In Montchavin – a small mountain village in the French Alps – 14 ALS cases were documented between 1990 and 2018. Statistically, one would have been expected. No shared genetic factor. All patients had consumed wild-harvested fungi with documented neurotoxins. The cluster was published in 2021 in the Journal of the Neurological Sciences.
Dr. Andrew Reid published a hypothesis as early as 2006: ALS as a consequence of mycotoxin exposure and secondary immune paralysis. In every patient he examined, he found elevated mycotoxin levels and suppressed immune parameters – T-2 toxin as the central finding.
Ustekinumab – a monoclonal antibody against IL-12 and IL-23 – blocks TH1 and TH17, the primary immune defenses against fungi. An FDA analysis of over 69,000 adverse event reports identified Ustekinumab with an unusual signal for ALS onset. When TH1 and TH17 are deliberately suppressed – fungi can grow unchecked.
Three independent data points. The same direction: Fungus → Toxins → Neurotoxicity → Motor neuron damage.
Studies
The following findings were obtained at my own expense – they are not part of standard clinical care. I present them because together they form a consistent picture that no one has yet connected.
Trichothecenes / T-2 Toxin in Urine
5× positive
Including after 32h fasting → internal source, not dietary
Fumonisins
Detected in gut after biofilm disruption
Second colonization in intestine – Fusarium most likely source
CD25 (IL-2 Receptor)
2.0 – 3.1 %
Reference ≥ 13% · 6 measurements over 12 months
IFN-γ (TH1)
79.5 pg/ml
Reference ≥ 118
IL-17 (TH17)
5.4 pg/ml
Reference ≥ 9.6 · Lab note: Candida predisposition
Kynurenine
Elevated
Vitamin B6 severely depleted → impaired gut enzyme function
LTT Stachybotrys
Negative
Stachybotrys unlikely as primary source – other trichothecene-producing molds possible
EMG 2022
Neurogenic remodeling
All tested muscles affected
IFN-γ, IL-17, IL-10 and CD25 are simultaneously and persistently suppressed. This is not an autoimmune pattern – where the immune system shifts in one direction. Here everything is suppressed. This matches the known profile of trichothecene mycotoxins: global inhibition of hematopoietic and lymphatic cells without selective imbalance.
Elevated kynurenine – the biochemical evidence: tryptophan is being converted to kynurenine instead of serotonin. Every step of this pathway is measurably documented in my case.
Studies on T-2 Immunosuppression
A mold fungus in the fundus and upper stomach – hidden behind a biofilm, invisible to endoscopy – continuously produces trichothecene mycotoxins. The toxins suppress the immune system globally. Simultaneously, through molecular mimicry, they trigger a cross-reaction: the immune system confuses fungal antigens with motor neuron surface proteins. The result is persistent hyperstimulation of the motor neurons.
The mechanism operates across three levels – which reinforce each other:
Level 1 — Tension: Mycotoxins directly
The mycotoxins themselves are the first and most fundamental trigger. They directly contact the afferent fibers of the vagus nerve on the gastric mucosa – nerve fibers that detect a threat and transmit signals from the stomach to the brainstem. There, where motor nuclei and the autonomic nervous system sit in close proximity, this sustained signal raises the baseline tension of the motor neurons. A 2025 review in Pharmacological Research describes exactly this anatomical route: afferent vagal fibers from the upper gastrointestinal tract project directly into the nucleus tractus solitarius – from where signals are relayed into motor nuclei.
Level 2 — Hyperstimulation: TLR and the Cross-Reaction
TLR sits on the gastric mucosa and detects the fungus behind its biofilm. When TLR is active, IFN-β is released, neuronal excitability rises via PKC. TH1 fights for years against the biofilm – without breakthrough. In this vacuum, TH1 begins to attack its own motor neurons through molecular mimicry. The result: twitching. cramps. fasciculations. hyperstimulation. It felt as though electricity was running through the muscles.
Level 3 — Nerve Inflammation: Dectin-1 when biofilm breaks
When the biofilm ruptures and beta-D-glucan is exposed, Dectin-1 activates microglia via Syk-CARD9. The immune system shifts mode – attacks more directly. The TLR activation drops. Instead of hyperstimulation: inflammation directly at the nerve. Pain like burning. First in the spine, then spreading across the back toward the limbs over months. When the biofilm regrows: back to Level 2.
My Current State
The fungus is still present. The mycotoxin burden has so completely suppressed the immune system that it no longer actively fights – no cross-reaction, no fasciculations. But the toxins are sufficient to maintain the baseline tension on their own. Motor neurons remain preserved – because the fungus is not yet gone.
This is the core dilemma: What is currently protecting me from muscle degeneration is suppressing my immune system to a minimum.
When the fungus is eliminated → TLR signal drops → no IFN-β production → mycotoxins disappear → afferent baseline tension collapses, cross-reaction collapses → motor neurons return to resting tone → degeneration begins. This is what I have unconsciously prevented – through constant stimulation of the fungus and the strong TH1 activation from mirtazapine. Exactly this chain – fungus gone, toxins gone, protection gone – may also explain what happened in Montchavin: the patients ate the fungi, the toxins arrived, the cross-reaction began. When the exposure ended – the protection disappeared.
Studies on the Mechanism
July 2021: First symptoms – twitching, cramps, weakness, muscle pain. November 2021: EMG unremarkable. May 2022: Neurogenic remodeling in all tested muscles – six months after a normal result. July 2022 only the foot extensor still affected. Between May and July, high-dose NR and TUDCA were added to mirtazapine. Progression stopped. Stable since.
I have been observing, documenting, and experimenting with my own body for years. And I found studies that describe what I had already experienced – before I knew those studies existed. Mirtazapine was prescribed in 2021 for anxiety – not for the fungus. It happened to activate the right receptor pathway at the right time. Without that one prescription, the course of disease today would likely be very different.
Mirtazapine — two effects, one paradox
TH1/TH17-Shift ↑ · H1 blockade
IFN-γ, IL-17 and IL-2 rise directly. IFN-γ amplifies the TLR signal via TH1 and macrophages – motor neurons remain under tension.
Simultaneously, H1 blockade on the mucosa suppresses the local inflammatory response: no vasodilation, no immune cell recruitment, no acute defense. The fungus is less effectively repelled. It stays. And as long as it stays – TLR runs.
Mirtazapine kept me stable – by keeping alive the same fungus that is making me ill. Until the mycotoxin burden grew so large that the toxins alone maintained the tension.
TUDCA & Nicotinamide Riboside — high dose
Biofilm openers / NAD⁺ ↑
TUDCA modulates pH in the upper gastrointestinal tract via bile acid receptors and reduces ER stress in motor neurons. NR raises NAD⁺ and activates macrophages and SIRT enzymes that strengthen the immune response against fungi. Together they likely opened the biofilm – exposing more beta-D-glucan, releasing more mycotoxins. Short-term increase in toxin load, but simultaneously the system maintains its tension.
Probiotics
Mucosal immunity ↑
Helped raise the TH1/TH17 response on the mucosal surface.
This hypothesis emerged from five years of experimentation. When I stopped the substances – the motor symptoms returned. Mirtazapine was the most important substance. Not because I knew it. But because it happened to hit the right pathway.
Fucoidan, Omega-3 & Sucralose — three proofs of the signaling pathway
Fucoidan and omega-3 are documented TLR modulators. In my case, both completely removed muscle tension – within five minutes. Simultaneously, weakness began. TLR blocked → cross-reaction gone → nerve releases → muscle weakness begins.
Sucralose acts differently – and therefore shows something different. A 2023 Nature study demonstrates that sucralose blocks T-cell proliferation via calcium signaling inhibition. Less TH17 → less antifungal defense → hyperstimulation gone. But no weakness – because TLR is still running. Three substances, the same underlying pattern. I chewed sucralose gum daily for years. Possibly not without consequence.
Studies on Substances
TH17 in the Cerebrospinal Fluid of ALS Patients
IL-17 and IL-23 are significantly elevated in the CSF of ALS patients – detected directly in the cerebrospinal fluid, not just peripherally. A 2026 meta-analysis confirms: TH1 and TH17 are elevated in blood, CSF and CNS tissue in ALS, while regulatory T-cells are reduced. The higher TH17 relative to Treg – the more aggressive the progression. What is TH17 fighting against in the CNS?
Masitinib – Long-term Survival April 2026
Masitinib inhibits mast cells and microglia – both of which respond to fungal antigens via Dectin-1 and TLR. Long-term survivors under masitinib: 121 months median survival vs. 42 months projected. The authors explicitly describe a specific subgroup in which disease progression is primarily driven by microglial and mast cell activity.
Two studies. The same direction: the immune system is active in the CNS. It is attacking motor neurons. A subgroup benefits from inhibiting exactly the cells that respond to fungi.
If the theory is correct – ALS may be stoppable in this subgroup.
The approach would be two-stage. Stage one: Completely eliminate the fungus – open the biofilm, expose the fungus, destroy it, without overwhelming the immune system. Stage two: Synthetically replace the TLR signal. Once the fungus is gone, the natural TLR activation disappears. Motor neurons lose their stimulus and begin to degenerate.
Studies
I am not a physician. I am a patient who has systematically observed, documented and researched for five years.
The complete theory – its development, all self-observations, scientific references and the personal course of disease – will soon be available in:
Book
One More Summer
Stephan Winkler · 2026