Subject: Mold Toxicity & Peptides: A Comprehensive Walkthrough
From: Derek from Research Radar <[email-masked]>
To: [email-masked]
Date: Tue, 28 Apr 2026 23:52:08 +0000
List-Id: <derekpruski.substack.com>

View this post on the web at https://derekpruski.substack.com/p/mold-toxicity-and-peptides-a-comprehensive

Read this first: Everything below is for research and educational purposes only. Nothing here is medical advice. All peptide references are framed for research subjects (RS), not for human consumption. If you think you’re dealing with mold illness, work with a qualified clinician who knows this terrain.
Section 1: What Mold Toxicity Actually Is
You’ll hear this called several names — mold illness, biotoxin illness, or its clinical name CIRS (Chronic Inflammatory Response Syndrome). They all describe the same thing: a multi-system illness that develops when someone with a susceptible immune system gets exposed to water-damaged buildings and the toxins they harbor.
Those toxins include:
Mycotoxins — poisonous compounds produced by mold itself
Endotoxins — fragments of bacterial cell walls (water damage breeds bacteria too, not just mold)
Beta-glucans — pieces of fungal cell walls that trigger immune responses
Inflammagens — a catch-all term for anything in the environment that drives inflammation
Here’s the part most people miss: healthy immune systems generally clear all of this. The people who end up stuck in CIRS almost always had something else going on first — chronic infections (Lyme, Epstein-Barr, co-infections), a heavy metal burden, prior viral hits, or significant unrelenting stress. Mold is usually the straw that breaks the camel’s back, not the only problem in the barn.
This is why one family member can be completely wrecked while everyone else in the same house feels fine. Same exposure, different immune terrain.
Section 2: How Mold Wrecks The Immune System
This section gets a bit technical, but it matters because the peptide protocol makes a lot more sense once you understand what’s actually broken.
The TH1/TH2 imbalance. Your immune system has two main “arms”:
TH1 is your killer side — natural killer cells, cytotoxic T-cells, the parts that hunt down and destroy infections, abnormal cells, and cancers
TH2 is your antibody/inflammatory side — useful in normal amounts, but when it dominates you get allergies, autoimmunity, and mast cell problems
In CIRS, TH1 gets suppressed and TH2 goes up. So your ability to fight infections drops while your ability to inflame and react to everything goes through the roof. Worst of both worlds.
T-cell exhaustion. Imagine an employee who’s been overworked for years. They still show up, but they’ve checked out. That’s what happens to immune cells under chronic insult. They’re physically present in lab tests but functionally useless. Same thing happens in cancer.
Mitochondrial dysfunction. Mitochondria are the energy producers inside your cells. When they break down, the cell can’t generate enough ATP (cellular energy) to do basic things — including pushing toxins out. This is why people on binders for years still don’t detox. The garbage trucks are running, but the houses can’t carry the trash to the curb.
Immune activation of coagulation. When the body senses chronic infection or inflammation, it lays down fibrin (a sticky protein web) trying to wall off invaders. The problem: that fibrin coats your cells and slows everything down. Oxygen that normally takes about 2 seconds to enter a cell can take up to 2 minutes. That’s where the “air hunger” feeling comes from — your lungs are fine, but your cells are starving.
Pineal/HPA axis dysfunction. The pineal gland and hypothalamus-pituitary axis run the body’s master hormonal commands. When they get dysregulated, you see the classic CIRS pattern — suppressed TSH, low T3, “tired but wired,” disrupted sleep, and standard thyroid panels that look “normal” while the person feels like they’re dying.
Barrier collapse. The gut lining and the blood-brain barrier are supposed to be selective walls. In CIRS they get leaky, which is part of why MCAS (mast cell activation syndrome — basically an immune system that reacts to everything) so often shows up alongside mold illness.
The biomarkers clinicians track for this: C4a, TGF-β1, MSH, VIP, MMP-9, and natural killer cell activity. A note on testing — Quest tends to mishandle the NK activity test. LabCorp is more reliable for that one specifically.
Section 3: The Two Approaches — Downstream vs. Upstream
The classical approach to mold treatment uses binders (compounds like cholestyramine that grab toxins in the gut and carry them out). This works, but it’s downstream — you’re catching toxins after they’re already loose, hoping to clear them faster than they’re being released. It can take 5 to 8 years on this approach, and a lot of people stall out.
The newer framework looks upstream — fix the immune system and mitochondria first, then detox. The logic:
If your immune system is broken, it can’t recognize or clear what’s colonizing you
If your mitochondria can’t make energy, your cells physically can’t push toxins out
If your barriers are leaky, you’re re-absorbing what you just excreted
Fix the upstream problems and the downstream cleanup goes from years to months. Binders still have a role — they just work way better when the system is primed to actually use them.
Section 4: Why Peptides Fit Here
Peptides are short chains of amino acids (the building blocks of proteins). They’re naturally occurring signaling molecules — your body makes thousands of them. They tell cells what to do.
There are two main categories worth knowing for this conversation:
Peptides (general category) — usually 5 to 50 amino acids long. They sit on cell surface receptors and trigger a cascade of effects inside the cell. Think of them as keys that fit specific locks.
Bioregulators — a smaller subcategory, only 2 to 4 amino acids long. Because they’re so small, they slip into the cell, into the nucleus, and bind directly to genes. They work epigenetically, meaning they influence which genes get turned on or off without changing the DNA itself. Bioregulators are gentle, slow-onset, and rarely cause reactions — which makes them ideal for sensitive research subjects.
The reason peptides work so well together: unlike pharmaceuticals, where stacking drugs multiplies side effects, peptides tend to complement each other. You can layer a bioregulator with two or three peptides and get a synergistic effect rather than a toxicity problem.
A note on oral peptides: when a peptide is capped (chemists add an acetyl group to one end and an amide group to the other), it survives stomach acid and absorbs well. Uncapped peptides get destroyed before they can work. The “arginine salt” version of certain peptides looks similar on a label but doesn’t survive — it’s marketed as “stable” but functionally less effective.
Section 5: The Layered Research Framework
This is the sequencing that’s emerging from clinical observation. Each layer prepares the system for the next. Skipping ahead causes problems — running offensive peptides before defensive ones is a common mistake that produces severe reactions.
Layer 1 — Calm and Modulate
For sensitive research subjects (which most CIRS-affected RS are), bioregulators come first. They’re the gentlest entry point and rarely produce reactions.
Thymus bioregulator — modulates the immune system as a whole, the foundation peptide
Pineal bioregulator (Epitalon class) — supports the master hormonal axis. Dosing note: research models support AM dosing rather than PM, even though it influences melatonin. PM dosing can keep the RS wired at night
Vascular/blood vessel bioregulator — supports the coagulation piece
Standard cycling in older literature: 1 cap twice daily for 1–2 months, then 10 days per month thereafter. Important context: that 10-day cycle came from anti-aging research where cost and pill burden were the main constraints (24+ separate organ bioregulators stacking up). For research subjects with active illness, longer continuous use during the active recovery phase usually makes more sense. Cycle down once the system stabilizes.
Layer 2 — Repair the Barriers
Before pushing the immune system harder, you need the walls intact. Otherwise everything you do leaks.
Larazotide — repairs tight junctions (the seals between gut cells). Sourced through compounding pharmacies for research only, since it’s a pharmaceutical compound
Rebamipide (Lexinox) — a mast cell stabilizer that’s also approved in Japan for sinus inflammation. Has a side benefit of regulating blood sugar in research models. Compounding pharmacy sourcing
Peptide-S (the body protection compound class) — the workhorse for gut and systemic barrier repair. The properly capped oral form survives digestion; injectable also works well
KPV — an anti-inflammatory mast cell stabilizer that’s also antimicrobial against staph and candida in research. Important sequencing note: in RS with heavy candida or staph colonization, KPV can produce die-off symptoms because it’s actually killing those organisms. That’s why it’s often staged later, not first
Layer 3 — Rebuild the Immune System
Now that the barriers hold, you can push TH1 up and pull TH2 down without the system rebelling.
Thymogen Alpha-1 / Thymosin Alpha-1 class — the cornerstone for raising TH1. Used internationally in research for respiratory infections, immune deficiency, and as a cancer adjunct
TB-4 fragment (the N-terminal immune fragment) — this is a critical distinction. The full TB-4 molecule has a middle section that stimulates mast cells, which is the opposite of what you want in MCAS-presenting RS. Most “TB-500” products on the market are actually that middle (actin-binding) fragment — useful for tissue regeneration, not for immune work. Make sure you know which fragment you’re researching
Thymalin/Vilon bioregulator combinations — oral bioregulator route to similar TH1 support
Layer 4 — Clear the Burned-Out Cells (If Needed)
Some research subjects have so many senescent cells (zombie cells — cells that should have died but didn’t, and are now leaking inflammation) that mitochondrial peptides backfire on them. The mitochondria are too damaged to respond.
If that’s the case, run a senolytic protocol first to clear the zombie cells:
FOXO4-DRI peptide — research compound for clearing senescent cells
Dasatinib + Fisetin combination — small-molecule alternative used in research, typically 3 days per month
Start very low. If you have a lot of senescent cells to clear, going in hot causes a significant reaction.
Layer 5 — Restore Mitochondrial Function
With the burned-out cells out of the way, you can rebuild cellular energy.
SS-31 (Elamipretide class) — heals the inner membrane of the mitochondria (the cristae) rather than just stimulating. Good for already-stressed mitochondria
MOTS-c — a mitochondrial peptide that’s more stimulating. Important sequencing point: don’t run this early in CIRS RS because it pushes already-inflamed mitochondria to do more, which produces more reactive oxygen species and more inflammation. It’s a Layer 5 tool, not a Layer 1 tool
Humanin — got its name because it made Alzheimer’s research subjects functional again. Strong neuroprotective profile in research literature
Layer 6 — Now Detox Actually Works
This is where binders, sauna, glutathione support, and all the standard detox protocols suddenly start producing results in weeks instead of years. The immune system can recognize what to clear, the mitochondria have the energy to push toxins out of cells, and the barriers hold so you don’t re-absorb what you just excreted.
This is also where addressing chronic infections fits — Lyme, co-infections, chronic candida, persistent viral reservoirs. LL-37 belongs here, which gets its own section below because it’s frequently misused.
Layer 7 — Brain and Nervous System Recovery
A lot of CIRS RS have significant neuroinflammation — brain fog, anxiety, sleep disruption, autonomic dysregulation.
Selank — calming, immune modulating, useful for anxiety presentations
Semax — more activating, cognitive support
Cerebral peptide blends — research dosing often needs around 4 caps per day for full effect (lower doses tend to underperform)
Cognitive peptide (Pinealon class) — works subcortically, ~100mcg roughly comparable to ~200mg of cerebral peptide blends in research
GHK-Cu — useful for connective tissue, neuropathy, and anxiety. Subcutaneous injection can be irritating; some research protocols dilute it and inject intramuscularly to reduce skin reactivity
Sequencing note for nasal sprays: a lot of CIRS RS have fungal or bacterial colonization in the sinuses that doesn’t belong there. Spraying Selank or Semax into a colonized sinus underperforms — clear the terrain first, then nasal delivery works as intended. Until then, injectable performs more reliably.
Section 6: VIP — Why It Gets A Special Warning
VIP (Vasoactive Intestinal Peptide) is positioned in the classical mold protocol as the “final step” — the peak of the pyramid you climb toward once everything else is corrected. Research subjects often report feeling better on it initially. That’s exactly what makes it tricky.
Looking at the actual mechanism: VIP raises TH2 and lowers TH1. That’s the opposite of what CIRS RS need. It does suppress both arms somewhat, but the net shift goes the wrong direction for sustained recovery.
What this looks like in practice: RS feel better on VIP, but the moment they get re-exposed to mold, perfume, or any inflammatory trigger, they crash hard. The immune system never actually got rebuilt — it got pharmacologically suppressed into a temporary equilibrium. The crash threshold stays low.
There’s also the sinus colonization issue layered on top. VIP nasal sprayed into a colonized sinus isn’t reaching what it’s supposed to reach, and may actually be feeding the wrong response.
The research-informed alternative is what’s outlined in the layered framework above — rebuild TH1, modulate barriers, fix mitochondria, clear infections, detox. The “feeling better” comes from actual recovery rather than pharmacological masking, and re-exposure resilience improves.
If VIP gets used in a research context, it’s short-term, late-stage, after the upstream work is already done — never as the primary intervention.
Section 7: LL-37 — Why It Gets Its Own Section Too
LL-37 is the human cathelicidin — an antimicrobial peptide your immune cells naturally produce. It’s effectively the body’s broad-spectrum endogenous antibiotic, with research activity against:
Gram-positive and gram-negative bacteria
Fungi, including Candida species
Some enveloped viruses
Biofilms — and this is the critical one for CIRS
A quick definition: a biofilm is a slimy protective matrix that microbes build around themselves. Lyme, co-infections, chronic staph, candida — they all hide inside biofilms, and conventional antimicrobials can’t penetrate the matrix. The infection persists even after years of treatment because the drugs literally can’t reach the bugs.
LL-37 in research has shown the ability to disrupt those biofilm matrices, exposing the organisms to clearance. That’s huge. It’s also what makes LL-37 dangerous to use early.
The catch — and this matters for CIRS research subjects:
LL-37 is not a Layer 1 peptide. Running it early in an RS who has high inflammation, MCAS, broken barriers, and dysfunctional mitochondria can produce severe Herxheimer-style reactions because:
Rapid microbial die-off releases endotoxins into a system that can’t process them
The TH2-skewed immune system interprets the die-off as more insult, ramping inflammation higher
Biofilm disruption releases sequestered metals and toxins (biofilms hoard heavy metals as part of their defense), and the mitochondria can’t yet clear them
The sequencing rule: LL-37 belongs after immune modulation, after barrier repair, and with mitochondrial support already running. It’s an offensive weapon. You don’t deploy offense before the defense is built.
Research dosing in the literature varies considerably. The principle that holds across the published work: start at a fraction of the target dose and titrate up. If an RS reacts to half a Peptide-S capsule, they’re going to react to LL-37 — period. Some research protocols start at 10% of the eventual target dose and ramp slowly over weeks.
LL-37 also has a specific role in research models for chronic sinus colonization, often paired with biofilm-disrupting compounds. This ties back to the nasal spray point earlier — clearing sinus terrain is often what unlocks the rest of the protocol working properly.
Section 8: The Practical Takeaways
CIRS isn’t one thing. It’s an immune dysfunction that lets multiple problems compound on each other — mold, infections, metals, barrier damage, mitochondrial collapse, autonomic dysregulation. Anyone selling a single peptide as the answer is missing the picture.
The summary of the research-informed sequencing:
Get out of the exposure first (no peptide undoes ongoing exposure — this is non-negotiable)
Start with bioregulators to gently modulate the immune system
Repair barriers before pushing harder
Rebuild TH1 and rebalance TH2
Clear senescent cells if mitochondrial response is sluggish
Restore mitochondrial energy production
Now detox effectively
Address chronic infections — this is where LL-37 fits, not earlier
Rebuild brain and nervous system
Transition to long-term maintenance with cycled bioregulators
Section 9: A Few Final Notes
On cycling. The “10 days on, then break” model from older research came from anti-aging populations where cost and pill burden were the main constraints. For research subjects with active multi-system dysfunction, the literature and clinical observation both support longer continuous use during the active recovery phase, transitioning to cycling once the system has stabilized. There’s no single right protocol — it depends entirely on where the RS is in the recovery arc.
On sourcing. Oral bioregulator quality varies wildly. The capping (acetylation and amidation) determines whether the molecule survives stomach acid. Uncapped or salt-form versions look identical on a label but perform very differently. For research-only pharmaceutical compounds like Larazotide and Rebamipide, compounding pharmacy sourcing is the standard route.
On expectations. This framework typically cuts recovery time significantly compared to binder-only approaches — the kind of timeline where what used to take 5 years takes 1 to 2, and milder cases sometimes resolve in months. But CIRS is genuinely complex, and individual response varies. Working with a clinician who understands this terrain is the difference between a structured recovery and another decade of trial and error.
Drop questions below — happy to go deeper on any specific layer, biomarker, peptide class, or sequencing question.

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