Mycotoxins & the Brain
Lauren Tessier, ND
If you’ve worked with people suffering from mold and mycotoxin exposure, you are aware of the vast array of symptoms they report. It is not uncommon for people to experience a litany of cognitive symptoms, including, but not limited to, brain fog, confusion, inattention, disorientation, and difficulties with memory, problem solving, following conversation, reaction time, and learning. Additional neurocognitive effects can manifest as mood complaints, such as depression, anxiety, obsessive-compulsive disorder (OCD)-like behavior, and social withdrawal. Meanwhile, strictly neurological complaints vary wildly and may involve reports of sensations of dizziness, internal vibration, numbness (which may be non-dermatomal), tingling, ataxia, vertigo, sharp pain, photophobia, changes in smell and taste, and tinnitus. Symptoms such as atypical seizure presentations, syncope, tremor, tics, depersonalization, and derealization may also occur, but to a lesser extent.
Many of the aforementioned neurocognitive complaints have been demonstrated in various studies of mold-exposed cohorts.1-7 A 2003 study found that 70 of 100 patients exposed to mold in their homes exhibited neurological symptoms that included ataxia, dizziness, and neurocognitive complaints.8 Moreover, assessment of their autonomic nervous system, via heart rate variability, demonstrated abnormalities in all who were tested. Neurocognitive assessments of a portion of study participants (limited due to cost) revealed deficits in problem solving, executive functioning, judgment, hand/eye coordination, and memory. Moreover, SPECT scans demonstrated a neurotoxic pattern in approximately 86% of a subgroup that clinically demonstrated imbalance.8 Another 2003 study, examining 182 mold-exposed patients, found hypoactivation of the frontal cortex, as demonstrated on quantitative electroencephalogram.9 These findings, in addition to the degree of exposure, correlated significantly to abnormal cognitive testing outcomes. It is obvious that the aforementioned neurological complaints are shared with many other serious conditions; therefore, it is imperative that all pertinent differential diagnoses are considered and ruled out. However, it should be noted that a proper work-up of mold illness should be included, as one should not underestimate the profound neurological impact of mold exposure.
Unfortunately, the nervous system stands to suffer grave ill effects following mold and mycotoxin exposure. The reason for this is multifactorial. Firstly, the brain is largely made of fatty tissue, and many mycotoxins are small and lipophilic in nature, thus able to pass through lipid-rich cell membranes with ease. Many lipophilic mycotoxins, such as enniatin B, beauvercin, and aflatoxin, have been found in high concentrations in tissues and organs with high fat content, such as liver and adipose tissue.10-12 Of course, the fatty tissue of the nervous system is no exception; such lipophilic mycotoxins do not spare the brain. In mice, in-vivo systemic administration of beauvercin and enniatin resulted in their deposition in brain tissue, demonstrating their ability to cross the blood-brain barrier (BBB).13
The lipophilic nature of mycotoxins presents additional concerns when one considers the direct communication between the olfactory bulb of the nose and the brain.14 In a 2006 mouse study, intranasal exposure to satratoxin G, the mycotoxin produced by the “infamous” black mold, Stachybotrys chartarum, resulted in apoptosis of olfactory sensory nerves.15Another mouse study delivered a similar apoptotic finding, in conjunction with bilateral atrophy of the olfactory nerve layer of the olfactory bulb of the brain.16
The high lipid content of the brain also places it at increased risk for lipid peroxidation, which is potentially made worse by the brain’s great demand for energy and oxygen. Oxidative damage, including lipid peroxidation, happens to be one of the most widely understood mechanisms of action of damage imparted by mycotoxins.17-36
Mycotoxins and the BBB
Understanding the impact of mycotoxins on the brain requires a quick refresher on astrocytes. These glial cells are an important part of the nervous system, as they are integral to the proper maintenance of the BBB.37 Astrocyte “endfeet” interact with the endothelial cells of the BBB to help direct production of various enzymes, development of tight junctions,38,39 and alteration of BBB permeability to various nutrients.40,41
There is direct evidence supporting mycotoxin-induced damage to astrocytes. A 2005 study of rat astrocytes demonstrated that sub-cytotoxic levels of ochratoxin A exposure damage the cytoskeleton of astrocytes, in conjunction with an upregulation of genes responsible for a neuroinflammatory response.42 Meanwhile, T-2 toxin, a Fusarium-generated trichothecene, has been shown to be cytotoxic to cultured human astrocytes at low concentrations and with relatively short exposure times.43 When astrocytes are injured, there is a disruption of ion homeostasis, specifically an intercellular calcium wave that propagates to endothelial cells, resulting in abnormalities of BBB permeability and transport.44 Direct evidence of such disruption has been demonstrated with human astrocyte exposure to ochratoxin A, which resulted in an increase in cytosolic calcium and apoptosis.45 It is without coincidence, then, that research has demonstrated mycotoxin-induced alterations of the BBB.46,47 An in-vivo mouse study revealed alterations of BBB permeability as a result of percutaneous exposures of brain and spleen tissue to T-2 toxin.48 Such T-2-induced alterations can impact permeability of amino acids,49 thereby shifting amino acid-dependent metabolism, such as the synthesis of neurotransmitters. However, mycotoxins/BBB abnormalities are not limited to alterations of permeability. Numerous mycotoxins have been shown to cross the BBB, such as aflatoxins,50-51 ochratoxin A,52 fumonisin B1,53 tricoherences,47,54-59 beauvericin,13 and enniatins,13,60 with some resulting brain deposition.
Mycotoxin Damage to Brain Regions
Research has also demonstrated that different mycotoxins may be toxic to various parts of the brain. For instance, intragastric administration of ochratoxin A has been shown in rats to result in brain deposition of the mycotoxin, leading to damage to the hippocampus, ventral mesencephalon, striatum, and cerebellum.52 Additional research in rats confirmed severe focal ochratoxin A-induced neurotoxicity of the hippocampus, as compared to other brain regions.61 Meanwhile, in mice, intraperitoneal injections of ochratoxin A resulted in marked damage to the midbrain, caudate putamen, and hippocampus.17 In a rat study, subchronic exposure of ochratoxin A caused a downregulation of NDMA receptors,62 which are crucial for learning and memory.63 An in-vivo study of the mouse subventricular zone, known for its neurogenic potential, demonstrated drastic changes when the tissue was exposed to ochratoxin A.64 Of note was a significant decrease in cell viability, cellular proliferation, differentiation, astrocyte counts, and neurogenesis.
A 2000 rat study revealed reduced excitability of the neocortex following fumonisin exposure, which manifested as disturbances in information processing.65 Fumonisin exposure has also been implicated in the demyelination of the forebrain in rats.66 In a 2017 in-vivo study, the pituitary gland was implicated as a target organ for T-2 toxin injury.67 While specific brain regions may suffer damage at the hands of mycotoxins, general tissue injury has also been widely documented. Fumonisin B1 is a known disruptor of myelination in both in-vivo68 and in-vitro rat studies,69 and has been shown to inhibit axonal growth in cultured hippocampal neurons.70 Gliotoxin has been demonstrated to be neurotoxic in numerous human in-vitro studies.71-73
Mycotoxin Damage to Brain Metabolism
Mycotoxins can also cause shifts in brain metabolism. For instance, ingestion of ochratoxin A-contaminated feed resulted in alterations of amino acid metabolism in the brains of rats.61 This mycotoxin has also been shown to interfere with the activity of phenylalanine hydroxylase,74 which is an integral enzyme in the formation of tyrosine and also a precursor of L-dopa and other downstream catecholamines. Mouse studies have revealed such a depletion of striatal dopamine,17,75 while in-vivo chicken studies have demonstrated dopamine depletion via exposure to deoxynivalenol,76 and serotonin and noradrenaline depletion as a result of ochratoxin A exposure.75 Fumonisin B1 has been shown to alter rat neurotransmitter metabolism in various brain regions of rats77 and to alter neurotransmitter concentrations in mice.78 In female rat models, acute systemic administration of T-2 toxin resulted in decreased brain stem and cerebellar serotonin, while chronic exposure resulted in elevated levels of serotonin in the cerebellum.79 Meanwhile, studies of T-2 exposed male rats showed elevated levels of monoamines80 and serotonin.80-82 In another in-vivo study, exposure to T-2 in male rats resulted in an increase in serotonin globally throughout the brain, as well as regional increases and decreases in norepinephrine.83 Of note, the dose used in this study was 0.1 mg/kg body weight, which represents only 2% of the LD50 value for T-2.
While much of the research regarding mycotoxin impact on the brain comes from animal studies, it is very important that we pay attention to these findings. Many clients I see have been given a clean bill of health by their neurologist and primary care physician, but they continue to suffer. It is in these clients that mold and mycotoxin exposure should be considered. Clearly, it is typically the last thing to be ruled out, but that does not make the work-up unimportant. Many clients with proper support will see drastic improvements in their neurocognitive complaints – some in a few short weeks, whereas in others it may take 1 to 2 years.
When working with neurologically impacted mold-exposed clients, please be very mindful of the diagnosis codes you employ. In the world of preexisting conditions, one needs to be particularly cautious to avoid incorrect or overzealous diagnoses. For instance, a patient who is acutely mold exposed, demonstrating cognitive deficits and difficulties with short-term memory, may clinically present as an “inhalational Alzheimer’s” case.84 In 6 short months, they may have completely recovered, yet the poorly chosen diagnosis of “Alzheimer’s” may continue to impact their life, especially in the realm of disability insurance or life insurance. Thus, please be sure to only code what is truly diagnosable, understanding that your choices can impact the patient’s future for years to come.
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Lauren Tessier, ND, is a licensed naturopathic physician specializing in mold-related illness. She is a nationally known speaker and is the vice president of the International Society for Environmentally Acquired Illness (ISEAI) – a non-profit dedicated to educating physicians about the diagnosis and treatment of environmentally acquired illness. Dr Tessier’s practice, “Life After Mold,” in Waterbury, VT, draws clients from all around the world who suffer from chronic complex illness as a result of environmental exposure and chronic infections. Dr Tessier’s e-booklet, Mold Prevention: 101, has been widely circulated and its suggestions implemented by many worldwide.