In August 2025, Jordan Peterson's daughter Mikhaila announced that her father had been diagnosed with Chronic Inflammatory Response Syndrome — CIRS — after years of debilitating symptoms that no one could fully explain. Profound fatigue. Cognitive decline. Food sensitivities so severe he could tolerate nothing but meat. Canceled tours, paused podcasts, and what Mikhaila described as pain-induced weepiness that the public had been watching for years without understanding its cause.
What made Peterson's case so striking wasn't just the severity. It was the timeline. His family now believes CIRS has been the underlying driver of his health problems since at least 2017. The formal diagnosis didn't come until 2025 — after a severe flare triggered by mold exposure while cleaning out his late father's home sent him into a spiral that ultimately landed him in the ICU with pneumonia and sepsis.
Peterson's experience put a name and a face on a condition that millions of people are living with — most of them undiagnosed.
At Global Apheresis, we've been treating patients with CIRS using plasmapheresis — also known as therapeutic plasma exchange — and seeing a pattern that traditional CIRS protocols alone often can't address. This article explains why, and what plasmapheresis offers that other approaches do not.
What Is CIRS?
Chronic Inflammatory Response Syndrome is a multi-system, multi-symptom illness first characterized by Dr. Ritchie Shoemaker. It occurs when the body's innate immune system becomes locked in an activated state, typically because it cannot clear certain environmental biotoxins.
The most common trigger is exposure to water-damaged buildings: mold, bacteria like actinomycetes, and volatile organic compounds. But CIRS can also follow Lyme disease, cyanobacteria exposure, and other biotoxin encounters. The trigger starts the process. The immune system's inability to shut it down is what makes it chronic.
The genetic component is significant. Roughly 25% of the population carries HLA-DR/DQ haplotypes that impair the adaptive immune system's ability to recognize and tag these biotoxins for removal. In these individuals, biotoxins don't get cleared. They recirculate through the blood and plasma, triggering inflammation that persists long after the original exposure has ended.
Why CIRS Is So Difficult to Diagnose
The symptom profile of CIRS reads like a medical catch-all. Patients present with clusters that span nearly every organ system: crushing fatigue unresponsive to rest, executive dysfunction and memory impairment that patients describe as “brain fog,” ice-pick headaches, joint pain and morning stiffness, shortness of breath, chronic sinus congestion, night sweats, excessive thirst, frequent urination, and sensitivity to light.
These symptoms overlap extensively with fibromyalgia, chronic fatigue syndrome (ME/CFS), and long COVID , which is not a coincidence. We'll return to that.
The diagnostic workup involves markers that most conventional physicians don't routinely order: Visual Contrast Sensitivity testing, MSH (melanocyte-stimulating hormone), VIP (vasoactive intestinal polypeptide), C4a, TGF-Beta 1, and ADH/osmolality panels. These markers paint a picture of immune dysregulation that standard bloodwork misses entirely.
This diagnostic gap is exactly what the Peterson family described. Years of symptoms. Multiple specialists. No unifying diagnosis until a clinician who understood CIRS finally connected the dots.
The Shoemaker Protocol, and Where It Falls Short
The standard treatment framework for CIRS follows the Shoemaker Protocol, a tiered approach that begins with removing the patient from the source of exposure and progresses through biotoxin binding with agents like cholestyramine, eradication of nasal biofilms (MARCoNS), and targeted hormonal correction.
This protocol helps many patients. For some, it resolves the condition entirely. But for a meaningful subset, particularly those with prolonged exposure, high toxin burden, or genetic profiles that make clearance especially difficult, oral binders and nasal protocols are not enough. The toxins continue to circulate. The inflammatory cascade continues. Symptoms persist.
This is where the conversation about plasmapheresis begins.
How Plasmapheresis Addresses What Oral Protocols Cannot
Plasmapheresis, also called therapeutic plasma exchange (TPE), works on a fundamentally different level than oral binders.
Cholestyramine and similar agents bind biotoxins in the small intestine, interrupting the enterohepatic recirculation loop. This is effective for toxins that cycle through the gut. But many of the inflammatory mediators driving CIRS (autoantibodies, cytokines, complement proteins like C4a, and the biotoxins themselves) circulate in the plasma. They are not accessible to oral binders.
Plasmapheresis removes the plasma directly. The patient's blood is drawn, separated into cellular components and plasma, and the plasma, carrying the accumulated inflammatory burden, is discarded and replaced with clean albumin solution. The blood cells are returned. The procedure takes two to three hours and is performed outpatient.
What this achieves is a reduction in circulating inflammatory mediators that oral protocols cannot reach. For CIRS patients who have done the foundational work but remain symptomatic, plasmapheresis addresses the residual burden that keeps the immune system locked in its activated state.

