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 with a fierce amount of scientific inquiry.
Part Two: Addressing the needs of the CIRS patient. We take a look at two clinicians who focus on the most sensitive patients.
Part Three: Mycotoxins and the immune response. Examining the diagnostic method of Dr. Andrew Campbell, a clinician who looks at the immune system’s antibodies response.

*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.

Unfortunately, this level of dismissal can (and often does) occur from well meaning Shoemaker Practitioners. I’ve seen a large number of patients that had horrendous reactions to Welchol or CSM. Unfortunately, their concerns were brushed off by the practitioner. You may have been told that CSM and Welchol aren’t absorbed so there’s no possible way they could trigger your headache/fatigue/brain fog/pain etc.

There’s far more that we don;t undertand about CIRS and chronic illness than what we do. Taking a place of humility and honouring the patient’s lived experience is our job as healers. Most patients have been gaslit for years. The last thing they need is another practitioner telling them their reactivity is in their head.

Enter Neil Nathan and Jill Crista. Dr. Nathan and Dr. Crista have built their entire approach around the patient that the rigorous protocols leave behind. They’re the ones looking out for the patient 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 (the innate immune system), 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 react to nearly everything. One of my more severe patients presented to me only be able to eat lamb. And the lamb had to be cooked from frozen. There was nothing else this patient could tolerate.

How do you think this patient would have reacted if I suggested they take four grams of Choelstyramine four times per day?

In these patients, the 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 go slow.
Stabilize mast cells first
Address limbic and vagal dysregulation 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.

I love this approach. It’s human. And 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.

Now I want to add an important caveat. All too often, what I find to be the underlying cause of the histamine, the mast cells, the ultra-reactive nervous system is ongoing exposure. And this is what Ritchie gets so very right. No patient is going to heal until they’ve solved for exposure. Remember, it’s not just mold. It’s all the other biotoxins that may be keeping you profoundly reactive. Always start with your environment.

The deep divide: mold as colonizer

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 shapes the lens in which Crista and Nathan view mold illness through. 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.

Does mold colonize you?

Now we have to talk about the elephant in the room: mold as a colonizer of the human body. This where Shoemaker and Nathan/Crista diverge sharply.

Dr. Shoemaker 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.

Ritchie goes even further; He talks about how -azole antifungal drugs can actually close the voltage dependent anion channel (VDAC) in your mitochondria. In a CIRS patient, this has the potential to make your fatigue much more intense. (source) Worse still, Ritchie posits (with evidence, i might add) that these -azole antifungal drugs will cause grey matter nuclear atrophy: shrinkage or loss of neurons and synaptic connections within the deep, structurally dense clusters of grey matter (nuclei) in the brain.

Now, what we don’t know is whether or not herbal anti-fungals can cause similar VDAC closures and grey matter nuclear atrophy. They might… I think caution is warranted. Especially since I haven’t seen compelling evidence to suggest that the body becomes a storehouse for molds. Even if that did hold to be true, we know that the vast majority of CIRS cases aren’t driven by mold anyways!

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

So, who’s right?

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.

More importantnly, this is so easily tested for. Swab the sinus. Send it to the lab for analysus. In a week you’ll know if there’s a fungal resevoir or not. Clinically, I find MARCoNS to be far more common than fungal colonies.

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.

My concern with this point of view is that mold has become the new candida. Candida was one of those naturopathic diagnosis that seemed impossible to disprove. Everyone had it! From gut tests, to antibody test, to spit in a cup tests, they all pointed towards candida overgrowth.

I don’t want CIRS and mold illness to go down the same path: a catch-all diagnosis that doctors roll their eyes at.

Laboratory testing a la Nathan & Crista

Lab testing is a particular divergence that 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 may be bacterial endotoxins, actinobacteria, beta-glucans, microbial volatile organic compounds, and inflammagens. Some of these have nothing to do with fungi at all. Dr. Shoemaker’s framework takes this seriously. Ritchie is constantly looking for other pathogens that could drive the illness. CIRS 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 endotoxins or actinobacteria 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… this is a real problem.

And with that in mind, we turn our attention to the hotly contested topic of urinary mycotoxin testing!

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The problem with urinary mycotoxin testing

I’ve referred a couple of times now to urine mycotoxin testing as “unvalidated,”. Now, we jump into why I take this stance. This test is woven through how the Nathan-Crista world identifies fungal burden and tracks progress. Unfortunately, it has more failure points than most patients realize. I want you to understand this 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 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 we run into issues. Here’s the paper Ritchie wrote about why he is not a fan of urinary mycotoxin testing. I’ll pull out the highlights in the below paragraphs.

Urinary mycotoxin testing measures excretion, not illness.

Urine is how the body gets rid of things. So a positive result confirms that mycotoxins passed through you. That’s good news. It does not suggest that mycotoxins are 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

Which one is it?

The test can’t tell you which one it is.

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. These tests 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. Taking glutathione 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. Remember, mycotoxins are found on food and what you ate areound test time is going to alter your results!
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.

Perhaps 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 by the patient is “too sick to excrete,” the toxins are “trapped in the cells,” they’ll “show up once detox begins.” 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’m not picking on the technology. 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. I’m confident all of you reading this agree that mold makes one sick. But what I’m trying to get at here is 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.

Binders, food, and other points of divergence between the camps

Approaching from the a patient-centered perspective has helped expand options for a CIRS/mold patient. In the beginning, Cholestyramine (CSM) was the only game in town. That was the only binder on offer. If you didn’t tolerate it, there was something wrong with you.

Crista and Nathan have taken holistic and naturopathic approach to binding. And I love that they’re doing it. The majority of my patients cannot tolerate CSM. If I’m to adhere strictly to the Shoemaker protocol, I have two levers in which I can pull when it comes to binding: CSM or welchol. Neither of these work for a large portion of my patients.

Enter natural binders.

Now, most natural binders get it wrong. They extrapolate binding for heavy metals (lead, mercury, etc.) and apply it to biotoxins. Wrong. Lead and mercury are positively charged elements. To bind them, you would want to use a negatively charged binder. Things like chorella, chitosan, bentonite clay, charcoal.

But biotoxins are not elements. Nor are they positively charged. In fact, they’re negatively charged. So when you use those natural binders, you’re actually repelling the very thing you’re trying to bind.

To properly bind biotoxins, you need positively charged binders. Ideally, this binder sequesters your bile acid. We want this to happen as the biotoxins reside in your gallbladder. They’re secreted when you gallbladder squirts bile into your digestive tract. In order for a binder to work, it needs to bind to the bile acid (and thus the biotoxin).

Ritchie Shoemaker is clear that CIRS is an inhalational illness. We do not get CIRS from eating mold. Blue cheese does not cause CIRS. Nor does consuming any food high in mycotoxins. CIRS is an illness that comes from inhaling biotoxins from a water damaged building. Low mold diets don’t solve for CIRS. The low mold diet is just the candida diet rebranded.

I won’t sit here and say that diet is unimportant. It is incredibly important. But it won’t solve for CIRS. For a lot a people, starting a low mold diet is the first step in dietary change. It’s the transition from a standard American/Canadian diet to a whole food based diet. That transition will inevitably help some of your symptoms. But let’s be clear: most of us will feel better when we swap hot dogs, twinkies, and soda for salmon, kale, and filtered water.

What I take from Nathan and Crista

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. Protocols ignore the human being sitting in front of you. Protocols suggest that you can treat everyone the same. You can’t. Jill Crista and Neil Nathan have done an incredible job focusing on the individuality. The meeting the person where they are at. I love their focus on:

Calming the nervous system.
Stabilizing mast cells.
Go low and go 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. Most natural binders miss the mark completely. And a low-mold diet isn’t going to solve this illness.

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: why the test at the center of it is the most contested in the field.