Who’s Right About Mold Illness?

Your guide to the 4 thought leaders in mold treatment

This is part 1 of 4 where I map the major thinkers in CIRS and mold-related illness: what each one believes, where each one is strong, and where each one breaks down.

This four-part series is a passion project for me. It’s something I’m thrilled to be writing about!

For decades, mold illness and CIRS had been some wacko diagnosis that had zero traction in the health and wellness space. At this time, I spent the majority of my days reaching out to individuals given a diagnosis like fibromyalgia or chronic fatigue syndrome and educating them that there’s a better way. You don’t have to be stuck with a diagnosis that offers no hope of healing. You don’t have to be stuck taking antidepressants for the rest of your life. And that no amount of stress reduction practice or graded exercise is going to ever solve this.

I encouraged patients not to settle for a CFS or fibromyalgia diagnosis. I wrote countless letters to primary care physicians that CIRS was far more of a legit diagnosis that CFS of fibromyalgia ever was. For those of you that trusted me in the early days, I offer you my profound thanks. Hope propelled us to work together. Hope in that maybe this guy knew something your doctors didn’t.

More often than not, it worked. People who had been sick for decades got better. Through that experience, I became a better clinician. I had to. Every week a patient would present with a symptom or reaction that I had never seen before. My patients made me a better practitioner. And for that I will be forever grateful.

Today, mold illness is a new world. Today, patients come to me saying they have CIRS or mold illness and that they want treatment. It’s quite rare for me to be educating patients that their CFS/fibromyalgia might actually be CIRS/mold illness.

I’m grateful for the profound shift in public awareness surrounding mold. No longer does it sound crazy to say that mold makes someone sick. We now (mostly) agree that mold in an indoor air environment is not conducive to human health.

And with this shift in awareness, we have new interpretations and understandings of how mold illness should be diagnosed and treated. This is a most wonderful development for the space. But with this explosion in knowledge, we inevitably have conflicting points of view.

Here lies today’s problem in the CIRS/mold illness space:

Patients are confused. 

They’ve read about CIRS and the Shoemaker Protocol. They’ve also read Jill Crista and Neil Nathan’s books – Break the Mold and Toxic. Andrew Campbell is saying that he is the only one with real published studies. Meanwhile, Kent Holtorf is ushering in a new era of treatment using peptides.

If you’ve suspected your symptoms are being driven by mold, without a doubt you’ve come across the above names. After spending a short time researching, you’ve probably noticed something disorienting: the experts don’t agree with each other. They’ll go on long rants about why their work is correct and the other’s is “garbage science.”

Shoemaker tells you the answer is in your bloodwork; that there’s a specific pattern of inflammatory markers that define the illness. Crista and Nathan tell you the bloodwork misses the point, urinary mycotoxins are how to test and what really matters is whether your nervous system is calm enough to tolerate treatment at all. Campbell says you should be measuring your body’s immune response to mycotoxins. Holtorf says you’re chasing the wrong thing; the real problem is a broken immune system, and you can fix it with peptides.

For a patient who is exhausted, cognitively foggy, and desperate for a clear path, this is maddening. It can feel like the field is a mess, or that nobody really knows anything.

I want to offer a different way to read it.

After years of treating complex chronic illness (specifically, patients who don’t respond to or tolerate treatment), I’ve come to believe these camps aren’t really contradicting each other. They’re answering the same question in four different ways. Once you see the question they’re each answering, the whole field stops looking like chaos and starts looking like a map.

The question is this:

What is the actual lesion?

When someone gets sick from a water-damaged building, what is the thing that is actually wrong with them? Where, precisely, is the broken part? Every major thinker in this space has staked their entire approach on a different answer. And because they’re answering different questions, they end up building different tests, different treatments, and different definitions of what “better” even means.

Before I introduce you to the four thought leaders in mold illness, I should name my biases and where I’m coming from:

I’m intimately familiar with the Shoemaker protocol. I studied directly with Ritchie and have been following his work for more than a decade. I have read all of Neil Nathan’s and Jill Crista’s books. I took Jill Crista’s practitioner training but stopped before completing it as I did not find the information was at the level I needed it to be for my complex patients. I’m familiar with Andrew Campbell through my readings on his research and the information posted on his website. I’m using Kent Holtorf as a placeholder for the use of peptides to treat complex chronic illness. I’ve read Holtorf’s work on why he thinks the Shoemaker protocol is misguided and I greatly appreciate how he is integrating and shifting the thinking around peptides and complex chronic illness.

I integrate Jack Kruse’s quantum biology principles into my thinking; especially in the context of mitochondrial health and function. Robert Naviaux’s work on the Cell Danger Response is truly remarkable. I use his philosophical lens to explain and understand how cell physiology changes in the face of chronic illness. I also took Bruce Hoffman’s practitioner training course where he integrates a unique point of view that blends Naviaux’s Cell danger Response with Kruse’s quantum biology through a practical approach as a clinician, not a researcher. I did not complete the training with Hoffman as I found the information was not at the level I needed it to be for my patient population.

All this to say, I’m writing this series of posts as someone who has invested a lot of time in each expert’s point of view. They all make great arguments for their cases and they all have glaring blindspots (as do I). My hope is that this article ameliorates your confusion between the camps and shows you that to help the chronically ill, you need to set aside being right and focus instead on the unique individual in front of you.

Camp 1: Ritchie Shoemaker

The lesion is the host

This is the position of Dr. Ritchie Shoemaker, the physician who coined the term CIRS: Chronic Inflammatory Response Syndrome. If not for Ritchie, there would be no mold illness revolution. he built the framework most of this field is reacting to, for or against.

Shoemaker’s argument is that the problem isn’t really the mold. It’s what your body does in response to the mold. In genetically susceptible people, biotoxin exposure triggers a sustained, self-perpetuating activation of the innate immune system. That cascade is measurable. There is a specific signature of inflammatory markers, and a  specific pattern of gene expression that defines the illness.

To help you better understand Shoemaker’s POV, think of CIRS as though it was an autoimmune disease. Just to be clear, CIRS is not an autoimmune disease but thinking through the lens of autoimmunity should help you better understand it. In autoimmunity, your immune system mistakenly attacks healthy cells or tissue. A virus might trigger autoimmunity but the root of the issue is a misguided immune system. CIRS is the same. Mold is the trigger. But your symptoms are maintained by a wayward innate immune system.

What makes the Shoemaker camp distinctive is its insistence on objectivity. You can prove someone has CIRS. You can prove when they no longer have CIRS. The treatment is a defined, rigidly sequential protocol. You don’t move to the next step until you’ve completed the prior.

The Shoemaker camp is the most rigorous, most reproducible, most published approach in the field. It is also the most demanding; of both the patient and of the practitioner. And as we’ll explore later in this series, that rigor is both its greatest strength and the source of its most important limitation.

Camp 2: Neil Nathan and Jill Crista 

The lesion is the patient’s tolerance state

This is the territory of Dr. Neil Nathan and Dr. Jill Crista, who now teach together and represent, in different flavors, a more individualized and patient-centered school of thought.

Their argument starts from an observation that anyone treating real patients eventually runs into: some people are so sensitive that they can’t tolerate treatment at all. Give them a binder, and they crash. Try to detox them, and they get worse. For this population, the bottleneck isn’t identifying the right protocol, it’s that their system is too reactive to receive any protocol.

So this camp reframes the lesion. The problem isn’t only the inflammation or the toxin; it’s the state of the patient’s nervous and immune system.  The cell danger response, limbic and vagal dysregulation, mast cell activation. Before you can treat anything, you have to calm the system down. The watchword is “low and slow.” Crista adds an accessible, naturopathic, food-and-foundations-first layer; Nathan brings the framework for the hypersensitive patient.

This is the most humane corner of the field. It meets patients where their physiology is at, and it rescues exactly the people the rigid protocols leave behind. Its weakness, as we’ll see, is the flip side of that flexibility: when the endpoints are soft and the diagnosis leans on clinical intuition, it gets harder to say objectively what’s wrong and when it’s fixed.

Camp 3: Andrew Campbell 

The lesion is the immune system’s reaction to the toxin

This is the position of Dr. Andrew Campbell, an immunologist who has spent his career on toxic exposures.

It’s tempting to summarize this camp as “just measure the toxin,” but that’s not quite what Campbell argues. Campbell is openly skeptical of measuring mycotoxins via urine (urinary mycotoxin tests). He states that urine is excretion, and a high level there may mean your body is successfully clearing the poison, which is a good sign rather than a diagnosis.

What Campbell wants to measure instead is your immune system’s response to mycotoxins: the IgG and IgE your body produces when it reacts to them. If you’ve ever had a food sensitivity test done… Yes, the ones that measure an IgG response to many different types of foods. You’re getting closer to Campbell’s reasoning; he states that your immune system is a fingerprint (unique to each person) so there is no one-size-fits-all protocol, and the right question is simply whether this patient has mounted an immune reaction to mold’s toxins.

The appeal here is a kind of biological logic. Rather than chasing toxin levels that come and go, you ask whether the body has registered the toxins as a threat and responded. What is very appealing about this point of view is that you can track that response over time. Lessen the mycotoxin burden and you’ll see your immune system respond in favourable direction.

The trouble is that the antibody test at the center of this approach hasn’t been independently validated the way its strongest claims suggest, and Campbell himself directs the laboratory that sells it.

Anyone that’s been in Shoemaker’s orbit will know that mold makes up a very small percentage of CIRS cases. We need to know about main drivers of this illness: actinomycetes, endotoxins, and beta glucans. This is something all the other camps are missing and we’ll dig into this in much more detail in the coming posts!

Camp 4: Kent Holtorf

The lesion is underlying immune dysfunction

This is the most directly oppositional camp to Dr. Shoemaker’s work.

Holtorf’s argument cuts underneath all the others. He says: why do some people get devastatingly ill from a building that barely affects the person sitting next to them? His answer isn’t genetics and it isn’t the dose of toxin. It’s that the susceptible patient already had a dysfunctional immune system; a characteristic shift in immune signalling, exhausted T cells, impaired natural killer cells, premature immune aging. The mold didn’t create the problem so much as expose a problem that was already present.

Treat the immune dysfunction directly (primarily with what he calls bioregulators) and Holtorf argues you can augment or even replace large parts of the Shoemaker protocol, faster and with better tolerance. He’s explicit that this is a challenge to the established approach, not a supplement to it.

For a clinic like mine that spends its days with non-responders, this camp is impossible to ignore, because it offers tools for exactly the patients who have been unable to tolerate everything else. But bold claims like “rapid,” or “superior efficacy” currently run well ahead of the published evidence, and the entanglement between the protocol and the products it requires deserves a critical look. We’ll give it one.

What every camp is missing

Here’s the thing I most want you to take from this opening piece: These four camps are presented as rivals. Patients and practitioners side with one and call the other camps bogus. But look again at what each one is actually claiming:

• Shoemaker is describing the host’s inflammatory response: the body’s reaction.
• Nathan and Crista are pointing at the nervous system’s tolerance: the patient’s capacity to be treated at all.
• Campbell is pointing at the immune system’s reaction to a toxin.
• Holtorf is pointing at the underlying immune dysfunction: the terrain that made the patient vulnerable in the first place.

Those aren’t four competing answers to one question. They’re four different layers of the same sick patient. The exposure, the immune terrain that let it take hold, the inflammatory cascade it set off, and the nervous-system state that now governs how much treatment the patient can handle.  All of these are real, and all of them are present, in varying proportions, in the people I see.

The thing that keeps patients stuck is practitioners arguing that their point of view is the only point of view. It isn’t. The art of treating complex cases is figuring out which layer is needing your attention for the patient sitting in front of you in this moment and starting there.

That’s the lens I’ll carry through the rest of this series. In the posts that follow, we’ll go through each thinker’s POV and lay out its strongest points and identify the blind spots.

In my opinion, to best serve the chronically ill, we need to set aside our desire to be right and instead focus on the human being in front of us. The goal of this series is to understand where each camp is right, what each camp misses, and how to discern which POV to focus on for each patient (as well as when to focus on it and when to pivot).

Because the patients who land in my office are usually the ones for whom a single camp’s answer already failed. Helping them starts with understanding the whole map.

Next in the series: Dr. Ritchie Shoemaker and the case for CIRS.