The Dr. Neil Nathan & Dr. Jill Crista Approach to CIRS

Note: This is part 2 of 4 of a series of blogs where I map the major thinkers in CIRS and mold-related illness: what each one believes, where each one excels, and where each one breaks down.

Introduction: I argued that the four major camps of CIRS treatment aren’t actually contradicting each other. Each one is answering the same question in a different way: Where is the illness?
Part One: Does the Shoemaker Protocol Work? This post looks at the camp that addresses the question scientifically.
Part Two: Addressing the needs of the CIRS patient. We take a look at two clinicians who focus on the most sensitive patients.

*Note: this blog was written by me, Mark Volmer. All spelling mistakes, misquotes, errors, and omissions are my own doing. It is not AI generated. *

If Dr. Shoemaker’s contribution to CIRS was making the illness measurable, Dr. Neil Nathan and Dr. Jill Crista‘s contribution is making the sickest, most fragile patients feel treatable. That is not a small contribution. The majority of patients suffering from CIRS have been give the runaround, or completely dismissed from mainstream medicine.

Dr. Nathan and Dr. Crista have built their entire approach around the patient that the rigorous protocols leave behind — the one who is too sensitive, too reactive, too dysregulated to tolerate standard treatment.

They work and teach together now, so I’ll treat them as one camp, while noting where they diverge. Dr. Nathan, an MD, is the author of Toxic and the dominant voice on the hypersensitive patient. Dr. Crista, a naturopathic doctor and author of Break the Mold, brings the more accessible, plant-and-foundations-first version of the same philosophy. Together they anchor the individualized, “low and slow,” nervous-system-first school of mold treatment.

Expert Recap: Dr. Neil Nathan and Dr. Jill Crista Mold Illness Treatment Viewpoint

Dr. Neil Nathan and Dr. Jill Crista’s approach is specific to the subset of CIRS patients who are too sick to begin treatment. Their approach revolves around increasing the patient’s tolerance for treatment with a gentle approach. However, to diagnose these patients, they use the discredited urinary mycotoxin test. The urinary mycotoxin test can be affected by diet, supplements, and hydration, which makes it an unreliable indicator of illness.

Where Dr. Neil Nathan and Dr. Jill Crista say the illness lives

Recall the original framing question, “Where is the illness?”. For Dr. Shoemaker, the illness is the body’s inflammatory response, and the genetics that prime it. For Dr. Nathan and Dr. Crista, the problem is the patient’s tolerance level.

Their starting observation is one every honest mold practitioner eventually confronts. A subset of patients — often the sickest — cannot tolerate treatment. You hand them a binder and they don’t slowly improve; they crash for weeks. Their mast cells are on a hair trigger, their nervous system is locked in a defensive crouch, and almost any intervention registers as a threat. For this patient, Dr. Nathan argues, the bottleneck was never identifying the right protocol. It’s that their system is too reactive to receive any protocol until you’ve calmed it down.

So the whole approach revolves around patient tolerance:

Go low and slow
Stabilize mast cells first
Address limbic and vagal dysregulation — the trauma-shaped, threat-locked nervous system — as foundational, not optional.

Dr. Nathan is explicit that many of these patients carry what he calls iatrogenic PTSD, injured as much by years of medical dismissal as by the mold itself. Dr. Crista’s version softens the entry even further: she leads with bioflavonoids and bile support before binders, on the logic that you can open the body’s own drainage and clearance pathways before you ask it to tolerate anything aggressive. Her belief is that you shouldn’t have to feel “hit by a truck” to get better — the crash isn’t a sign of progress, it’s a sign you went too fast.

This is humane medicine. It meets the patient where their physiology actually is. And for the reactive patient, it is frequently the only thing that works, because it’s the only approach that treats being too sick to be treated as the first problem to solve.

The deep divide: mold as colonizer

Here’s where the approach makes a claim that puts it on a collision course with Dr. Shoemaker — and it’s the part patients rarely understand.

For Dr. Nathan and Dr. Crista, mold isn’t just something you were exposed to in a building. It’s something that has taken up residence inside you. Dr. Crista puts it vividly: the people who get sick are the ones whose internal flora has fundamentally shifted — they have, in her words, become the moldy building. Mold moves into the sinuses, the respiratory passages, the gut. It forms biofilms. It colonizes.

That single premise reshapes the entire treatment. If mold is colonizing you, then you have to kill it where it lives — and that means antifungals. This is the core of what they do:

Intranasal antifungals. The sinuses are treated as a fungal reservoir whether or not the patient has any sinus symptoms at all — Dr. Crista is explicit that sinus exposure, not sinus symptoms, is the indication.

Gut antifungals and biofilm disruption. Both treat fungal overgrowth in the gut, typically with biofilms first and then layering in antifungals.

The Brewer lineage. This colonization-and-antifungal thinking traces substantially to Dr. Joseph Brewer’s work on intranasal antifungal treatment, which Dr. Nathan integrated into his protocol. It’s a genuinely different intellectual lineage than Dr. Shoemaker’s.

Why this is the crux — and where I get cautious

Now we have to talk about the elephant in the room, because this is the single sharpest disagreement in the entire field.

Dr. Shoemaker’s camp — and, notably, the Centre for Disease Control (CDC) — holds that mold illness from a water-damaged building is an inflammatory condition, not a fungal infection. Patients suffering from CIRS were poisoned by toxins and inflammagens; fungi are not actively growing inside your body. And antifungals are drugs designed to treat active fungal infections. From Dr. Shoemaker’s viewpoint, prescribing systemic antifungals for a toxin-and-inflammation illness is treating a disease the patient doesn’t have.

This isn’t a fringe objection. In 2014, the CDC published a report specifically criticizing the practice of diagnosing patients with “mold toxicity” via urine mycotoxin testing and then prescribing antifungals. They noted plainly that antifungal medications treat fungal infections, not illnesses caused by toxins produced by fungi. The agency’s position is that:

Mycotoxins show up in the urine of healthy people,
No validated threshold predicts disease, and that
There is no FDA-approved urine mycotoxin test.

Urine mycotoxin testing is woven into how the Nathan-Crista world identifies and tracks fungal burden. However, Dr. Crista’s own materials acknowledge that diet, binders, and glutathione can all affect the results, which is a quiet admission of how unreliable the test can be.

Is the Nathan/Crista approach to mold illness treatment right?

So who’s right? Here’s my honest read, and it’s not a clean verdict.

I think the model of fungal colonization is overused, but not without merit. There genuinely are patients with fungal colonization of the sinuses. Fungal sinusitis is a real diagnosis, and some CIRS patients do have an actual fungal component that responds to anti-fungals. The problem is the leap from “some patients have fungal colonization” to “mold illness is fundamentally a colonization problem, so nearly everyone needs antifungals.” That is an unproven generalization. When a protocol treats the sinuses as a fungal reservoir regardless of symptoms, and uses an unvalidated urine test to justify months of systemic anti-fungals, you are exposing a lot of patients to real drugs with very real risks. The prolonged use of anti-fungals is not benign.

The most defensible position, I think, sits between the two camps: antifungals are appropriate when there’s actual evidence of infection or colonization: imaging, culture, a genuine clinical picture. However, they are being overused when they’re prescribed reflexively to anyone with a positive urine mycotoxin result. Dr. Nathan and Dr. Crista are right that some patients have a fungal component that the pure-inflammation model misses. They go too far when colonization becomes the default explanation for every patient.

What their workup leaves out

There’s a second, quieter divergence that matters just as much, and it’s the one that most directly explains why I keep the Shoemaker Protocol as my foundation.

The Nathan-Crista model is built around mold and mycotoxins. But a water-damaged building is not just a mold problem. Alongside the mold and its mycotoxins, there are bacterial endotoxins, actinobacteria, beta-glucans, microbial volatile organic compounds, and inflammagens that have nothing to do with fungi at all. Dr. Shoemaker’s framework takes this seriously — the illness is a response to the whole inflammatory load of the building, not just the fungal fraction.

A workup organized around mycotoxins and fungal colonization can overlook all of that. If a patient’s dominant driver is endotoxin or actinobacterial exposure, a treatment plan built around killing fungus and binding mycotoxins may be aiming at the wrong target. The patient who doesn’t get better then gets told they need more anti-fungals, longer, when the actual inflammagen was never fungal to begin with.

The individualized, symptom-and-tolerance-driven approach is often light on those measurements. That’s the trade-off baked into a model that prioritizes how the patient feels and tolerates over what the labs show: you gain enormous flexibility and humanity, and you lose the external referee. It becomes harder to say objectively what’s driving the illness, and harder to know when it’s truly resolved versus when the patient simply feels better for now.

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The problem with urinary mycotoxin testing

I’ve referred a couple of times now to urine mycotoxin testing as “unvalidated,” and I owe you a fuller accounting, because this test is woven through how much of the Nathan-Crista world identifies fungal burden and tracks progress — and it has more failure points than most patients realize. This is worth understanding in detail, because if the test is unreliable, every treatment decision built on top of it inherits that unreliability.

Here is what a urine mycotoxin test actually does: it detects mycotoxins in your urine. That’s it. The interpretive leap — from “mycotoxins are in your urine” to “mold is making you sick” — is where the problems pile up.

It measures excretion, not illness.

Urine is how the body gets rid of things. So a positive result confirms that mycotoxins passed through you — not that they’re harming you. In fact, you can construct exactly opposite stories from the same number:

A high level might mean a big toxic burden = Bad

A high level might mean your body is clearing toxins efficiently = Good

The test can’t tell you which.

Mycotoxins are in healthy people’s urine

Mycotoxins are common contaminants of ordinary food — grains, coffee, nuts, dried fruit. The CDC has pointed out that precisely because of dietary exposure, mycotoxins show up in the urine of healthy people. So a positive test may be measuring your breakfast, not your basement. The test generally can’t distinguish a food source from an environmental one.

There’s no validated threshold for disease

This is the biggest problem. For a lab value to mean something clinically, somebody has to have established what level predicts illness. This is the work that turns a number into a diagnosis. For urine mycotoxins, that work hasn’t been done. No study has demonstrated an association between a given urinary mycotoxin level and any specific disease state. There also is no FDA-approved urine mycotoxin test. The “elevated” cutoffs on these reports are lab-defined, not disease-validated.

The result swings based on how you prepared

This one should trouble anyone who values reliability. The number you get depends heavily on what you did before collecting:

Glutathione binds to mycotoxins and chemically changes them so the mass spectrometer can’t detect them — so taking it before a test can drive results falsely low. The labs themselves instruct patients to stop it for days beforehand.
Hydration moves the number: dehydration can inflate some labs’ results, over-hydration can dilute them.
Diet in the days before collection changes dietary mycotoxin load and therefore the result.
Binders taken beforehand alter what’s excreted.

When a test result depends this much on patient prep, you’re no longer measuring a stable property of the patient. You’re measuring a moment, shaped by a dozen variables.

Different labs give different answers

Run the same patient through different laboratories and you can get materially different results, because they use different methods, different panels, and different reference ranges. Even Dr. Crista’s own materials acknowledge that different labs test differently and that results vary accordingly. A test that doesn’t agree with itself from one lab to another is a shaky foundation for a treatment plan.

And — most revealing — a negative result rarely ends the inquiry

Here’s the tell that should give any careful clinician pause. Within this world, a negative urine test is frequently explained away: the patient is “too sick to excrete,” the toxins are “trapped in the cells,” they’ll “show up once detox begins.” One major lab states outright that you can be negative on the urine test while mycotoxins are still present in the cells causing damage. Now, sometimes that’s biologically true. But notice what it does to the logic. If a positive result confirms mold illness and a negative result also confirms mold illness, then the test results will never change the conclusion. A test that can only ever support the diagnosis isn’t functioning as a diagnostic. It’s functioning as a confirmation.

I want to be fair: the underlying laboratory technology is real. Mass spectrometry can genuinely detect mycotoxins at tiny concentrations, and some labs do thoughtful things like creatinine-correcting for dilution. The problem isn’t that the machines don’t work. It’s that detecting a molecule and diagnosing a disease are two very different things. Urinary mycotoxin testing quietly slides from the first to the second without the validation that move requires.

None of this means mold doesn’t make people sick — it plainly does. It means that this particular instrument can’t reliably tell you whether mold is making this particular patient sick, or how sick, or whether they’re getting better. And when a model leans on that instrument to justify months of anti-fungals, the unreliability of the test becomes the unreliability of the whole treatment plan.

What I take from this camp

I want to be careful not to let the criticism eclipse the genuine contribution, because the contribution is real and I use it.

Dr. Nathan and Dr. Crista are right about the thing that matters most for the patients who end up in my office: you cannot run a protocol on a patient whose system won’t receive it. This is what the rigid protocols are missing:

Calm the nervous system,
Stabilize mast cells,
Go low and slow
Respect the limbic and vagal state before pushing detoxification

For the reactive patient, this is the difference between a patient who recovers and a patient who crashes and quits.

Where I diverge is on the model underneath the kindness. I think the colonization-and-antifungal framework is applied too broadly, leans on testing that can’t bear the weight placed on it, and risks missing the non-fungal inflammagens.

The honest synthesis, the one I try to practice, is to take their sequencing wisdom and graft it onto Shoemaker’s objective foundation. Meet the sensitive patient where they are, calm the system first, go slow — but keep measuring, and stay humble about whether the problem is really fungal at all.

Mold Illness Treatment Viewpoint Three: Dr. Andrew Campbell

Which brings us to the third camp that says the whole argument is misframed. This camp says that you should stop fighting the body’s response and the colonization, and just measure the toxin directly.

Next in the series: Dr. Andrew Campbell and the case for measuring the toxin — and why the test at the center of it is the most contested in the field.