients with cognitive decline. For the public, awareness of the potential neurological effects of mycotoxins highlights the importance of addressing water damage promptly and maintaining healthy indoor environments.
As one researcher noted, "There are at present a number of highly effective antifungal compounds with little toxicity" 10, suggesting that if the fungal/mycotoxin connection is confirmed through further research, new therapeutic options could be developed specifically targeting this mechanism of neurodegeneration.

Citations:

VitaminDWiki - End of Alzheimer's videos, transcripts and many studies

Research concludes vitamin D may treat or prevent allergy to common mold – Sept 2010

from news release http://www.eurekalert.org/pub_releases/2010-08/lsuh-rcv080610.php
CLICK HERE FOR TECHNICAL PDF

New Orleans, LA – Research conducted by Dr. Jay Kolls, Professor and Chair of Genetics at LSU Health Sciences Center New Orleans, and colleagues, has found that vitamin D may be an effective therapeutic agent to treat or prevent allergy to a common mold that can complicate asthma and frequently affects patients with Cystic Fibrosis. The work is scheduled to be published online August 16, 2010, ahead of the print edition of the September 2010 issue of the Journal of Clinical Investigation.

The environmental mold, Aspergillus fumigatus, is one of the most prevalent fungal organisms inhaled by people. In the vast majority, it is not associated with disease. However, in asthmatics and in patients with Cystic Fibrosis (CF), it can cause significant allergic symptoms. Up to 15% of CF patients develop a severe allergic response called Allergic Bronchopulmonary Aspergillosis (ABPA). Since the mold is so common, the researchers wanted to identify the factors that determine why only a subset of patients develop the allergy and what factors regulate tolerance or sensitization to the mold resulting in the development of ABPA. To gain insights, the group studied two groups of patients with CF. Both groups were colonized with A. Fumigatus, but only one had ABPA.

The researchers focused on Th2 cells–the hormonal messengers of T-helper cells that produce an allergic response. They found that a protein called OX40L was critical in driving Th2 responses to A. fumigatus in the CD4+T cells isolated from patients with ABPA and that this group had a much greater Th2 responses to A. Fumigatus. The CD4+T cells from the group of patients that did not have ABPA had higher levels of the proteins, FoxP3 and TGF-ß, critical to the development of allergen tolerance. The researchers discovered that heightened Th2 reactivity in the ABPA group correlated with a lower average blood level of vitamin D.

"We found that adding vitamin D not only substantially reduced the production of the protein driving an allergic response, but it also increased production of the proteins that promote tolerance," notes Dr. Jay Kolls, Professor and Chair of Genetics at LSU Health Sciences Center New Orleans.

According to the National Institutes of Health, Cystic fibrosis (CF) is the most common, fatal genetic disease in the United States. About 30,000 people in the United States have the disease. CF causes the body to produce thick, sticky mucus that clogs the lungs, leads to infection, and blocks the pancreas, which stops digestive enzymes from reaching the intestine where they are required in order to digest food. It is estimated that about 70,000 people worldwide have the disease.

Recent research has suggested that low levels of vitamin D may contribute to heart disease, a higher risk of diabetes, certain cancers, and depression as well as asthma, colds, and other respiratory disorders.

"Our study provides further evidence that vitamin D appears to be broadly associated with human health," notes Dr. Jay Kolls, Professor and Chair of Genetics at LSU Health Sciences Center New Orleans. "The next step in our research is to conduct a clinical trial to see if vitamin D can be used to treat or prevent this complication of asthma and Cystic Fibrosis."

Vitamin D and Mold Allergies - Mercola 2010

Mercola Sept 2010 - Who Knew this Vitamin Could Prevent Mold Allergies?

Mycotoxins from mold can massively effect human health and decrease Vitamin D in 4 ways

Mycotoxins restrict Vitamin D in intestine, liver, kidney, and cells

Disruption of Vitamin D Metabolism Pathways

Impaired Absorption and Activation

Vitamin D Receptor Interference

Impact on Calcium Homeostasis and Bone Health

Altered Mineral Metabolism

Clinical Manifestations in Animals and Humans

Mycotoxins and Immune Function: The Vitamin D Connection

Immunomodulatory Effects

Microbiome Interactions

Clinical Recognition and Intervention Strategies

Diagnostic Considerations

Mitigation Approaches (want 60-90 ng/mL of vitamin D)

Conclusion

Citations:

Mycotoxins and Their Impact on Human Health

Origins and Types of Mycotoxins

Exposure Routes and Global Prevalence

Acute Toxicity and Poisoning

Chronic Health Effects by Organ System

Hepatotoxicity and Kidney Damage

Neurotoxic Effects

Immunosuppression and Immune Dysregulation

Carcinogenic Properties

Other Health Effects

Specific Mycotoxins and Their Health Impacts

Aflatoxins

Ochratoxin A (kidney)

Trichothecenes (brain)

Fumonisins

Vulnerable Populations

Prevention and Treatment Strategies

Conclusion

Citations:

Mycotoxins and Alzheimer's Disease: Exploring the Toxic Connection

Understanding Mycotoxins and Their Sources

Types and Sources of Mycotoxins

Neurotoxic Properties of Mycotoxins

Toxic Alzheimer's Disease: A Distinct Subtype

Dr. Bredesen's Classification (type 3 due to toxins)

Connection to Chronic Inflammatory Response Syndrome

Evidence Linking Mycotoxins to Alzheimer's Disease

Fungi and Fungal Material in AD Brains

Neuroinflammatory and Oxidative Processes

The Candida Connection

Epidemiological Observations

Mechanisms of Mycotoxin Neurotoxicity

Blood-Brain Barrier Disruption (can be compromised by mycotoxins)

Oxidative Stress and Mitochondrial Dysfunction

Amyloid-Beta and Tau Protein Effects

Neurotransmitter Disruption and Excitotoxicity

Additional Metabolic Mechanisms

Diagnosis and Genetic Susceptibility

Genetic Susceptibility Factors

Biomarkers and Laboratory Testing

Clinical Presentation

Treatment Approaches for Mycotoxin-Related Cognitive Decline

The Shoemaker Protocol

Environmental Remediation

Supportive Measures

Prevention Strategies

Indoor Environment Quality

Food Safety Practices

Conclusion: Future Directions and Implications

Citations:

VitaminDWiki - End of Alzheimer's videos, transcripts and many studies

Research concludes vitamin D may treat or prevent allergy to common mold – Sept 2010

Vitamin D and Mold Allergies - Mercola 2010

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