A patient recently forwarded me Dr. Russell Blaylock’s newsletter “Rethinking Dimethyl Sulfoxide.” In it he cites cell-culture and developmental-animal data suggesting low-dose DMSO can promote α-synuclein aggregation, impair astrocytes, damage mitochondria, and harm developing neurons. The concern is real and deserves a direct response—especially for those enrolled in or considering our registered pilot, DART-TINN (NCT07567274).

I am the principal investigator of that study, which is funded by the non-profit Rebuild Medicine. We are testing a dual-route, compounded DMSO regimen specifically for refractory subjective tinnitus that began or worsened after PASC or COVID-19 vaccine injury. More than 500 of our roughly 4,000 patients carry this symptom; for many it is relentless and life-altering. “Nothing we can do” is no longer an acceptable answer.

What the two perspectives actually say

A Midwestern Doctor has spent the last two years assembling the largest accessible review of DMSO’s history, toxicology, and clinical use. He documents decades of human exposure (hundreds of thousands of patients), high-dose toxicology studies across species that found no major organ toxicity, and protective effects—radical scavenging, improved microcirculation, anti-inflammatory action, and the ability to revive stressed cells. Common effects are garlic odor and transient skin irritation. Severe reactions are rare. AMD frames the FDA’s long-standing restrictions as political and economic rather than driven by genuine safety signals. Mary Beth Pfeiffer’s recent investigative piece, “Stanley Jacob’s Remarkable Medicine Was Buried by Government. But DMSO Lives,” reaches a similar conclusion after reviewing the historical record, patient outcomes, and the work of clinicians who have brought DMSO back into practice.

Blaylock focuses on specific preclinical findings: a 2022 Scientific Reports paper showing DMSO accelerates α-synuclein oligomerization in vitro and in cells (though the oral mouse arm showed no pathology); a 2014 study in which 1 % DMSO impaired mitochondrial function and glutamate handling in cultured astrocytes; and developmental work demonstrating apoptosis in the immature mouse brain. These are legitimate signals that any responsible clinician must weigh.

The tension is largely one of model, dose, and route. Culture-medium concentrations and direct exposure of developing neurons are not the same as short-course, local adult human use.

How DART-TINN is designed

We are not giving high-dose systemic DMSO. Participants receive two compounded formulations for 30 days:

• An otic liquid (50 % DMSO + betahistine + low-dose dexamethasone + lidocaine) instilled into the external canal every four days.

• A transdermal cream (DMSO base with N-acetylcysteine and levocarnitine) applied once daily to the periauricular skin, mastoid, and upper neck.

This dual local route concentrates the solvent’s penetration, anti-inflammatory, and vasodilatory properties at the cochlear microvascular bed—the precise territory we believe is compromised by spike-related fibrin microclots, iron dysregulation, and endothelial injury—while keeping systemic exposure low. The design modernizes a 1975 open-label series in which a similar DMSO combination produced complete or substantial, sustained resolution of tinnitus in most patients, accompanied by a rise in tympanic temperature consistent with improved local perfusion.

Primary endpoint is a ≥50 % drop in Tinnitus Handicap Inventory score at Day 30 in at least half the cohort. We collect safety data, secondary symptom clusters, and longer-term follow-up precisely so we can detect any unexpected neurological signal early.

Why we are proceeding—and why patients should stay engaged

The α-synuclein and mitochondrial findings deserve respect. They do not, however, override the accumulated human safety data at the concentrations and routes we are using, nor the historical tinnitus signal, nor the mechanistic fit with the microvascular pathology we see every day in clinic. Local delivery plus the antioxidant and mitochondrial-support adjuncts in the cream further reduce the theoretical risk Blaylock highlights.

We monitor closely. Any new or worsening neurological symptom triggers immediate review. Iron indices, fibrin markers, and inflammatory panels remain part of our broader evaluation so we can test whether auditory improvement tracks systemic microvascular recovery.

Blaylock’s caution is useful; it keeps us precise about dose, purity, route, and duration. AMD’s and Pfeiffer’s work remind us that a compound with this breadth of historical clinical activity should not be abandoned on the basis of cell-culture data alone—especially when patients are suffering a refractory, spike-linked symptom for which conventional options offer little.

If you are in the study or considering it, bring every concern. We will walk through the data, the design choices, and the monitoring plan together. The goal remains the same: generate a clear signal—positive or negative—while protecting every participant.

Tinnitus in this population is not “just ringing.” It is often a sentinel of the same iron–fibrin–microvascular injury we track elsewhere. DART-TINN is one careful attempt to meet that injury where it lives. We will follow the results wherever they lead.

Scott Marsland, FNP-C
Principal Investigator, DART-TINN

Over the past few years at Leading Edge Clinic, tinnitus has stopped being a niche complaint and started to look like a signal.

Among more than 4,000 patients with Long COVID (PASC) and post‑COVID vaccine injury, over 500 now live with intrusive, often refractory tinnitus. Many had normal audiograms before the pandemic. Many developed tinnitus in temporal proximity to SARS‑CoV‑2 infection or mRNA vaccination. And many also show clinical and lab evidence of microcirculatory dysfunction: fibrin pathology, autonomic instability, and signs of impaired tissue oxygenation. This is not the usual “older guy with noise exposure” story.

DART‑TINN (NCT07567274) is our attempt to formally study that signal—a first‑in‑the‑world, DMSO‑centered tinnitus trial that treats DMSO as part of the therapy itself, not just background chemistry, in adults with Long COVID and post‑COVID vaccine injury.

The patient who started it all

The immediate inspiration for DART‑TINN wasn’t a journal article. It was a patient.

He lives in the Midwest and has suffered immeasurably from post‑COVID vaccine tinnitus and hearing loss—the kind of suffering that doesn’t fit neatly into a THI score box: sleepless nights, constant noise, the feeling that his auditory world has been hijacked.

After one particularly difficult visit with him, I went looking for something—anything—that might offer a different angle. That search led me to a 1975 paper I had vaguely heard of but never read. The PDF wasn’t free. I paid the $40 anyway, and it turned out to be the best $40 I’ve spent in a long time.

The forgotten 1975 DMSO paper

In that paper, Aristides Ziga Caro reported on “Dimethyl Sulfoxide Therapy in Subjective Tinnitus of Unknown Origin,” treating 15 adults with constant subjective tinnitus.

His regimen:

• A medicated DMSO spray into the external auditory canal every four days

• Daily intramuscular injections containing DMSO plus anti‑inflammatory and vasoactive agents

Nine of the fifteen reported complete resolution of tinnitus that did not return over a year of follow‑up; the remaining six improved to varying degrees.

By modern standards, the study is anything but perfect: no control group, tiny sample size, subjective endpoints, and a mechanistic story that leans on “microcirculatory malnutrition” of auditory nerve cells. But the basic idea—that tinnitus in some patients might respond to focused microcirculatory and anti‑inflammatory therapy using DMSO as a penetrant and potentiator—refused to leave my mind, particularly in the context of spike‑related endothelial injury and fibrin microclots. [3–6]

We are not copying 1975 ENT lore. We are re‑examining it with today’s PASC/post‑vaccine lens and testing it with modern tools and oversight.

How tinnitus looks now, in science and in clinic

Since Caro’s time, tinnitus research has exploded. We now think of chronic subjective tinnitus as a neural network phenomenon: reduced input from the inner ear, maladaptive “central gain” in the brain, and emotional/attentional circuits that determine how intrusive the phantom sound becomes. [7–9]

In simplified terms:

• The ear gets injured—by noise, infection, toxins, or microvascular compromise—and sends less signal.

• The brain turns up the volume to compensate, and some circuits become hyperactive and synchronized.

• Limbic and attention systems decide whether that activity is barely noticeable or utterly overwhelming.

Vascular, immune, and metabolic factors are part of the upstream story. They help explain why certain cochleas and pathways get injured, rather than being the whole picture.

In our Long COVID and post‑vaccine cohort, tinnitus rarely arrives alone. It rides in with dysautonomia, cognitive fog, neuropathic pain, and evidence of spike‑associated microclots and endothelial dysfunction. [3–6,10] Seen through that lens, Caro’s focus on microcirculation looks less quaint and more prescient—he was nudging an upstream mechanism we now have much better language for.

Why DMSO, and why dual‑route?

DMSO is a controversial molecule. It has been called everything from snake oil to miracle solvent. The reality, as usual, is more nuanced.

What interests us are its practical properties:

• It penetrates skin and mucosa, including external ear canal and periauricular tissues

• It modulates inflammation and can alter microvascular tone and rheology

• It carries other small molecules with it, enhancing tissue penetration [11–13]

In DART‑TINN, we use DMSO in two key ways:

• As a primary vehicle and potentiator for an otic solution containing betahistine, dexamethasone, and lidocaine, applied into the external auditory canal every four days

• As a transdermal carrier for levocarnitine and N‑acetylcysteine, applied nightly to the mastoid, periauricular skin, and upper posterior neck

The therapy is adjacent to, not a replacement for, systemic treatment of spike‑induced coagulopathy. We still use systemic tools—anticoagulant or antiplatelet strategies, endothelial support, autonomic regulation, and therapies aimed at fibrin amyloid microclots—for many PASC and vaccine‑injured patients. DART‑TINN lives next to that work: a focused ear‑ and neck‑level intervention aimed at the auditory end‑organ and nearby microvasculature. [3–6]

The hypothesis is simple:

If tinnitus in Long COVID and post‑vaccine injury is driven, in large part, by microcirculatory injury and neuroinflammation in the auditory system, then concentrated local modulation of those processes—while delivering neuroprotective and rheologic co‑agents—may relieve the burden enough for central gain to downshift.

The unsung heroes: compounding, logistics, and a lot of NAC smell

None of this would exist without people who live and breathe compounding and logistics.

Vitahealth Apothecary in NYC—owner and pharmacist David Restrepo and compounding pharmacist Boris—helped turn Caro’s conceptual model and our updated formulation ideas into actual medications. Creating the cream used in the study has at times meant stinking the pharmacy to high heaven with the unmistakable sulfur/egg smell of N‑acetylcysteine. They kept at it anyway.

Infuserve America in St. Petersburg, FL—particularly Director of Case Management Ashley Kramer and pharmacist Jenrose Kratz—helped us tackle a practical problem: water‑based ear drops are fragile and expensive. Infuserve worked with us to adapt the formulation, using glycerin as a shelf‑stable base with added antibacterial function. That pivots the therapy from “theoretically interesting but logistically impossible” to something real people can use at home.

Behind these details are months of back‑and‑forth, tweaking concentration, base, stability, smell, and usability. The trial listing makes it look tidy. It wasn’t.

What DART‑TINN actually tests

DART‑TINN is a prospective, single‑arm, open‑label Phase 2 pilot in adults with refractory subjective non‑pulsatile tinnitus linked to Long COVID or post‑COVID vaccine injury. Key features include:

• Adults 18–70 years with chronic subjective tinnitus (≥6 months)

• Clinically significant tinnitus, defined by a Tinnitus Handicap Inventory (THI) score ≥ 20

• Documented PASC or post‑COVID vaccine injury, with tinnitus onset or clear worsening in that context

• Failure of at least two prior tinnitus therapies (sound therapy, counseling/CBT, pharmacologic treatments, steroids, etc.)

All participants receive 30 days of dual‑route DMSO‑based therapy. The primary outcome is the proportion of participants achieving a ≥50% reduction in THI score at Day 30. Secondary outcomes track:

• THI change over time

• Tinnitus loudness and annoyance (visual analog scales)

• Sleep and concentration

• Patient global impression of change

• Vertigo, insomnia, headache, and fatigue scores

with follow‑up out to 12 months for durability and safety.

To our knowledge, DART‑TINN is the only registered clinical trial in the world that uses DMSO itself as a therapeutic intervention for tinnitus, rather than simply as a solvent or inactive carrier for another drug. Most modern studies treat DMSO as background chemistry; we are deliberately testing its biological and delivery properties as part of the intervention in a clearly defined Long COVID and post‑vaccine tinnitus population. For patients and clinicians who are tired of “nothing we can do,” this kind of careful, mechanism‑driven innovation is exactly what we need more of.

This is intentionally a pilot. We want to know:

• Does this mechanistic bet produce clinically meaningful relief in an enriched PASC/vax‑injured tinnitus population?

• Is the regimen feasible and tolerable in real life?

• What signal, if any, justifies a larger, controlled trial?

Right now, the study is roughly 50% enrolled. Early recruitment focused on Leading Edge Clinic patients invited from our existing panel. It turns out that getting people to complete the THI questionnaire, schedule an ENT visit, and then actually get ENTs to fill out a study form (or at least send the required information) is a bit like herding cats. For my patients who know how much I love the felines of this world….

Safety, dosing, and our DMSO track record

DMSO is not a toy. Experimental work shows concentration‑ and time‑dependent toxicity in various cell types, including cochlear hair cells at higher doses and prolonged exposure. Clinical reviews describe adverse reactions ranging from garlic‑like body odor, warmth, and headaches to gastrointestinal upset and rare organ or hematologic effects, depending on route and dose. [11–15]

We designed DART‑TINN with that in mind:

• Concentrations and application schedules are chosen to avoid continuous high‑dose exposure to cochlear tissues while still leveraging DMSO’s penetration and carrier function

• Both formulations are prepared by licensed compounding pharmacies with strict quality control

• Safety monitoring is built in: telemedicine access, structured adverse‑event reporting, and 6‑ and 12‑month follow‑up visits to capture delayed effects

In our broader practice at Leading Edge Clinic, we have extensive experience using DMSO across multiple indications. Serious toxicity has been very rare. One notable adjunctive cancer patient developed chronic anemia that appeared to be related to oral DMSO; when the DMSO was stopped, the anemia improved. Cases like that have pushed us to tighten monitoring and be more conservative with systemic dosing. They have not suggested that carefully controlled local and transdermal use is inherently unsafe.

We are not ignoring DMSO toxicity data. We’re respecting them and designing around them—while also honoring the reality that, in the right dose and context, DMSO can be a potent, underutilized therapeutic tool.

Funding, access, and how non‑LEC patients can participate

DART‑TINN also exists because someone believed this kind of work was worth funding.

The non‑profit Rebuild Medicine accepted DART‑TINN as a project aligned with its mission: bridging the gap between real patients’ clinical needs and the thoughtful use of repurposed medicines. Funding from Rebuild—thanks to Ron Morris and Michael Barton, and to my practice partner Dr. Pierre Kory for facilitating that introduction—allows us to:

• Provide a stipend for the ENT visit prior to initiation of medication

• Cover the cost of the compounded medications themselves

Initially, enrollment was by invitation from within Leading Edge Clinic. At this point, it is possible to enroll Long COVID and post‑vaccine‑injured individuals who are not currently LEC patients.

To do that, they would:

• Become members of the First Nation Medical Board (FNMB), a tribal entity under which LEC operates (currently a $35 annual membership fee)

• Agree to be seen under the agreements we hold as tribal providers caring for public members of a tribal entity, which gives them access to a discounted visit price specifically for the study

Anyone interested in learning more can email DART‑TINNstudy@drpierrekory.com and ask about eligibility and next steps.

Why we’re doing this now

The easiest thing to do with tinnitus in PASC and post‑vaccine injury is to call it “anxiety,” hand out a sound generator, and hope for habituation. That hasn’t matched what our patients live through—or what their labs and clinical exams show.

When you see fibrin‑heavy blood, dysautonomia, microcirculatory signs, and tinnitus in the same person, the more honest answer is: this is probably vascular plus neural, not simply psychological. Spike protein’s effects on endothelium, fibrin(ogen), and microclots are now reasonably well described. The tinnitus literature has matured enough to map how peripheral injury feeds central gain and limbic distress. DART‑TINN sits at the intersection of those two bodies of work. [3–9]

If DART‑TINN fails, we’ll learn something important about the limits of localized microcirculatory therapy in this phenotype and refine where we focus systemic spike‑coagulopathy treatment and neural‑targeted interventions. If it succeeds—even partially—it will justify larger, controlled trials and help open a more nuanced conversation about how spike protein, fibrin, microclots, and auditory networks intersect in real patients.

Either way, the people who have been told for years that their tinnitus is “just stress” deserve more than reassurance. They deserve careful, mechanism‑informed experimentation and data that actually reflect the complexity of their condition—and a few stories about stinky pharmacies and $40 PDFs along the way.

DART‑TINN Eligibility Criteria (for reader reference)

Inclusion Criteria

• Adults 18 to 70 years of age

• Chronic subjective non‑pulsatile tinnitus for at least 6 months

• Bothersome tinnitus defined by a Tinnitus Handicap Inventory (THI) score ≥ 20 at screening

• Documented history of post‑acute sequelae of SARS‑CoV‑2 (PASC, Long COVID) or post‑COVID‑19 vaccine injury, with tinnitus onset or clear worsening temporally associated with that event

• Failure of at least two prior tinnitus therapies (for example, sound therapy, counseling or cognitive‑behavioral approaches, pharmacologic treatments, or steroid therapy)

• Willing and able to provide informed consent

• Able to complete telemedicine visits and electronic questionnaires in English and to attend a baseline in‑person otolaryngology (ENT) evaluation

Exclusion Criteria

• Objective or pulsatile tinnitus, or tinnitus primarily synchronous with the heartbeat

• Active middle‑ear infection, acute otitis media, tympanic membrane perforation, or current otorrhea

• Recent exposure (within the past 3 months) to known ototoxic medications associated with new or rapidly worsening tinnitus

• Known hypersensitivity or allergy to dimethyl sulfoxide (DMSO) or any component of the study formulations (betahistine, dexamethasone, lidocaine, levocarnitine, N‑acetylcysteine, or excipients)

• Pregnancy or breastfeeding

• Uncontrolled or severe psychiatric illness (for example, active psychosis, acute suicidality) that, in the opinion of the investigator, would interfere with participation or completion of questionnaires

• Inability to comply with study procedures, including telemedicine visits, electronic data capture, or topical/otic dosing instructions

• Any other otologic or neurologic condition judged by the investigator to confound tinnitus assessment or pose unacceptable risk with DMSO‑based therapy

Selected Bibliography

1. ClinicalTrials.gov. DMSO Dual‑Route Therapy for Refractory Tinnitus in Long‑COVID and Post‑COVID‑19 Vaccine Injury (DART‑TINN). NCT07567274.

2. Caro AZ. Dimethyl sulfoxide therapy in subjective tinnitus of unknown origin. Ann N Y Acad Sci. 1975; [PubMed PMID: 1055561].

3. Pretorius E, et al. Proteomics of fibrin amyloid microclots in long COVID/post‑acute sequelae of COVID‑19. Cardiovasc Diabetol. 2023.

4. Kell DB, Pretorius E. Amyloid fibrin microclots as a central feature of Long COVID. Hematology/Long COVID review.

5. Mao S, et al. Prevalence and prognosis of tinnitus in post‑COVID‑19 patients. Acta Otolaryngol. 2024. [PubMed PMID: 39512084].

6. Yih WK, et al. Tinnitus after COVID‑19 vaccination: Findings from the Vaccine Safety Datalink and VAERS. CDC Stacks.

7. Henry JA, et al. Underlying mechanisms of tinnitus: a review and clinical implications. J Am Acad Audiol. 2014.

8. De Ridder D, et al. Pathology of tinnitus and hyperacusis: clinical implications. J Neurol. 2015. [PubMed PMID: 26313440].

9. Langguth B, et al. The neuroscience and treatment of tinnitus. Physiol Rev. 2021.

10. Hearing Health Foundation. Tinnitus and COVID‑19 (overview article).

11. Gallardo‑Villagrán M, et al. Dimethyl sulfoxide: a bio‑friendly or bio‑hazard chemical? Molecules. 2022.

12. Qi W, et al. Cytotoxic effects of dimethyl sulphoxide on cochlear hair cells in vitro. Hear Res. 2007. [PMC2262105].

13. Hoyberghs J, et al. DMSO concentrations up to 1% are safe in zebrafish embryo assays. Front Toxicol. 2021.

14. Jacob SW, Rosenbaum EE, Wood DC. Dimethyl sulfoxide: basic concepts. New York: Marcel Dekker; 1971.

15. Petrillo S, et al. Adverse reactions of dimethyl sulfoxide in humans: a systematic review. Pharmacol Res. 2019. [PMC6707402].

Something else I’ve done during all of my medical leaves was watch movies. My wife and I have seen a lot of movies together. After all, she was working in the Ritz 5 in the Old City of Philadelphia when we met. But I can palpate the times when I was in recovery, because I’ll reference a film and she’ll say, “You must have watched that by yourself.” What’s implied in that statement is, “It’s not a movie I would have chosen to watch.” But I loved those movies.

There was Downfall (2004), a German film that shows Adolf Hitler’s final days in his Berlin bunker as World War II ends and the Nazis are defeated. Or, Lady Vengeance (친절한 금자씨, 2005), a stylish Korean revenge thriller in which a woman wrongly imprisoned for a child’s murder teams up with the families of the real serial killer’s other victims to collectively torture and execute him. There was the deadpan Belgian black comedy Aaltra (2004), two feuding rural neighbors—one a farmer—end up paralyzed in wheelchairs after a bitter argument leads to a tractor accident. Forced to rely on each other, they embark on a darkly humorous road trip across Europe toward Finland to seek compensation from the manufacturer, turning their animosity into reluctant companionship amid absurd mishaps. In the Icelandic film Children of Nature (1991), an elderly farmer named Þorgeir, unable to tend his remote sheep farm any longer, shoots his loyal shepherd dog, sells his flock, and moves to the city to live with his daughter’s family before ending up in a Reykjavík nursing home. (I’ll never forget the image of him wrapping the gun in a newspaper and the look of trust his dog gives him before he shoots it). There he reunites with his old childhood sweetheart Stella; after growing disillusioned with institutional life, the pair escapes by stealing a vehicle and embarks on a poignant journey back to her abandoned village in the remote Westfjords. Stella dies upon reaching her childhood home, and Þorgeir buries her as she wished, finding a final sense of peace and freedom in nature before his own story concludes.

Which leads me to another film I watched by recuperating. Noise (2007), the Australian drama-thriller directed by Matthew Saville, centers on Constable Graham McGahan (Brendan Cowell), a cop whose life is increasingly dominated by severe tinnitus following an on-duty incident. The condition of tinnitus is woven directly into the sound design and plot: Graham’s world is constantly interrupted by a persistent, high-pitched ringing that fluctuates in intensity, sometimes drowning out dialogue, traffic, or conversations so completely that he struggles to function. The film smartly uses a technique called point-of-audition audio—muffling ambient sounds while amplifying or isolating the ringing—to put the audience inside his head, making his isolation, frustration, and disorientation feel immediate and visceral.

This exceptional portrayal of tinnitus isn’t just a medical detail; it drives the story and themes. Assigned to a low-key night shift in a police information van in a troubled Melbourne suburb after requesting lighter duty, Graham becomes a reluctant listener to community trauma while barely able to hear himself. The ringing underscores his emotional detachment and vulnerability, especially as he gets entangled in the aftermath of local murders. It’s one of the most realistic and immersive depictions of living with constant ear noise I’ve seen—raw, unrelenting, and deeply human—turning a personal affliction into a powerful cinematic device.

When I watched Noise sixteen years ago, I did not have tinnitus. The closest I had come to it was when I was a boy, playing with firecrackers, and one went off in my hand right next to my ear. My ear(s) rang for hours, but that faded away. The Covid shots changed that in 2021, and bilateral tinnitus and hearing loss have been my constant companions since then. But Brendan Cowell’s performance in Noise had elicited my empathy for others with this condition long before it impacted my own life.

There is a tool used by ENTs call the Tinnitus Handicap Inventory or THI. It was developed and validated in 1996 by Craig W. Newman, Gary P. Jacobson, and Jack B. Spitzer. Published in the Archives of Otolaryngology–Head & Neck Surgery, it is a 25-item self-report questionnaire designed to quickly measure how tinnitus affects daily life across functional, emotional, and catastrophic domains. Initial validation studies showed strong reliability (high internal consistency and test-retest stability) and good validity through correlations with depression scales and tinnitus severity ratings. It provides a total score (0–100) with severity grades and has since been adapted and validated in many languages, becoming one of the most widely used tools for assessing tinnitus handicap in both clinical practice and research.

As the Principal Investigator of a pilot study using two compounded medications to treat tinnitus in patients with PASC and injury from the Covid shots, I have been administering and evaluating the THI for study candidates. In order to qualify for study participation, patients need to have a score of at least 20. Most have scores of 60 or above. What those numbers confirm for me is that these patients are suffering tremendously, but they have not been offered viable treatments. I hope that we can change that.

What makes the movive Noise so effective, is how completely it commits to letting the audience feel tinnitus rather than just being told about it. The sound design doesn’t simply add a ringing tone in the background; it actively sabotages Graham’s ability to navigate the world in real time. Conversations drop out mid-sentence. Sirens and traffic become distant murmurs one moment and overwhelming the next. The ringing doesn’t stay politely in the background—it takes over, exactly the way people with severe tinnitus describe. You don’t just watch a man struggling with a medical condition; you’re pulled inside the exhausting, disorienting experience of trying to function when your own ears are betraying you.That immersion reveals how tinnitus reshapes identity and relationships far beyond the physical noise. Graham is a cop who can no longer fully trust his own senses at a moment when the job demands sharp attention and human connection. His assignment to the quiet night shift in the information van is both a practical accommodation and a kind of exile. He becomes a reluctant listener to other people’s trauma while his own inner noise constantly threatens to drown everything out. The film shows, without melodrama, how something invisible can isolate you even when you’re surrounded by people who need you.

It strikes me that the movie treats tinnitus as both a personal affliction and a kind of unwanted superpower. The same ringing that disrupts Graham’s life also forces him into a different way of being present. He can’t tune things out the way he used to. In a strange way, the condition keeps him tethered to the raw, unfiltered reality of the neighborhood he’s been sent to observe. It’s not romanticized, but it’s honest about the complicated ways chronic conditions can change how someone moves through the world.Most of all, Noise captures the quiet, grinding toll—the way tinnitus erodes sleep, concentration, patience, and the simple ability to be in your own head without interference. There are no dramatic breakdowns or miracle cures. Instead there’s the steady, relentless presence of the ringing and the small, daily negotiations it demands. That restraint is what makes the portrayal feel so true. It doesn’t turn tinnitus into a plot device; it lets tinnitus be the atmosphere the story moves through.

Through all these films—whether it was watching Hitler unravel, families exact collective revenge, feuding neighbors bond in wheelchairs, an old farmer bury his dog and his past, or a cop navigate a ringing world—I was quietly learning how to sit with suffering, limitation, and the strange grace that can emerge from both. Now, as I evaluate the THI scores of patients in our pilot study, those solitary recovery watches feel less random. They were preparation: a reminder that the most powerful stories don’t always fix the pain, but they help us witness it more clearly and, sometimes, find ways to ease it.

Most of all, I remember the chemical outgassing smell from the N-95 I had to wear for the 13 hours of a 12 hour shift. The stale air of an overcrowded Emergency Department. The plastic. The sweat. The metallic edge of panic when a young person is running out of time and everybody in the room knows it. I was working at SUNY Upstate then, in the Level-1 trauma center, and I can still picture twenty-year-olds coming in by EMS in acute respiratory distress, then getting intubated in the hallway because there was nowhere else to put them. Some nights it still feels like I’m walking those hallways, only now the stretchers roll past on a Zoom screen instead of linoleum. Back then, the disease often had a rhythm to it. A patient would seem to be hanging on, and then around day 8, the floor could drop out from underneath them. That was often the day they arrived in the ED.

Years later, most of my work happens through telemedicine at Leading Edge Clinic’s Long COVID program and its post-vaccine syndrome program. The setting is different now: no beeping monitors, no transport stretchers, no ventilators humming in the background. Instead, I stand in front of a screen and meet people in bedrooms, kitchens, home offices, parked cars, and the occasional closet where they’ve hidden from the rest of the household to have enough quiet for a medical visit. But what I hear all day long is not peace. It is the aftersound of that same protein.

Call her Vesni. Before all this, she was the sort of person who walked fast on purpose, just to burn off the day; now she plans her week around two loads of laundry, and she cannot walk around the block without paying for it for three days. Another was a CEO who used to run meetings and now loses the thread of a sentence halfway through speaking it. Another tells me she feels as though her body has become allergic to life itself: food, heat, cold, perfume, exertion, stress, the wrong supplement, the wrong cup of tea. A middle-aged man who had always been sturdy and useful says, with embarrassment, that he now has to sit down to fold laundry. An older woman says she misses herself. That one stays with me.

These aren’t ICU patients in the old sense, but they are not mild.

Two recent papers by Gerlach et al. have helped me put words to a pattern I have been circling around for years. The first, Unprecedented Pathological Features of the SARS-CoV-2 Spike Protein and Their Conservation across Variant Evolution: A Source-Agnostic Feature Inventory, lays out a source-agnostic inventory of unusual features of the SARS-CoV-2 spike protein and argues that most of the deeper pathological machinery of spike was conserved, and in some cases strengthened, as the virus evolved into late Omicron lineages. The second, A Proposed Mechanism for Reduced COVID-19 Severity with Omicron: Could Systematic NTD Loop Deletions Have Eliminated Allergenic Determinants in SARS-CoV-2 Spike Protein?, offers a structural hypothesis for why the acute face of COVID changed so dramatically with Omicron: three short, surface-exposed loops in the ancestral N-terminal domain may have functioned as allergenic determinants, and those loops were systematically deleted in Omicron.

If that hypothesis is right, it explains something that has otherwise been hard to name cleanly. Omicron may have removed one of the most explosive short-term triggers for acute respiratory collapse while leaving behind the rest of spike’s pathological toolkit. In plain English: the fire alarm got quieter, but the wiring in the walls stayed hot.

What the wards taught us

Early in the pandemic, many of us were learning with our hands; the Emergency Department has a brutal way of teaching fast. We were trying to understand what kind of illness this was by watching bodies fail in real time. Long before there was consensus language for it, there was a sense among some bedside clinicians that a subset of these patients were not simply drowning in viral pneumonia. There was something immunologic, allergic, or mast-cell driven happening in at least some of the worst crashes.

Dr. Pierre Kory went to Washington and testified before the Senate about the role of steroids in saving lives. At the time, he was mocked for it. History hasn’t been kind to the mockers. It would also be wrong to tell this story without paying homage to Dr. Shankara Chetty, our common colleague at RAPID, who was the first physician to clearly identify the day-8 hypersensitivity pattern and adapt that model into clinical practice. Long before this hypothesis had structural language, Dr. Chetty was seeing the pattern at the bedside and acting on it, and a great many clinicians recognized, in his work, something they had been witnessing but had not yet fully named. The Omicron loop paper doesn’t prove that those early day-8 crises were allergenic reactions to specific NTD loops, but it does provide a plausible structural framework for why antihistamines and corticosteroids sometimes worked so dramatically in the pre-Omicron era, and why that particular pattern largely faded afterward.

That matters to me because the memories are not academic. I remember bringing patients up to the ICU from the ED and walking back down knowing I would probably be doing it again in an hour. I remember the sheer wrongness of seeing previously healthy young adults vanish into ventilators. If we had understood then what these papers are proposing now, some of those scenes may have unfolded differently.

What Omicron lost

The second paper is the one that made me put my green Rooibos tea down, because every now and then a paper arrives that doesn’t merely add another citation to the pile but instead reaches back through the years, grabs a handful of half-formed clinical memories, and suddenly arranges them into something that looks less like coincidence and more like the edge of understanding.

Its core idea is simple: three short loops on the surface of the ancestral spike N-terminal domain, around H69-V70, V143-Y145, and N211, may have acted as allergenic determinants in susceptible patients. Omicron deleted all three while preserving spike trimer integrity through compensatory remodeling. If those loops were part of what was provoking the day-8 hypersensitivity phenotype, then their disappearance could help explain why the ICU story changed so abruptly once Omicron took over.

This is still a hypothesis. The authors are careful about that. They call for peptide allergenicity testing, mast-cell activation work, patient immunophenotyping, and structural-functional studies comparing ancestral and Omicron NTDs. Good. That is exactly what should happen. But a hypothesis does not need to be proven before it becomes useful. Sometimes a good hypothesis acts like a flashlight. It illuminates what you have already been stumbling around in.

For me, the light falls backward and forward at the same time. Backward, to the ward patients who crashed hard and fast. Forward, to the people I now see with mast-cell activation, dysautonomia, weird inflammatory surges, flushing, palpitations, burning skin, sleep disruption, and post-exertional misery who often do not look anything like the patients we were intubating in 2020, yet seem to belong to the same family of injury.

What spike kept

The companion Gerlach paper is, in some ways, even more unsettling. It asks a straightforward question: as SARS-CoV-2 evolved, which spike features actually disappeared? And the answer, according to their review, is basically none of the major protein-level pathobiologic ones. The furin cleavage site remained. The amyloidogenic epitopes remained. The superantigen-like and toxin-like motifs remained. The prion-like domains were modified but not abolished. The neuropilin-related loop remained. The glycosylation shield remained. ACE2 binding stayed strong or got stronger.

This is the part of the story that feels most consistent with what I see now in PASC and vaccine injury. Acute disease got softer up front, but the protein did not suddenly become gentlemanly. It kept the features that could contribute to vascular injury, abnormal clot architecture, autonomic chaos, neuroinflammation, and chronic immune disturbance.

Take the furin cleavage site. The paper argues that Omicron’s nearby mutations increase cleavability, which means more efficient generation of free S1 fragments. That matters because once you have more circulating S1, you still have access to the downstream problems: amyloidogenicity, neuropilin-1 engagement, inflammatory signaling, and all the rest. So while Omicron may have become less likely to trigger the spectacular day-8 crisis, it may not have become less capable of seeding slower, stranger systemic harm.

That rings true.

The people on my screen

Lightning Bug has never been, for me, just a place to summarize papers. It is where the papers and the people have to meet.

I think about the family story in “All Along the Watchtower”, where a physician father working in a busy clinic had unexpectedly low spike antibody levels compared with the rest of his household, and the clue turned out to be an old habit of sipping a homemade Baobab drink all day at work. That post was not just about a supplement. It was about what happens when you are paying close enough attention that an odd lab value turns into a hypothesis, and a hypothesis turns into a small act of care. The same thing happened with mast-cell activation. It did not arrive in my practice as an abstract theory. It arrived through patients who kept reacting to everything, until the pattern was too loud to ignore.

In “Table 12”, I wrote about a younger vaccine-injured patient who went in for dental work, got procaine, then later nearly died after a cascade that included an alpha-gal reaction and emergency epinephrine. I also wrote about an elderly patient with metastatic renal cell carcinoma whose swollen arm looked, to Dermatology, like mast-cell disease, but to Oncology looked like cellulitis. He then got hit with an IV cephalosporin and gadolinium MRI contrast, both of which likely worsened mediator release and delirium in an already fragile system. Those cases are messy, human, imperfect, and clinically real. They are also exactly the sort of cases that make the Omicron NTD hypothesis feel relevant. If ancestral spike really did carry an exposed allergenic cassette, and if later spike variants deleted it while leaving the deeper machinery intact, then the movement from acute respiratory hypersensitivity to chronic mast-cell, neurologic, and inflammatory instability starts to make a lot more sense.

I think too about “Do Not Go Gently”, where I wrote about my own family and the painful realization that what many people dismiss as “aging” may, in some cases, be vascular, neurologic, or inflammatory damage layered on top of time. That piece was personal because this work is personal. It is one thing to write “brain fog” in a chart. It is another to watch someone grieve the self they used to be. When a patient tells me she cannot read novels anymore because by page three she no longer remembers page one, no amount of tidy academic prose can improve that sentence. It can only honor it.

Microclots, fibrin, and humility

My own thinking about microclotting has changed over time. The signal is real. The spike inventory paper gives a plausible molecular basis for fibrinolysis-resistant fibrin through amyloidogenic segments like Spike685. And certainly there are patients in whom clotting biology looks front and center. I have seen blood that clots in the tube. I have seen patients with striking improvement on anticoagulation. I have also seen the opposite: patients whose microclot scores do not correlate neatly with how sick they feel, or whose symptoms improve only partly, or not at all, despite treatment aimed squarely at coagulation.

That is where humility has to enter. If you do this work honestly, the patients will eventually cure you of reductionism. If you read “You look mahvelous!”, you know how much I care about the small wins—hair growing back, color returning to a face. Those are the kinds of changes that tell me we are tugging on the right part of this knot.

More and more, I have found the perspective of Ruth Kriz, MSN, APRN helpful here. Kriz places fibrin in a broader terrain of chronic illness, not just as a marker of pathological clotting but as structural scaffolding for biofilm, persistent infection, poor perfusion, and immune evasion. In that framework, spike does not merely cause “microclots.” It may aggravate a fibrin-rich ecosystem in susceptible patients, especially those with hypercoagulation tendencies, where infection, inflammation, immune dysfunction, and sometimes cancer biology all begin feeding each other.

That feels closer to the truth of what I now see. Not a single mechanism. Not a silver bullet. More like a knot.

Outside my office, where I wrote this piece, is a view I usually only catch out of the corner of my eye between visits. Today was a rare day when there was time to stop and really take it in. The trees on the edges have already gone green, but the stand in the middle is still all branches and promise, late to leaf out but not dead. I’ve watched clouds my whole life; what was different today was how the ones in the foreground were rolling and roiling upward, almost boiling as they joined the higher layers and slowly covered the blue sky. It felt like a snapshot of where we are with spike now—new growth starting at the edges of life, older damage in the middle still catching up, and a sky that looks fine until you pay attention to how quickly it’s filling in.

Why this matters now

There is a temptation, especially among people who want to be done with all of this, to treat Omicron as the point where the problem solved itself. The hospital numbers improved, therefore the virus mellowed, therefore the rest is exaggeration. The people saying this are usually not the ones spending an hour with a patient who cannot tolerate a grocery store, a dentist appointment, a glass of wine, a family argument, a flight of stairs, or a night of poor sleep. I understand the impulse. It’s human to want the credits to roll. Biology doesn’t care about our narrative arcs.

The two Gerlach papers suggest a better framing. Omicron may indeed have lost something important: a set of ancestral NTD loops that made acute hypersensitivity crises more likely. But it may have kept, and in some respects enhanced, the structural elements of spike that drive chronic multisystem harm. That hypothesis does not explain everything. It does, however, explain a great deal about the historical difference between pre-Omicron and post-Omicron patients, both in Long COVID and in injury related to the COVID shots.

It also raises uncomfortable questions for future vaccine design -- not because every question has been settled, but because too many were never asked in the first place. If first-generation mRNA products encode the ancestral spike with most of these deeper features intact, then “safe enough” can no longer mean only “provokes antibodies” or “reduces hospitalization.” It also has to mean that the protein being expressed has been stripped of the structural liabilities that the virus itself has shown it can live without.

The quieter catastrophe

The catastrophe of 2020 was loud. Ventilators. Sirens. Body bags. The catastrophe that followed is quieter. It looks like someone canceling dinner again. Someone lying flat in a dark room. Someone losing a job they loved. Someone carrying Benadryl, Cromolyn, Ketotifen, a pulse oximeter, an EpiPen, and a private fear that their body is one bad input away from going off the rails.

The loud catastrophe was easier for the world to recognize. This story is not only about what the virus did in 2020, but also about what spike keeps doing after the world has decided to look away.

The quiet one is harder. It unfolds in kitchens and bedrooms, on Zoom calls, in the silence after a patient says, “I just want my life back.”

That is why these papers matter. Not because they prove everything, but because they offer a coherent, testable framework for what so many of us have witnessed. The ancestral spike may have carried an allergenic front end that helped drive the day-8 crash. Omicron may have deleted that front end. But the deeper spike toolkit—furin cleavage, amyloidogenicity, neuroactive motifs, neuropilin access, glycan shielding, vascular and neurologic potential—appears to have stayed.

Which means the story was never simply that the virus got mild.

It may be closer to this: the scream faded, but the injury kept talking. If your body is still telling you that story, you are not crazy, you are not weak, and you are not alone. You are living in the long echo of a protein the world has not fully faced yet.

P.S. This post of Lightning Bug is dedicated to Faith. Thank you for supporting Lightning Bug and being an engaged reader. We will find our way forward, together.

References

1. Gerlach J, Baig AM, Jaeger B, et al. *Unprecedented Pathological Features of the SARS-CoV-2 Spike Protein and Their Conservation across Variant Evolution: A Source-Agnostic Feature Inventory*. ResearchGate preprint. February 2026. DOI: 10.13140/RG.2.2.16496.11521. Available at: https://www.researchgate.net/publication/401309711_Unprecedented_Pathological_Features_of_the_SARS-CoV-2_Spike_Protein_and_Their_Conservation_across_Variant_Evolution

2. Gerlach J, Baig AM, Jaeger B, et al. *A Proposed Mechanism for Reduced COVID-19 Severity with Omicron: Could Systematic NTD Loop Deletions Have Eliminated Allergenic Determinants in SARS-CoV-2 Spike Protein?* ResearchGate preprint. May 2026. DOI: 10.13140/RG.2.2.16772.49280. Available at: https://www.researchgate.net/publication/404805453_A_Proposed_Mechanism_for_Reduced_COVID-19_Severity_with_Omicron_Could_Systematic_NTD_Loop_Deletions_Have_Eliminated_Allergenic_Determinants_in_SARS-CoV-2_Spike_Protein

3. Whittaker GR, Daniel S. SARS-CoV-2 spike and its adaptable furin cleavage site. *Journal of Molecular Biology*. 2023;435(16):167375. DOI: 10.1016/j.jmb.2023.167375.

4. Johnson BA, Xie X, Kalveram B, et al. Furin cleavage site is key to SARS-CoV-2 pathogenesis. *Nature*. 2021;591(7849):293-299. DOI: 10.1038/s41586-021-03237-4.

5. Peacock TP, Goldhill DH, Zhou J, et al. The furin cleavage site in the SARS-CoV-2 spike protein is required for transmission in ferrets. *Nature Microbiology*. 2021;6(7):899-909. DOI: 10.1038/s41564-021-00908-w.

6. Nyström S, Hammarström P. Amyloidogenesis of SARS-CoV-2 spike protein. *Journal of the American Chemical Society*. 2022;144(20):8945-8950. DOI: 10.1021/jacs.2c01829.

7. Westman J, Hammarström P, Nyström S. Spike685 amyloid fibrils template fibrin and generate fibrinolysis-resistant clots. *Biochemistry*. 2025;64(2):336-350. DOI: 10.1021/acs.biochem.4c00593.

8. Boschi C, de Candia P, Catapano AL, et al. SARS-CoV-2 spike protein amyloid fibrils impair fibrin polymerization and promote fibrinolysis resistance. *International Journal of Molecular Sciences*. 2025;26(22):12321. DOI: 10.3390/ijms262212321.

9. Cheng MH, Zhang S, Porritt RA, et al. Superantigenic character of an insert unique to SARS-CoV-2 spike supported by skewed TCR repertoire in patients with hyperinflammation. *Proceedings of the National Academy of Sciences USA*. 2020;117(41):25254-25262. DOI: 10.1073/pnas.2010722117.

10. Cheng MH, Zhang S, Porritt RA, et al. A monoclonal antibody against staphylococcal enterotoxin B superantigen inhibits SARS-CoV-2 entry in vitro. *Structure*. 2021;29(9):951-962.e3. DOI: 10.1016/j.str.2021.06.006.

11. Tetz G, Tetz V. Prion-like domains in spike proteins of SARS-CoV-2 differ across its variants and enable changes in affinity to ACE2. *Microorganisms*. 2022;10(2):280. DOI: 10.3390/microorganisms10020280.

12. Daly JL, Simonetti B, Klein K, et al. Neuropilin-1 is a host factor for SARS-CoV-2 infection. *Science*. 2020;370(6518):861-865. DOI: 10.1126/science.abd3072.

13. Cantuti-Castelvetri L, Ojha R, Pedro LD, et al. Neuropilin-1 facilitates SARS-CoV-2 cell entry and infectivity. *Science*. 2020;370(6518):856-860. DOI: 10.1126/science.abd2985.

14. Wrapp D, Wang N, Corbett KS, et al. Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation. *Science*. 2020;367(6483):1260-1263. DOI: 10.1126/science.abb2507.

15. Iuliano AD, Brunkard JM, Boehmer, et al. Trends in disease severity and health care utilization during the early Omicron variant period compared with previous SARS-CoV-2 high transmission periods — United States, December 2020-January 2022. *MMWR Morbidity and Mortality Weekly Report*. 2022;71(4):146-152. DOI: 10.15585/mmwr.mm7104e4.

16. Adjei S, Hong K, Molinari NM, et al. Mortality risk among patients hospitalized primarily for COVID-19 during the Omicron and Delta variant periods — United States, April 2022-June 2022. *MMWR Morbidity and Mortality Weekly Report*. 2022;71(37):1182-1189. DOI: 10.15585/mmwr.mm7137a4.

17. Nyberg T, Ferguson NM, Nash SG, et al. Comparative analysis of the risks of hospitalisation and death associated with SARS-CoV-2 Omicron (B.1.1.529) and Delta (B.1.617.2) variants in England: a cohort study. *The Lancet*. 2022;399(10332):1303-1312. DOI: 10.1016/S0140-6736(22)00462-7.

18. Abdullah F, Myers J, Basu D, et al. Decreased severity of disease during the first global Omicron variant COVID-19 outbreak in a large hospital in Tshwane, South Africa. *International Journal of Infectious Diseases*. 2022;116:38-42. DOI: 10.1016/j.ijid.2021.12.357.

19. Meng B, Abdullahi A, Ferreira IATM, et al. Altered TMPRSS2 usage by SARS-CoV-2 Omicron impacts infectivity and fusogenicity. *Nature*. 2022;603(7902):706-714. DOI: 10.1038/s41586-022-04474-x.

20. Hui KPY, Ho JCW, Cheung MC, et al. SARS-CoV-2 Omicron variant replication in human bronchus and lung ex vivo. *Nature*. 2022;603(7902):715-720. DOI: 10.1038/s41586-022-04479-6.

An observational clinical account from my practice as Scott Marsland, FNP-C at Leading Edge Clinic

In November 2025 I published the initial case study of a woman whose chronic fatigue and long-standing infertility shifted dramatically after targeted mineral repletion with a liquid volcanic mineral solution chemically similar to EPA-approved water purification formulations such as Aurmina. I updated this case study in March of 2026. The pregnancy remains fully viable with an expected delivery in July 2026. The patient continues to be healthy and active overall, with only expected pregnancy-related fatigue.

Patient Update (May 2026)
The patient shared the following:

• Continuing 5 mL oral twice daily (morning and evening) in treated water.

• Walking one hour daily and practicing yoga every day.

• Feeling tired, which she attributes to pregnancy, warmer weather, recent extensive travel, and periods of less optimal water/food access. She also wonders about prior Celtic salt use.

• No recent bathing, but consistently using the treated mineral water for drinking, tea, coffee, and cooking.

• Recent midwife blood work: no urinary protein (reassuring for renal health), low ferritin with high serum iron. She suspects insufficient vitamin C co-administration with her iron supplement affecting conversion/storage; she is addressing this.

• Fetal monitoring via Doppler shows strong heartbeat and active movement (kicking). Formal ultrasound scheduled at 34 weeks.

Lab Timeline & Key Changes (April 20, 2026 Results)

Figure 1: Mercury Speciation (Quicksilver Scientific)

Figure 2. Summary of Mercury Changes Over Time

Overall from baseline (June 2025): MeHg –79%, Total Hg –78%.
Urine mercury indicates strong excretion capacity (total Hg –54% from prior). Hair mercury at 1,550 ng/g consistent with ongoing mobilization.

Whole-Blood Elemental Panel (April 20, 2026)
Figure 3: Nutrient + Toxic Elements

Notable trends:

• Mercury continued declining to 1.7 µg/L

• Zinc improved to 662 µg/dL (77th percentile)

• Magnesium improved to 3.04 mg/dL

• Selenium stable at 295 µg/L (80th percentile)

• Lead stable/low; other toxics well-controlled

Discussion

Despite recent travel and reduced bathing, the patient’s consistent oral intake and use of treated water for daily cooking/drinking appear sufficient to sustain impressive mercury reduction (–39% since February, –79% overall for MeHg). The low ferritin/high iron pattern is common in pregnancy and is being addressed with added vitamin C. Fetal status remains reassuring.

These patterns continue to align with the mineral displacement, selenium-supported demethylation, and enhanced clearance mechanisms explored in Dr. Pierre Kory’s water chemistry framework.

The temporal association between sustained mineral support, heavy-metal mobilization, and a healthy ongoing pregnancy remains striking. The patient’s tolerance and continued progress speak to the protocol’s gentleness and adaptability even under the physiologic demands of late pregnancy and travel.

Disclaimers
Aurmina is an EPA-approved water purifier only and is not a supplement or drug. This is a single observational case. It is not intended to diagnose, treat, cure, or prevent any disease.

Next Steps
Third-trimester labs, 34-week ultrasound, and postpartum retesting at 6–8 weeks (once plasma volume normalizes) to assess sustained improvements.

Thank you for reading. I welcome thoughtful questions in the comments.

Scott Marsland, FNP-C
Lightning Bug | Leading Edge Clinic

Come for the science, stay for the stories.
Personal reflections (including the My Vietnam series, Part 1, Part 2, and Part 3) live in the opt-in Personal Insights section—toggle it on in your account settings if they speak to you.

REPUBLISHING FOR GOOD REASON

I originally posted this Substack on August 27th, 2024. Since that time, the Leading Edge Clinic has grown, and we now have thirty five employees and thousands of patients. The providers have multiple electronic chats, and we meet in different ways during the week in order to research, learn, update and continually grow in our efforts to provide care for patients with complex chronic conditions. Today the question arose in a chat about whether or not other providers prescribe Epi-Pens to patients with MCAS. In my response to the conversation, I referenced Afrin’s Table 12, and when my colleague replied, “What is Table 12 from Afrin?” I realized that it was time to share this Substack again. Whether you are a patient with PASC or injury from the Covid shots, a patient with MCAS for some other mysterious reason, or simply someone who has “bad allergies”, you should know about Table 12. It could save your life. If you are a medical provider, and you are caring for these same patients, you absolutely should know about Table 12. Cheers.

PROLOGUE

After working in the Emergency Department (ED) for more than fourteen years, I cannot count the number of abdominal pains, chest pains, broken bones, lacerations, heart attacks, strokes, MVCs, stabbings, and gunshots I encountered. I also saw patients in anaphylaxis, which is when an acute allergic reaction leads to swelling of the airway, tongue, lips, and face so that a person’s ability to breathe is compromised. Sometimes a relative rolled them in the door, the patient arching back in a wheelchair as they took their last gasp. But, there actually weren’t that many of them. I can count them, just like the number of cases of priapism (an erect penis that just won’t stop being erect!), or foreign objects mysteriously lodged in a rectum (you can scarcely imagine). I would put the number of anaphylaxis patients over fourteen years at...twenty.

You might then understand that when six of my patients at the Leading Edge Clinic have either approached anaphylaxis or come within a minute of dying from the same, over the short period of six months, well, it got my attention.

What is going on here? To give you an answer, we’ll have to go back in time a few years.

RECENT PAST

In my Substack Honest Fight I wrote about my 2019 trip to Sweden and Norway with Ellen David Friedman, a veteran union organizer and international labor leader. While we were there, we spent most of our time with teachers, but had a visit with dockworkers, and also met some nurses and doctors. I had a fascinating one-on-one meeting with Anne Lindgren Berndt, President of Vårdförbundet. Also known as the Swedish Association of Health Professionals, Vårdförbundet is the trade union and professional organization of four registered professions; nurses, midwives, biomedical scientists and radiographers. It represents more than 80 % of the workforce.

During our conversation, Anne shared a story which stuns me to this day. A young couple made a trip to the countryside outside of Stockholm for a picnic with their two young children. After a bee stung their not-yet-one-year-old daughter, her lips began to swell and her breathing turned raspy. They called emergency services and within ten minutes a helicopter with an emergency nurse and physician landed in a nearby clearing. They administered a lifesaving epinephrine injection, and within minutes the girl was breathing more easily. Then they bundled up the girl and flew off to the nearest hospital right? Nope. The pilot, nurse, and doctor hung out for more than thirty minutes, monitoring the little girl, getting a health history, providing a pair of epi-pens, providing education about how and when to use the pens, and ensuring that there would be a followup the next day with her pediatrician. Then they returned to their helicopter and flew away, leaving the young family to enjoy the rest of their picnic. True story.

Sweden is not nirvana, or Ellen and I wouldn’t have been there meeting with union members across several sectors. The neocons strategically, methodically, almost invisibly, have hollowed out the strength and influence of Swedish labor over a period of decades. And still, the story above demonstrates what is possible when a country dedicates more than a fraction of its resources to rational healthcare instead of endless wars.

PAST

Dr Lawrence Afrin is considered by many to be the expert on mast cell activation (MCAS) in the United States, and Dr Gerhard Molderings his equivalent in the United Kingdom. An aside—would you agree that someone with the last name Molderings sounds like he should be in a Harry Potter movie? Anyway, in 2016, Afrin, Molderings et. al. wrote a review of how to treat MCAS. It was titled Pharmacological treatment options for mast cell activation disease. If I could wave a magic wand and bring the medical establishment up-to-date on the post-Covidian world, I would make these twenty three pages of clinical wisdom required reading. But seeing as how this isn’t a Harry Potter movie, and I misplaced my magic wand, I’m going to write you dear readers and try to arm you with some potentially lifesaving information.

The meat of the article lays out a step-wise approach to treating MCAS. Some of these therapies should be familiar by now to most patients with post-acute sequelae of Covid (PASC) and injury from the Covid shots: H1 and H2 anti-histamines, Cromolyn, Ketotifen, etc. What evaded my attention for months, but which rose in prominence with each successive instance of anaphylaxis, was Table 12.

As I pay tribute to Dr Afrin, I also feel compelled to share some small insight into the complexity of this man’s mind and expertise. When a hero fails to live up to the expectations in one’s mind, does it make a sound? For me, it sounds kind of like a “whumpf.” It turns out that “whumpf” has been adopted as technical avalanche term, which describes the sound made when a heavier lay of snow collapses under the weight of a person or machine walking over a lighter/weaker layer of snow, sometimes preceding an avalanche. Sounds auspicious to me! So, Dr Afrin has been a hero of mine, shedding light on the topic of MCAS through his prolific writing on the topic. My “whumpf” moment came when a patient told a provider in our practice that a nurse in Dr Afrin’s practice said he believes in the safety and efficacy of the Covid shots, and thinks that Paxlovid is an effective first-line treatment for acute Covid. In case that was hearsay, I checked with another colleague who has been in regular communication with Dr Afrin, and she/he said, “ Yup, that’s about right.” If the poignancy of this is lost on you, give it time.

PRESENT

The origin of mast cells helps explain why hyperactivation in MCAS is so problematic. When life on this planet leapt from single to two-celled organisms, mast cells were the second cell to arrive. They were the original bouncers of life, and tasked with protecting the organism. They developed a wide repertoire of tools, which included mediators. We can count the birth, life and death of a platelet or white blood cell in about a week. Red blood cells last up to two months. Mast cells last—get this—two to four years! How would you like to really, really, really piss off your mother-in-law, and then find out she was moving in with you for the next four years? No bueno.

When a person is exposed to the spike protein, whether from infection, shedding, or vaccination, the spike protein hyperactivates the mast cells. In a person who didn’t have mast cell disease before the pandemic, this may not have significant consequences. But in a person who had some degree of mast cell disease before Covid, this can be disastrous. These are people who may have had environmental allergies, food sensitivities, rashes, unexplained headaches, irritable bowel disease, asthma, etc.

So what are mediators? They are substances released by mast cells with characteristics that promote, manage and resolve our immune response, particularly in allergic and inflammatory processes that lead to healing. When they spin out of control, or stay around too long, they cause lots of trouble. E.g. cytokines. Remember all the people who died during the pandemic in the winter of 2021 from cytokine storm? Those cytokines were coming from mast cells. What other mediators are there? Histamines, heparin, proteases, leukotrienes and prostaglandins.

Back to Table 12. I’ll skip down to local anesthetics, because I think this point touches the largest number of people. Procaine is what most of us know as Novacaine. It’s the most commonly used local anesthetic in dentistry, because of it’s rapid onset and short duration. In post-Covidian times, in mast cell activated patients, there is a big downside to Novacaine—it can provoke release of mediators from mast cells. If you’re a person without any history of MCAS, perhaps this is no big deal. But what if you are limping along with PASC or vaccine injury?

One of my patients is in his mid-30s, and vaccine injured. He needed to have some involved dental work, and rather than it taking a day or two to recover, it took eight to nine days. A few days after this, he went out to eat with his family and at ate some elk meat. Before the meal was over, he was starting to have trouble breathing, and his throat felt like it was closing. He had an old epi-pen in the glove compartment of his vehicle, and used it. His family drove him to the nearest ED, and he lost consciousness on the way due to diminished breathing and lack of oxygenated blood flow to his brain. He literally came within minutes of losing his life.

Why did this happen? If we go back to the period after he received the Covid shots, one conclusion of the exhaustive testing by system doctors who couldn’t find any abnormal tests, or almost none, was that he had Alpha-gal Syndrome. Ever heard of it? Me neither. It’s a potentially life threatening condition which can occur after a tick bite, and results in a delayed allergic reaction to mammalian meat. Mammals have tits and nurse their young, so we’re talking about the four-leggeds, such as pigs, cows, sheep, but also deer, rabbits, and elk. The likelihood of developing Alpha-gal are pretty slim, or at least they used to be, with estimates as low as 1-2% of the pediatric and adult population. Having never encountered it during thirty years of practice, I’ve now encountered it twice in the last year in our practice.

The patient had experienced some difficulty breathing and throat scratchiness after diagnosis with Alpha-gal, and before eating elk meat, enough to be cautious and have an Epi-pen, but what sent him over the edge? A dental procedure with Procaine, or Novacaine led to a close call.

Table 12 doesn’t just point out the dangers, it also points towards the solutions, or alternatives. In the case of Novacaine, there is the alternative of Bupivacaine. This is a local anesthetic which takes longer to numb tissue, up to fifteen minutes, and lasts longer, up to eight hours. That makes it a lot less convenient for dentists and patients, but most dentists will have it on hand. It just requires some advanced planning and communication.

It’s worth noting that Lidocaine is on the naughty list too. If you cut yourself badly and go to the local Urgent Care for some stitches, the chances are that the suturing physician will use Lidocaine to numb up the site first. It may be worth discussing your options.

If we go back up the list of Table 12, we’ll find SSRIs. This is the one instance where there literally is no alternative. Examples are citalopram, escitalopram, fluoxetine, fluvoxamine, and sertraline. And how many people take SSRIs? In the United States, about 13% of the adults or 43 million people. Worldwide, estimates suggests 4-5% of the global population or 300-400 million people. Hey, I’m sorry to put a damper on pharma profits, but I think that we’ve got a problem here. MCAS + SSRIs= mediator release → increased potential for anaphylaxis.

Moving back down the list, we find peripheral acting analgesics such as Aspirin and Ibuprofen. This is where I would caution the reader, and say, “Hey, let’s not go overboard here.” Any decision about whether to use or not use a therapeutic, at what dose, and for how long, is based upon a risk vs benefit decision. We can do this! Heck, most adults drive a car, and that is one non-stop rolling series of risk-benefit decisions. Ibuprofen? Well, if you’re well hydrated, and take it with food, and haven’t just eaten a high-histamine meal with avocado, leftovers, and alcohol (inhibits diamine oxidase or DAO, which breaks down histamine) then you could be fine. But what if you take an SSRI, and you just had dental work with Novacaine, and then you had a high histamine meal. Perhaps Tylenol might be a better choice, or rather least worst choice.

Next up on the list are some opiate analgesics, some of my favorites: morphine and codeine. Meperidine or Demerol is there too, but very rarely used these days.

Trying to quit smoking or fending off the blues with Wellbutrin / Bupropion? I’m sorry to say but that’s on the naughty list too.

How about antibiotics? Not to feel left out, we have some of those too, including Cefuroxime (I think there was a typo leaving the e off the end on the list) and Vancomycin. You’ll generally encounter these in the hospital setting via IV administration. Which is also where you’ll find iodinated contrast medium (think CT contrast) and gadolinium chelate (think MRI contrast). It is into this spiderweb of therapeutics that one of my patients recently landed, with serious adverse consequences.

This patient is in his eighties, and being treated with adjunctive cancer care for renal cell carcinoma which has metastasized to his lungs and bones. One of his arms swelled up to three times the size, and his wife took him to the ED. There was a turf war there, in which the Dermatologist opined that his arm was the biggest hive she had ever seen, and recommended antihistamine treatment (think MCAS). Oncology opined that he had cellulitis, brushed aside Dermatology’s recommendations, and ordered IV antibiotics with a cousin of Cefuroxime; these are antibiotics called Cephalosporins, commonly used to treat skin infections. They also ordered an MRI with contrast. Hours later, the patient was streaking down the hallway, trying to escape, exhibiting what would be called delirium, and powerfully pushing aside his wife in his rush. After being home for several days, she reports that his mind still isn’t the same, his sleep is disrupted, and “it has been rough.” So who was right, Dermatology or Oncology? I would vote Dermatology, and say that Oncology picked two therapeutics interventions, an IV Cephalosporin and an MRI with gadolinium chelate which both ramped up mediator release from his already hyperactive mast cells and created a pro-inflammatory and disruptive environment in his brain which contributed to delirium in this vulnerable, elderly patient.

How could mast cell mediators contribute to delirium? Cytokines such as TNF-alpha and IL-6 can cross the blood brain barrier and promote inflammation. Histamine increases blood brain barrier permeability, allowing inflammatory molecules and other immune cells to enter the brain, ramping up neuroinflammation and disregulating neuronal connections. Histamine can also directly bind to histamine receptors in the brain and impact neurotransmitter release and signaling, particularly with acetylcholine and dopamine, both strongly associated with delirium. Mediators can cause dilation and increased permeability of blood vessels in the brain which affect cerebral blood flow negatively. Mediators like proteases and reactive oxygen species can induce oxidative stress which can damage neurons and lead to cognitive dysfunction and delirium.

The therapeutics on the bottom of Table 12 are ACE inhibitors, such as Lisinopril, and beta blockers, such as Metoprolol. ACE inhibitors relax veins and arteries to lower blood pressure, and are often first-line therapies for hypertension due to concurrent protective impact upon kidney function. Beta blockers block the effect of the hormone and neurotransmitter epinephrine, causing the heart to beat less forcefully and more slowly. We can’t and shouldn’t throw the baby out with the bath water, understanding that patients are often on these medications for good reason, but also expanding our focus, and realizing that use of these medications in a post-Covidian era can prime an individual for a spillover of mast cell mediators, which could in some cases lease to anaphylaxis.

An example in this case is my patient who never had any allergies to seafood, but is on an ACE inhibitor for blood pressure, and takes LDN, Ketotifen, takes Antronex with meals, and as needed H1/H2 antihistamines for her MCAS. She went out to dinner with her husband and was in a restaurant which was sparsely populated, so less risk of shedding. She had a glass of wine (inhibits DAO production to break down histamine) and ordered seafood Alfredo, which had shrimp, scallops and clams. When she began eating her entree, it started to feel like her lips were swelling and her throat was tightening, but it wasn’t obvious to the dining companion observing her. She stopped eating the dish, and this sensation of throat tightness continued for more than twelve hours afterwards. When we discussed this during a followup visit, I suggested that we order her an Epi-pen, and reviewed Table 12 with, explaining that I think she was approaching an anaphylactic reaction.

A very important teaching around Epi-pens is that they come in pairs for a reason. Remember that the Swedish helicopter nurse and physician left a pair of epi-pens? Epinephrine is a short-acting medication, and its effects can wear off before a person reaches emergency medical providers. If the patient separated the pens, and put one in a car and one in their home for instance, they may have just one Epi-pen on hand in an emergency. That is what happened with my 30-something patient with Alpha-gal Syndrome, and without a second pen to administer, he nearly died before his family got him to the ED.

My final words of advice are to print out Table 12 and carry it with you. Discuss it with your PCP, dentist, surgeon and anesthesiologist. In a post-Covidian era, our bodies are different, and we need to be smart about how we may respond to drugs and agents which never troubled us before. Be prepared.

P.S. Thank you to Deb for her original artwork, the feature image of this Substack, a tribute to Pierre and I, and our work at the Leading Edge Clinic in treating PASC and injury from the Covid shots.

P.S.S. If you’ve ever heard the Beatles song Revolution 9 (you need to listen to it with a set of ear buds or headphones), you might appreciate why I wanted to call this Substack Table 12. It’s not a zinger of a title, but it should be, because Table 12 is so darned important. I hope that after reading this Substack you’ll agree.

A clinical case from practice

This case involves a woman in her 30s with prior vaccine-injury history, chronic fatigue, significant symptom burden, and laboratory-confirmed iron deficiency anemia with reactive thrombocytosis. All protected health information has been removed or generalized. Dates, identifying details, and nonessential specifics have been minimized to preserve privacy while retaining the clinical pattern.

The patient initially presented with profound fatigue and a sense of feeling generally unwell. Her broader history included a baseline vaccine-injury syndrome with ongoing systemic symptoms, polypharmacy, dysautonomia/POTS physiology, and complex nutritional and inflammatory issues. Initial laboratory workup showed a classic iron-deficiency pattern: low hemoglobin, low hematocrit, low MCV, low MCH, low MCHC, elevated RDW, very low serum iron, very low iron saturation, and an elevated platelet count consistent with reactive thrombocytosis.

At one point in the course, there was also a mild ALT elevation. That raised concern for possible medication or supplement irritation, but the rest of the liver profile remained reassuring, and the abnormality later normalized.

Why this case mattered

This was not just a lab abnormality. The patient felt terrible. The degree of fatigue and systemic depletion was functionally significant, and the iron-deficiency pattern appeared to be contributing not only to poor stamina and exertional intolerance, but also to a reactive platelet elevation that could have added thrombotic concern in the context of her broader medical history.

The clinical question was straightforward: could a more targeted oral strategy improve marrow response, improve symptoms, and reduce the reactive thrombocytosis without creating gastrointestinal intolerance or hepatic stress?

Baseline pattern

The early laboratory pattern was strongly consistent with iron deficiency anemia:

- Low hemoglobin and hematocrit.

- Microcytosis and hypochromia.

- Elevated RDW.

- Markedly low serum iron.

- Markedly low iron saturation.

- Elevated platelet count consistent with reactive thrombocytosis.

A fecal occult blood test was negative, which was reassuring but did not fully exclude intermittent or occult gastrointestinal loss. Just as importantly, the patient menstruated during the study period, including a heavier-than-usual cycle during the later phase of treatment. That matters because it means the observed laboratory improvement occurred in spite of an expected source of ongoing monthly iron loss rather than in the absence of it.

Intervention

A consulting pharmacist recommended two products as part of the next phase of care:

- Sideral, an Italian sucrosomal iron, one capsule daily.

- Heart and Soil Lifeblood, six capsules daily, a whole-blood bovine extract product intended to provide heme-based nutritional support.

As part of a broader, whole-body approach, the patient was also guided to use organic castor oil liver compresses during this phase. The intent was to support bile flow, facilitate liver function, and help calm low-grade liver inflammation while iron repletion was underway.

She also remained on elements of a broader recovery protocol, including Vedicinals 9 oral liquid and Aurmina baths, while other therapies were held in reserve until iron stabilization improved.

Before moving to Sideral and Lifeblood, the first therapeutic step was a gentler, food-based liquid iron strategy using Floradix layered on top of ongoing lactoferrin. That choice was deliberate. It offered a low, steady dose of iron with generally good tolerability and was a reasonable place to begin in a patient with significant symptom burden and concern for gastrointestinal side effects.

Over the first several weeks, however, the response looked limited. The pattern remained one of marked depletion, with ferritin at 6, iron saturation at 5%, serum iron remaining low, and platelets still running in a reactive range. In other words, Floradix may have been tolerated, but by itself it did not appear to be generating the strength of response needed for the degree of deficiency present in this case.

Why Sideral was attractive in this case

Sideral uses a sucrosomal form of iron in which the iron is wrapped in a phospholipid and sucrose-ester matrix. That structure helps the iron pass through the stomach with less breakdown and less direct contact with the gastric lining, then reach the intestine for absorption. In practical terms, that is one of the reasons sucrosomal iron is often better tolerated than traditional oral iron salts, especially in patients who are sensitive to nausea, bloating, constipation, or general GI irritation. (Although not relevant in this case, this is also a consideration in patients who have had gastric bypass.)

That characteristic mattered here. This patient was already burdened by systemic symptoms and multiple therapies. A formulation that could move through the stomach more gently, remain more intact through the upper GI tract, and still deliver clinically useful iron made sense as a strategic oral option before escalating to infusion therapy.

Why Lifeblood may have helped

Heart and Soil Lifeblood is formulated from grass-fed whole blood extract, spleen, and liver. From a nutritional perspective, that means it is not just an iron product. It also provides heme-based iron along with cofactors and tissue-derived nutrients relevant to red blood cell production, oxygen delivery, and metabolic recovery.

The liver and spleen components are especially interesting in a case like this because they offer a broader package of naturally occurring nutrients associated with hematopoiesis, including compounds related to B-vitamin support, trace minerals, peptides, and iron-handling biology. In clinical terms, that may help explain why some depleted patients feel supported by organ-based formulations even before full normalization of standard iron indices occurs.

No conflict statement

There is no financial relationship, sponsorship, affiliate relationship, paid endorsement, or conflict of interest with either Sideral or Heart and Soil Lifeblood in the care of this patient.

Gratitude

Tremendous thanks to David Restrepo, pharmacist and owner of Vitahealth Apothecary in New York City, for his thoughtful consultation and product guidance in this case.

Laboratory trend tables

Iron Studies Trend

Ferritin crept from 6 to 14 ng/mL over this window and transferrin drifted down from 327 to 299 mg/dL, small but meaningful signs that true iron stores were beginning to replete as the Sideral + Lifeblood phase progressed, after only limited impact from the initial Floradix‑based approach.

Liver and CMP Trend

Subjective improvement during follow-up

What makes this case more compelling is that the patient did not just improve on paper.

At follow-up, she reported significant improvement and described having real bursts of energy and more good days overall. She was still dealing with swings, sometimes feeling better one day and then very tired the next, but the pattern had clearly shifted away from unrelenting depletion.

That distinction matters. Early recovery from iron deficiency often does not feel smooth or linear. Patients may feel enough better to overdo it on a good day, only to crash the next. In a patient with overlapping POTS and vaccine-injury physiology, those oscillations are even easier to misread. But in context, the presence of genuine higher-energy windows is often a sign of improving physiologic reserve, not treatment failure.

She also reported that her most recent menstrual period was heavier than usual, yet the laboratory trajectory still improved. That makes the trend more impressive, not less.

Why IV iron was considered — and held in reserve

At several points, referral for intravenous iron infusion was seriously considered. The patient felt profoundly unwell, the iron panel looked alarming, and the threshold for escalating to IV iron in that context is appropriately low.

What kept that from happening immediately were the early objective signals that the marrow was already responding to oral therapy. Hemoglobin and hematocrit were rising across sequential draws. Platelets, which had behaved in a clearly reactive pattern, began to fall. The transient ALT bump also normalized, suggesting the broader regimen was being tolerated rather than driving ongoing hepatic stress.

Just as importantly, these gains occurred even though the patient menstruated during the study period, including a heavier-than-usual cycle near the later phase of follow-up. That makes the response more impressive, because the therapy appeared to work in spite of an expected ongoing route of iron loss.

Those signals argued that the patient was demonstrating rapid replication under oral dosing; in practical terms, the marrow appeared to be taking the available iron and putting it to work. With creatinine, eGFR, and liver enzymes (AST/ALT/alkaline phosphatase) remaining stable in the normal range over six weeks, it was reasonable to hold intravenous iron in reserve rather than escalate, especially once the patient also began to report meaningful symptomatic improvement.

Interpreting the changes

Several things stand out.

First, the platelet count fell from an originally elevated, reactive range into a clearly improved range and largely stayed there. Even with a slight week-to-week wobble, the overall pattern strongly supports reactive thrombocytosis rather than autonomous platelet overproduction.

Second, hemoglobin and hematocrit improved stepwise across serial testing. This was not a one-off fluctuation. It was a directional trend.

Third, the iron profile finally began to look better in a more obvious way on the latest draw. Serum iron rose from 12 to 37, and iron saturation rose from 3% to 10%. That remains suboptimal, but it is a meaningful directional improvement.

Fourth, the transient liver enzyme abnormality normalized and remained acceptable. ALT moved from mildly elevated back into a normal range, reducing concern about ongoing hepatic irritation from the broader treatment and supplement environment. The supportive use of organic castor oil liver compresses was part of that broader strategy aimed at helping calm low-grade hepatic irritation during the repletion phase.

Why the patient may have improved before the iron panel looked pretty

This is an important teaching point.

Many clinicians expect serum iron and saturation to normalize in parallel with how a patient feels. That is often not what happens. In real-world care, especially in complex and inflamed patients, the body may use incoming iron immediately for red-cell production. That means hemoglobin can start to climb and platelet reactivity can begin to settle before serum iron indices look impressive.

That appears to be what happened here. Only later did the iron panel begin to visibly catch up with the clinical story and CBC trend.

Clinical takeaways

- Severe iron deficiency can coexist with a high platelet count that is reactive rather than malignant.

- A falling platelet count during iron repletion is a reassuring sign.

- A temporary mild ALT elevation does not necessarily mean the treatment path is failing, especially when the rest of the liver panel is stable and the value normalizes.

- Iron saturation alone should not be overinterpreted in the early phase of response.

- In selected patients, a better-tolerated, more targeted oral strategy may begin to shift the trajectory even before full biochemical repletion is visible.

- Not every symptomatic iron-deficient patient needs immediate IV iron if serial data clearly show early marrow response and the patient is beginning to improve clinically.

- Improvement during an active menstrual window is a meaningful signal that the repletion strategy is overcoming ongoing physiologic iron loss.

Final reflection

The patient is now feeling significantly better. That improvement matters as much as the numbers.

The case is a reminder that recovery is often not linear and not all markers move at the same speed. In this patient, the combination of improved hemoglobin, improved hematocrit, a marked drop in platelets from baseline, normalization of liver enzymes, rising serum iron and iron saturation, and a meaningful clinical improvement suggests that the intervention helped move her out of a depleted, stressed physiologic state and into an early recovery phase.

There is still more ground to cover before full iron repletion can be claimed. But the direction is clear, the clinical response is real, and the lab pattern supports what the patient is already telling us: she is doing better.

Addendum 4/27/26

A subsequent laboratory draw on 04/27/26 strengthened the overall conclusion of the case. Hemoglobin rose to 11.1 g/dL, hematocrit to 39.0%, MCV to 82 fL, and platelets normalized to 381. Serum iron increased further to 40 ug/dL and iron saturation to 11%, while kidney and liver markers remained stable. Taken together, these later data points support a continued recovery trajectory and further reduce concern that intravenous iron will be necessary if the present trend continues.

P.S. If you recognize the clinical acumen and patient-focused care in this case report, please recommend the Leading Edge Clinic to friends and family with PASC, injury from the Covid shots, cancer (for adjunctive care), and other complex medical conditions.

The Curious Substack

Why Drinking Structured Water Doesn’t Work. What You Can Do That Does.

A full scientific theory paper complete with detailed mechanisms, experimental design proposals, and a comprehensive reference list can be found HERE…

Read more

5 months ago · 57 likes · 38 comments · Curious Outlier

The Curious Outlier is right… and also wrong

The piece “Why Drinking Structured Water Doesn’t Work. What You Can Do That Does” gets one big thing right: ingested “structured water” does not survive the stomach as a persistent, macro‑scale bulk‑phase structure. Hydrogen bonds in liquid water reconfigure on the order of picoseconds, and the warm, acidic, electrolyte‑rich environment of the gastric lumen rapidly equilibrates any imposed ordering. That is sound physical chemistry.

It also correctly points to real, experimentally documented EZ‑like water at hydrophilic interfaces—especially the endothelial glycocalyx—as a legitimate biophysical phenomenon, not a marketing gimmick. This is where Dr. Pierre Kory and others have increasingly shifted the conversation away from “bottled magic geometry” toward mineral‑defined cosmotropic water and interfacial organization at surfaces.

Where the argument founders is in its conflation of three very different questions:

• Can you drink “structured water” into your cells?

• Can RIC replace water purification and mineralization?

• Is the concept of ordered, EZ‑like water anything more than a marketing label?

The Substack piece mixes the first with the third and then uses that to dismiss the second, while simultaneously positioning RIC as a substitute for substrate decisions about water quality. A clinical thinker steeped in functional physiology, knows that signals and substrates are not the same thing.

RIC is a signal, not a purifier

Remote ischemic conditioning (RIC) is a remarkably elegant maneuver: a blood‑pressure cuff inflated and released on an arm or leg creates brief, controlled ischemia‑reperfusion cycles that trigger systemic vascular and end‑organ benefits. Studies have linked chronic RIC to improved endothelial function, reduced heart‑damage risk, better stroke outcomes, and kidney protection in high‑risk settings.pmc.ncbi.nlm.nih

The hypothesis tying RIC to EZ‑like water is plausible:

• RIC improves shear‑stress patterns and glycocalyx‑mediated flow‑mediated dilation.

• It upregulates mitochondrial health and infrared output, which can expand EZ layers at hydrophilic surfaces.

• It enhances antioxidant defenses and reduces oxidative damage, preserving the very protein‑and‑sugar surfaces on which EZ water forms.

But none of these mechanisms remove heavy metals, PFAS, pesticides, herbicides, or other organic and inorganic contaminants from the water you drink or the body burden you already carry. You can no more “RIC” chromium out of your liver than you can “walk” sewage into potable water. Movement and vascular conditioning improve how your body manages stress and toxins; they do not delete the pollutants. That is a physical and chemical problem—requiring filtration, sorption, and controlled mineralization—which is exactly the terrain which Lightning Bug and Dr Pierre Kory’s Medical Musings (Kory’s cosmotropic‑water framing) are trying to clarify.

From “structured water” to coherencing and minerals

Dr. Kory has recently distanced himself from some of the more fantastical “structured water” branding while simultaneously doubling down on the biophysical reality of mineral‑defined water organization. His language now emphasizes cosmotropic water and mineral‑driven interfacial order, rather than static “hexagonal” labels attached to machines.

In my Substack “Photophone in Our Cells”, I described how trace‑mineral‑rich structured‑water protocols can transiently lower the activation energy for EZ‑like, biophoton‑coherent water organization within the body’s existing interfacial architecture. That is not the same as claiming that bottled water arrives in your cells as a permanent hexagonal lattice. It is, instead, a claim about pre‑organized substrates that align with the body’s own glycocalyx‑ and membrane‑driven water‑ordering machinery.

The Curious Outlier’s Substack critique is right that hydrogen bonds break and reform on picosecond timescales, and that any imposed bulk‑phase structure is rapidly erased. But that is not the only way water can be “structured.” The bulk breaks; the interfaces persist. The glycocalyx already holds on the order of 0.7–1.7 L of interfacial water, and that is the real EZ environment we should be thinking about—not a marketing‑phase label on a bottle.

What Pierre and I are adding to the conversation is the clinical substrate bridge:

• How specific mineral profiles and ordered‑water protocols can ease the work the glycocalyx and membranes must do to form EZ‑like layers.

• How that, combined with vascular conditioning (RIC, exercise, breathwork), may optimize the thermodynamic window for biophoton‑driven coherence and ordered water in vivo.

This is not a contradiction of the hydrogen‑bond‑lifetime argument; it is a refinement of it, shifting focus from “bottled bulk‑phase structure” to mineral‑driven, interfacial, coherenced water within living systems.

Why “20‑plus references” do not erase decades of discovery

Curious marshals a sizable bibliography and uses it rhetorically to suggest that “structured water” is a myth, without sufficiently distinguishing between the marketing fluff and the real EZ and glycocalyx physics behind it. Pollack’s work on EZ water, the glycocalyx EZ reservoir, and the infrared‑driven expansion of ordered water layers are all peer‑reviewed, distinct literatures; they do not vanish because someone compiles a long list of unrelated references.

What Dr Kory and I are doing is operationalizing that physics:

• How mineral content, redox buffering, and interfacial conditions shape the ease with which the body can organize water.

• How modern environmental toxicants (PFAS, heavy metals, pesticides) and demineralized, dead water undermine that capacity.

RIC is a powerful signal for vascular conditioning, but it is not a water purifier, mineralizer, or coherencing device. Water quality, mineral content, and interfacial order still matter—in the body of the patient, the soil, and the plant. A blood‑pressure cuff cannot turn sewage into potable water; it also cannot replace the substrate decisions we make about what we drink.

RIC is a brilliant tool for training the vascular system to use water better; it is not a substitute for bringing the right water to the table in the first place.

For what it’s worth, Pierre has a lot of theories. So do I. It’s part of how we approach the world. When he told me months ago that he thought adding Aurmina to spring or tap water was more effective than adding it to distilled or reverse osmosis water, I wasn’t eager to hear more. In fact, I think that I had just made this video for Substack called Water Distilling 101. My wife and I have distilling water for thirty two years, thinking that we were doing the best thing for our health. It’s hard to admit that you were wrong after that much time.

In his Substack post titled “The Water We Thought Was Safe: Why Purity Isn’t Enough,” Dr. Pierre Kory highlights research from a 2004 Czech review on the health risks of drinking demineralized water, including reverse‑osmosis (RO) treated water. He summarizes the findings that long‑term consumption of such water can contribute to mineral deficiencies, muscle cramps, fatigue, cardiac‑rhythm disturbances, and higher risks for cardiovascular disease, osteoporosis, and adverse pregnancy outcomes. Readers can reference this section in context at: https://pierrekorymedicalmusings.com/p/the-water-we-thought-was-safe-why.pierrekorymedicalmusings

Distilled water is also demineralized water. Pierre’s theory was that it was better to start with spring or tap water, because even with pollutants in it, which the Aurmina would flocculate, there was also a basic mineral architecture which the Aurmina could organize. We are both fond of saying, don’t let the perfect be the enemy of the good, so I didn’t. I kept on drinking distilled water, but his theory was still chicken-scratching in the back of my mind.

There were also some practical considerations to negotiate. When I brought up the three bottle Lisa and Pierre Kory hamhock method of purifying water, Kerries’ face told me “Are you out of your mind? Do you think we have space in our little kitchen for that set up? Do you think that you’re getting any lovin’ tonight if you want to do this?” It’s funny how much a look can say when you have been married a long time. So, I had to figure out a different arrangement, for the water that is, which meant clearing out and cleaning up a section of the basement which needed it anyway. That took a few weekends and a trip to the dump. Then I had to set aside the money to buy the requisite Ikea containers and stands. What I ended up with was this:

I really, really wanted that setup to work. There was plenty of space, and it was aesthetically pleasing. The only problem is that the water still smelled and tasted like chlorine, even after three days, even after I used up to a quarter cup in the container (see middle one in this photo, thus the yellow-orange color in the bottom). I was going to need another filter. Because the South Korean filter which Pierre and Lisa are using is sold out (more coming soon to Aurmina by the way), I moved forward with a Berkey. That was another $400. The next incarnation looks like this:

This arrangement was a lot more crowded, but I can make it work. The more important thing is that the water is delicious.

The most important thing is how I feel after drinking the water. I’m not going to make any medical claims here. I’m just going to say that I’ve been drinking Aurmina in distilled water for months, and I think it has been helpful, but within twenty four hours of drinking Aurmina in Ithaca City tap water, I felt better.

Aurmina can be purchased here: https://www.aurmina.com/

The Ikea bottles and stands can be purchased here: https://www.ikea.com/us/en/p/vardagen-beverage-dispenser-60578319/

The Berkey can be purchased here: https://www.usaberkeyfilters.com/

For Cat Lovers in the Crowd

If I had known what a big hit the Ikea box and wrapping for the water bottles and stands would be in this household, I would have ordered it for Christmas.

This video is dedicated to Nathalie in Alaska. I hope this helps.

An observational clinical account from my practice as Scott Marsland, FNP-C at Leading Edge Clinic

In November 2025 I published the initial case study of a woman whose chronic fatigue and long-standing infertility shifted dramatically after targeted mineral repletion with a liquid volcanic mineral solution chemically similar to EPA-approved water purification formulations such as Aurmina. At that time we saw measurable mobilization of mercury and lead, plus the long-sought positive pregnancy test. Eight months later the story continues—and gets even stronger. The pregnancy remains fully viable with an expected delivery in July 2026. The patient has zero new physical complaints, and she continues the same multimodal regimen: daily oral ingestion plus regular bathing with the mineral solution.Below is the updated timeline with new lab data, precise percent changes, and mechanistic observations informed by water chemistry principles.

Patient Background (Recap)

• Adult female with chronic fatigue, history of renal inflammation, and >1 year of unsuccessful attempts to conceive.

• Primary exposure: Dietary methylmercury (fish consumption).

• Baseline (June 23, 2025): Markedly elevated blood mercury (see Figure 1).

Protocol (Unchanged from Original Post)

Practitioner-directed at Leading Edge Clinic:

• Liquid volcanic mineral solution (chemically similar to EPA-approved water purification formulations).

• Oral: 1 mL per 20 lbs body weight, mixed in water, twice daily.

• Bathing/soaks: Regular dermal exposure (frequency titrated to tolerance).

• Hydration: ≥½ body weight in ounces of pure water daily.

• Adjustments made for autonomic sensitivity, mild detox responses, and metabolic stability.

The combination of drinking (systemic mineral repletion) + bathing (transdermal uptake + mild sweat/excretion support) has been maintained continuously since mid-2025.

Lab Timeline & Key Changes1. Blood Mercury Speciation (Quicksilver Scientific) Figure 1: Baseline Mercury Speciation – June 23, 2025

Figure 2: Follow-Up Mercury Speciation – February 16, 2026

Figure 3: Timeline of Changes in Mercury

Key observations:

• Dominant drop in MeHg (the form most associated with fertility and mitochondrial interference).

• No rebound in inorganic fraction—consistent with successful hepatic demethylation + renal excretion.

• Total burden now approaching (but still above) typical suspect-population averages.

2. Whole-Blood Elemental Panel – Toxic & Nutrient Elements

Figure 4: Nutrient Elements + Ratios – December 16, 2025

Figure 5: Toxic Elements Close-Up – December 16, 2025

Selected changes (Dec 16, 2025 values vs. earlier prior result; further directional improvement noted in Feb speciation):

Ca/Mg and Cu/Zn ratios remain balanced. No new elevations in antimony, cadmium, or other monitored toxics.

Footnote: Mercury values vary slightly by matrix/method (Quicksilver speciation in ng/mL vs. whole-blood elements in µg/L), but directional trends are consistent across panels.

Current Clinical Status (March 23, 2026)

• Pregnancy: Viable, second trimester, due July 2026.

• Symptoms: None new. Energy stable, no complaints related to fatigue or renal issues.

• Regimen: Continues drinking + bathing with the mineral solution daily/regularly.

The patient reports feeling “steady” throughout gestation—no Herxheimer-type reactions, no new sensitivities, and no need for protocol interruption.

Scientific Context: Mineral-Water Interactions

The following framework draws from water chemistry research by Dr. Pierre Kory on geological water conditioning and Hofmeister chemistry principles. This provides theoretical context for understanding mineral-aqueous interactions but does not constitute medical claims. Note: while standard Hofmeister series literature uses “kosmotropic” (from Greek “kosmos,” meaning order) for structure-stabilizing ions, Dr. Pierre Kory uses the variant “cosmotropic” (with a “c”).

Hofmeister Chemistry Framework
The clinical observations in this case align with established principles of Hofmeister chemistry, which describes how different dissolved ions systematically influence water’s hydrogen-bond network and hydration shell stability. Cosmotropic ions—particularly sulfate, magnesium, and multivalent cations found in volcanic mineral sources—promote more ordered hydration structures and stable electrochemical environments compared to chaotropic conditions.

As Dr. Kory explains in his water chemistry analysis, dissolved ions influence water behavior in reproducible ways. Some ions stabilize the hydrogen-bond network of water (cosmotropic ions), while others disrupt it (chaotropic ions). These effects propagate outward into protein stability, enzyme function, membrane behavior, and the operation of living cells.

Geological Conditioning of Water
Natural waters acquire their biological compatibility through prolonged contact with mineral-rich geological formations. Dr. Kory’s research on geological conditioning suggests that water moving slowly through rock inherits electrical coherence and charge-balancing capacity that modern treatment systems often strip away.

Before water ever enters a root, a cell, or the bloodstream, it has already lived a geological life. After rain falls, it enters fractures, faults, and porous bedrock, where it travels slowly along mineral interfaces, exchanging ions, redistributing charge, and becoming chemically and electrically conditioned before re-emerging through springs, faults, or aquifers. Along that path, water acquires far more than dissolved ions—it inherits electrical coherence and structure.

Redox Buffering Capacity
The mineral spectrum in volcanic-derived solutions provides redox buffering capacity—creating reversible mineral couples (iron, sulfur, etc.) that can accept and release electrons in controlled increments rather than allowing energy to dissipate chaotically. This electrochemical architecture may support the body’s own gradient maintenance systems.

Dr. Kory distinguishes between redox buffering (the capacity of water and dissolved mineral systems to stabilize electron flow and oxidation-reduction potential) and the cosmotropic-chaotropic balance (how dissolved ions influence water structure, hydration, and molecular organization). In natural systems, these often reinforce one another.

If water is the medium through which energy travels, then redox buffering is the electrical regulation while cosmotropy is the architecture of the wiring.

Discussion & Mechanistic Observations

These serial reductions in mercury (especially MeHg), lead, arsenic, and strontium—achieved while pregnant—align with the known actions of full-spectrum volcanic minerals:

• Competitive displacement at binding sites (zinc, copper, magnesium, molybdenum crowding out Pb and Hg).

• Selenium-dependent glutathione peroxidase support for demethylation of MeHg → excretable inorganic Hg (with elevated Se levels likely contributing to sustained handling).

• Enhanced renal clearance pathways (aided by both oral and dermal routes).

Bathing provides additional transdermal mineral delivery and gentle sweat-mediated excretion—particularly useful during pregnancy when aggressive oral chelators are contraindicated. These patterns resonate with Dr. Kory’s emphasis on how kosmotropic mineral environments may restore coherent energy flow in biological systems, potentially aiding cellular resilience during detoxification and gestation. The temporal association between mineral sufficiency, heavy-metal mobilization, and successful conception remains striking. Pregnancy itself can increase mineral demand (explaining the modest Zn/Mg dip), yet the patient’s tolerance and continued progress speak to the protocol’s gentleness and adaptability.

Disclaimers

Aurmina is an EPA-approved water purifier only and is not a supplement or drug. This is a single observational case from my private NP practice at Leading Edge Clinic. It is not intended to diagnose, treat, cure, or prevent any disease.

Next Steps in Practice

We will continue monitoring with third-trimester labs (repeat mercury speciation + whole-blood elements) and post-partum follow-up. If you are a practitioner or patient interested in similar mineral-support approaches under supervision, the original November 2025 post contains the foundational protocol outline.

Thank you for reading. As always, I welcome thoughtful questions in the comments.

— Scott Marsland, FNP-C
Lightning Bug | Leading Edge Clinic

Come for the science, stay for the stories.
Personal reflections (including the My Vietnam series, Part 1 and Part 2) live in the opt-in Personal Insights section—toggle it on in your account settings if they speak to you.

Parasite Cleanses: Straight Talk for My Patients with PASC, Vaccine Injury, or Cancer Concerns

Many of you have been asking about parasite cleanses lately—whether herbal protocols with wormwood, black walnut, clove, or papaya seeds, or even over-the-counter “deworming” kits. This topic is trending heavily on social media right now, with influencers claiming hidden parasites are causing everything from fatigue to cancer. As a clinician focused on post-acute sequelae of COVID-19 (PASC), vaccine-related injuries, and adjunctive cancer care, I want to give you clear, evidence-based guidance so you can make informed decisions.

First, the reality of parasites in the United States:
In our modern sanitation, hygiene, and food-safety environment, most Americans are not “overrun” with intestinal worms. Classic helminths (like Ascaris or hookworm) are rare outside specific risk groups—recent immigrants, international travelers, or pockets of poverty. Common exposures include Toxoplasma (often from cats or undercooked meat, usually asymptomatic) or pinworms in children. If you have no travel history, no eosinophilia on bloodwork, and no persistent unexplained diarrhea, weight loss, or abdominal pain, the chance of a significant parasitic infection is very low. True infections are diagnosed with targeted testing (stool ova-and-parasite exams, blood serologies), not assumed. (For prevalence data, see CDC resources and reviews such as Jones et al., 2014, on neglected parasitic infections: https://doi.org/10.4269/ajtmh.13-0726; Woodhall et al., 2014: https://doi.org/10.4269/ajtmh.13-0722.)Cancer and parasites:

There are rare, well-documented links—but only in specific endemic regions overseas (e.g., schistosomiasis causing bladder cancer or liver flukes linked to bile-duct cancer). These involve decades of chronic inflammation in high-risk populations. Cancer in the United States is not caused by parasites. The idea that “everyone has worms causing cancer” is simply not supported by medical evidence. (See Li et al., 2021, on repositioning antiparasitic drugs: https://doi.org/10.3389/fphar.2021.670157.)

Why certain antiparasitic drugs can still help:
This is the biggest point of confusion. Drugs like mebendazole (and its cousin fenbendazole) show promise in adjunctive cancer care because they directly disrupt microtubules inside cancer cells, halting cell division, triggering cell death (apoptosis), and cutting off blood supply to tumors. This works whether or not parasites are present—the antiparasitic effect is incidental. Key studies include Sasaki et al., 2002 (mebendazole induces mitotic arrest and apoptosis via tubulin depolymerization: https://doi.org/10.1158/1535-7163.MCT-02-1-0001) and Doudican et al., 2008 (apoptosis via Bcl-2 inactivation: https://doi.org/10.1158/1541-7786.MCR-07-2159).

Similarly, ivermectin has been used successfully by many clinicians including myself, the practitioners at the Leading Edge Clinic, and my partner Dr. Pierre Kory, author of War on Ivermectin, for symptom relief in PASC and vaccine injury. The benefits come from its powerful anti-inflammatory and immune-modulating actions—reducing cytokines, calming NF-κB pathways, and possibly interfering with spike-protein effects—not from killing parasites. (See Zaidi & Dehgani-Mobaraki, 2022, on mechanisms: https://doi.org/10.1038/s41429-021-00491-6; Portmann-Baracco et al., 2020: https://doi.org/10.1016/j.nmni.2020.100831.)

A key source of confusion is the overlap in metabolism between parasites and cancer cells. Parasites and cancer are not the same thing, and parasites are not the cause of cancer. But some antiparasitic drugs appear to affect cancer cells because both rely on overlapping survival biology—microtubules, stress signaling, redox balance, and, importantly, how they produce energy.Many parasites exist in low-oxygen environments and depend on glycolysis—a more primitive, less efficient way of generating energy through substrate-level phosphorylation rather than mitochondrial respiration. Cancer cells very often shift in that same direction (known as the Warburg effect). Even in the presence of oxygen, they rely more heavily on glycolysis and less on efficient energy production, especially as they grow and adapt under stress. (See Medjkane & Weitzman, 2013, on reversible Warburg effect in Theileria-infected cells: https://doi.org/10.1371/journal.ppat.1003686; Mudassar et al., 2020, on targeting hypoxia and mitochondrial metabolism with antiparasitics: https://doi.org/10.7150/thno.49670.)

The overlap is not causal—it is functional. Both systems lean on similar survival pathways, and drugs that disrupt those pathways may impact both. This metabolic similarity explains why certain antiparasitic agents can have off-target effects on cancer cells, independent of any actual parasitic infection.

What about herbal parasite cleanses?
These products have limited high-quality human evidence. Some herbs show activity against parasites in lab dishes or livestock, but well-designed studies in people are scarce and often low-quality. Recent medical reviews describe this as a social-media-driven trend with little proven benefit for the average person. Potential downsides include gastrointestinal upset (sometimes mistaken for “die-off”), medication interactions, unregulated supplement quality, and—most importantly—delaying proper evaluation of your real symptoms. In my practice, these cleanses rarely move the needle compared to addressing inflammation, mitochondrial support, or targeted therapies. (For broader context on natural products, see Ndjonka et al., 2013: https://doi.org/10.3390/ijms14023395; Strothmann et al., 2022: https://doi.org/10.1016/j.heliyon.2022.e11300.)

My practical advice:
If you have symptoms that could suggest parasites, bring them up at your visit—we can order the right tests and treat accordingly with proven medications. For the vast majority of my patients with PASC, vaccine injury, or cancer, the focus should stay on what actually drives improvement: reducing chronic inflammation, supporting detoxification pathways, optimizing immune balance, and using repurposed drugs where the science and clinical experience align. Parasite cleanses are not a shortcut or a necessary routine step.

I’m here to answer questions honestly and personalize care based on your labs, history, and response to treatment—not trends. Let’s keep the conversation going at your next appointment. Your recovery and well-being are my top priority.

— Scott Marsland, FNP-C
(With input from current medical literature, my clinical experience, and collaboration with Dr. Pierre Kory and Dr Paul Marik)

Parasite Prevalence in the US

• Jones JL, Parise ME, Fiore AE. Neglected parasitic infections in the United States: toxoplasmosis. Am J Trop Med Hyg. 2014;90(5):794-799. DOI: 10.4269/ajtmh.13-0722

• Woodhall DM, Jones JL, Cantey PT, et al. Neglected parasitic infections: what every family physician needs to know. Am Fam Physician. 2014;89(10):803-811. (PMID: 24866216; full text available via PubMed Central or journal site; no separate DOI listed in primary sources, but commonly referenced in CDC/CDC-affiliated reviews)

Cancer and Parasites / Repurposing Antiparasitic Drugs

• Li Y-Q, Zheng Z, Liu Q-X, et al. Repositioning of Antiparasitic Drugs for Tumor Treatment. Front Oncol. 2021;11:670804. DOI: 10.3389/fonc.2021.670804

Mebendazole Mechanisms in Cancer

• Sasaki J, Ramesh R, Chada S, et al. The anthelmintic drug mebendazole induces mitotic arrest and apoptosis by depolymerizing tubulin in non-small cell lung cancer cells. Mol Cancer Ther. 2002;1(13):1201-1209. (PMID: 12479701; DOI not assigned in original publication, but widely cited; full text via journal archive)

• Doudican NA, Rodriguez A, Pavlick AC, et al. Mebendazole induces apoptosis via Bcl-2 inactivation in chemoresistant melanoma cells. Mol Cancer Res. 2008;6(8):1308-1315. DOI: 10.1158/1541-7786.MCR-07-2159

Ivermectin Mechanisms (Anti-Inflammatory / Potential in Viral Contexts)

• Zaidi AK, Dehgani-Mobaraki P. The mechanisms of action of ivermectin against SARS-CoV-2—an extensive review. J Antibiot (Tokyo). 2022;75(2):60-71. DOI: 10.1038/s41429-021-00491-6

• Portmann-Baracco A, Bryce-Alberti M, Accinelli RA. Antiviral and Anti-Inflammatory Properties of Ivermectin and Its Potential Use in Covid-19. Arch Bronconeumol. 2020;56(12):831. DOI: 10.1016/j.arbres.2020.06.011

Metabolic Overlap (Warburg Effect / Glycolysis in Parasites and Cancer Cells)

• Medjkane S, Weitzman JB. A reversible Warburg effect is induced by Theileria parasites to transform host leukocytes. Cell Cycle. 2013;12(14):2167-2168. DOI: 10.4161/cc.25540

• Mudassar F, Shen H, O’Neill G, et al. Targeting tumor hypoxia and mitochondrial metabolism with anti-parasitic drugs to improve radiation response in high-grade gliomas. J Exp Clin Cancer Res. 2020;39(1):208. DOI: 10.1186/s13046-020-01724-6

Herbal / Natural Products for Antiparasitic Activity

• Ndjonka D, Rapado LN, Silber AM, et al. Natural Products as a Source for Treating Neglected Parasitic Diseases. Int J Mol Sci. 2013;14(2):3395-3439. DOI: 10.3390/ijms14023395

• Strothmann AL, et al. Antiparasitic treatment using herbs and spices: A review of the literature of the phytotherapy. Braz J Vet Med. 2022;44:e004722. DOI: 10.29374/2527-2179.bjvm004722

As many of you know, I am co-owner of Aurmina alongside Dr. Pierre Kory and Lisa Kory. Aurmina uses a base Themarox solution imported from Japan, drawing from longstanding Japanese traditions around mineral-based wellness.

Disclosure: As a co-owner, I have a financial interest in Aurmina. This post reflects on an out-of-print 2005 book by Japanese physician Dr. Hisatake Nojima, Super Minerals Protect Your Health!, based on a translated version made possible through generous patient efforts (details below).

Important upfront disclaimer: This is a neutral, educational summary of Dr. Nojima’s personal opinions, clinical anecdotes, and hypotheses from 2005. These are not supported by modern randomized controlled trials, have not been evaluated or approved by the FDA, and do not represent current medical, nutritional, or scientific consensus. Nothing here is medical advice, a health claim, an endorsement of any approach (including mineral solutions), or promotion of any product, including Aurmina. The book’s ideas—particularly on cancer and disease—are historical, provocative, and based on one clinician’s observations in his practice. They predate major advances in genomics, oncology, and evidence-based nutrition. Science has evolved significantly since 2005; always consult a qualified healthcare provider for personal health matters.

A heartfelt thank-you: A patient from the Leading Edge Clinic and his family kindly tracked down five of Dr. Nojima’s out-of-print books and funded their full English translation. Copyright restrictions prevent sharing complete PDFs, so we’re limited to summaries like this. Many readers might find value in the full texts to explore these concepts further—we’re investigating compliant ways to potentially publish or share the translations (e.g., via permissions or proper channels). Our sincere gratitude to this patient and family for their commitment to broadening access to the insights of one of Japan’s most innovative and forward-thinking medical voices.

Dr. Nojima’s Background and Driving Motivation

Dr. Hisatake Nojima, a Doctor of Medical Science, trained at Nagasaki University School of Medicine and held roles including Assistant Professor at Kagoshima University, U.S.-based research, and directing public health centers in Chiba. By 2005, after over 13 years working with trace minerals, he ran Nojima Clinic, dedicating himself to “Super Mineral therapy” for conditions he linked to modern lifestyles—cancer, diabetes, atopic dermatitis, hay fever, and more. He observed these “modern day diseases” as rare in developing nations or pre-industrial eras, blaming industrial agriculture’s shift from organic to inorganic methods (chemical fertilizers/pesticides depleting soil minerals). He criticized huge investments in pharmaceuticals and early gene therapy as overlooking basics, echoing the Japanese adage that “medicine and food share the same origin.” In his view, correcting dietary mineral imbalances could address root causes simply, without costly interventions.

Core Thesis: Trace Elements as Life’s Fundamental Catalysts

Dr. Nojima portrayed trace elements (minute minerals like tungsten, titanium, vanadium, plus 40+ others) as essential catalysts for all life processes. He explained how primordial life emerged via minerals in rocks catalyzing organic matter from ancient atmospheres, with seawater’s mineral profile mirroring human blood composition (e.g., high chlorine/sodium). As life evolved, animals shifted from direct seawater absorption to plant-based intake—but modern inorganic farming, he argued, stripped soils of these elements, creating “mineral malnutrition” in advanced societies.He detailed minerals’ roles: activating enzymes (magnesium for ~300, zinc for ~250), enabling vitamins to function (e.g., vitamin E needing calcium, selenium, zinc), and partnering with genes for proper protein synthesis. Deficiencies, he hypothesized, disrupt metabolism, leading to abnormalities. He introduced “Super Mineral Water”—ionized, water-soluble minerals from natural ore—as a practical, low-cost, side-effect-free replenishment method, emphasizing synergy among elements rather than isolated supplements.

Chapter Breakdowns with Deeper Insights

Chapters 1-3: Deficiency as the Root of Modern Diseases

Dr. Nojima tied widespread issues to soil depletion: citing 1950s-2000s Japanese food tables showing spinach losing ~50% vitamin A, ~25% vitamin C, and ~83% iron; apples nearly all iron. He warned of “sub-healthy” states from deficiencies, exacerbated by stress or alcohol. He advocated agricultural fixes—ionizing trace elements into fertilizers, reviving organic practices with waste recycling (”mottainai”)—while suggesting individuals use mineral solutions interim. He stressed building resilient bodies for faster recovery and reduced drug reliance, cautioning against “drug-related harm” like immune damage from treatments.

Chapters 4-5: Minerals’ Hypothesized Role in Cancer and Diseases

He posited deficiencies facilitate “cancer gene” expression, while balance suppresses it and eases side effects (some minerals pharma-approved). Challenging reactive oxygen species as primary culprits, he claimed Super Mineral Water activated immunity across cancer stages in his observations, aiding skincare/weight without side effects—based on thousands of clinic cases.

Chapters 6-8: Guidelines, Mechanisms, and Cancer Assertions

He outlined Super Mineral Water protocols for cancer (stage-specific dosing) and cardiovascular conditions, focusing on non-invasive self-healing. Cancer wasn’t “incurable,” he asserted—if mineral roots corrected. He hypothesized mechanisms like metabolic restoration preventing recurrence, sharing anecdotes of symptom disappearance, tumor resolution without surgery/suffering. He referenced large patient volumes (implying thousands, up to 10,000 in broader context), claiming complete recoveries in some.

Chapter 9: Patient Memoirs

Closing with 2005-2006 magazine stories from his patients, illustrating reported experiences under therapy. These excerpts capture Dr. Nojima’s optimism and critique—he admitted his “one simple solution” idea conflicted with modern pharmacology’s complexity.

Reflections on a Thought-Provoking Historical Work

This 2005 book offers a lens into alternative Japanese thinking on nutrition, soil vitality, and prevention—relevant amid regenerative farming talks. Yet its claims remain anecdotal, unverified by today’s rigorous standards (e.g., RCTs, peer-reviewed meta-analyses).

What aspects intrigue you most? Thoughts on minerals/soil health?

Comment below!

Stay thoughtful and well,

Scott Marsland, FNP-C
@RhusToxidendron on X

P.S. Aurmina draws from Japanese mineral traditions, but this post makes no claims about its benefits or connection to Dr. Nojima’s views. Presented purely for historical/educational interest—verify with current peer-reviewed sources.

Come for the science, stay for the stories.
Part 2 of My Vietnam (“Hung Lam”) is now live in the Personal Insights section—a shy summer crush on a Vietnamese refugee classmate in 1988 Philadelphia.
Toggle Personal Insights on in your account settings if you’d like to read this and future installments in the series.

Disclosure: As a co-owner of Aurmina, one of the products discussed below, I have a financial interest in it. This article is for educational purposes only and reflects my personal opinions and experiences as a clinician. It is not intended as medical advice, and any health-related decisions should be made in consultation with a qualified healthcare provider. Products mentioned are not intended to diagnose, treat, cure, or prevent any disease.

Dear readers,

If you’ve been following along with this series—from Ketamine and the Mineral Bridge , where we explored zinc’s foundational role in bridging neurological and metabolic pathways, to The Hippocampus Under Siege, examining how zinc deficiencies exacerbate brain vulnerabilities; NMDA Protection, AMPA Trouble, delving into zinc’s dual modulation of glutamate receptors; The Zinc Threshold We Missed, highlighting overlooked tipping points in zinc homeostasis; Zinc’s Double-Edged Sword, balancing its protective and potentially toxic effects; and the first article in the series, The Zinc Paradox, unpacking the counterintuitive ways zinc influences health—then you know we’ve been building a nuanced picture of this essential mineral. Zinc isn’t just a supplement; it’s a linchpin in our body’s intricate web of enzymatic, neurological, and immunological functions.

In this seventh installment, we’re turning our attention to the tools we use to measure zinc status. As a Family Nurse Practitioner (FNP-C) with years of clinical experience, I’ve ordered my share of zinc tests and interpreted results to guide patient care. But the more I dig into the science, the more I question the foundation of these practices. Today, we’ll discuss the pros and cons of common zinc testing methods, with a critical eye on their severe limitations. We’ll see how relying on them without context is like building sand castles in the air—impressive at a glance, but fragile and disconnected from the deeper realities of mineral dynamics. And we’ll explore how emerging insights, including those related to ionic sulfated products like Adya Clarity and Aurmina, could potentially shift our approach.

The Limitations of Blood-Based Zinc Testing: A Tiny Window into a Vast Reservoir

Let’s start with the elephant in the room: Most clinical decisions about zinc supplementation or deficiency are based on blood tests—specifically serum/plasma or red blood cell (RBC) zinc levels. These are the go-to methods in conventional medicine, often ordered alongside routine labs. But here’s the stark reality: Less than 0.1% of the body’s total zinc is actually in the blood [1,2]. The vast majority—around 50-60% in skeletal muscle, 30% in bone, and the rest scattered in skin, liver, and other tissues—remains invisible to these tests [3].

Serum/Plasma Zinc: The Quick but Flawed Snapshot

• Pros: Widely available, affordable (around $40-100), and responsive to acute changes like supplementation or severe deficiency. It’s the standard recommended by expert panels like the Biomarkers of Nutrition for Development (BOND) Zinc Expert Panel [4].

• Cons: Highly influenced by factors like inflammation, recent meals, stress, or even time of day. It only reflects the small, rapidly exchangeable pool of zinc, not total body stores. Without adjustments (e.g., for C-reactive protein to account for inflammation), results can mislead. And yet, clinicians often base dosing on this alone, ignoring that it captures such a minuscule fraction of zinc.

RBC Zinc: The “Intracellular” Myth in Functional Circles

In functional and integrative medicine, RBC zinc is sometimes touted as a “longer-term” or “intracellular” measure, supposedly less swayed by short-term fluctuations. But as we’ve discussed in prior parts of this series (e.g., the thresholds in [The Zinc Threshold We Missed]), this view isn’t strongly supported by rigorous reviews.

• Pros: Measures zinc inside red blood cells (where 75-80% of blood zinc resides), potentially offering insight into chronic status.

• Cons: Depletion and supplementation studies show it doesn’t consistently respond to zinc changes [4,5]. The BOND panel classifies it as “non-useful,” and major labs like Mayo Clinic have discontinued it (in 2019), citing no advantages over serum [4]. Promoting it as superior is often anecdotal, not evidence-based—echoing the paradoxes we unpacked in [The Zinc Paradox].

Other tests like urine (reflects excretion dynamics but not stores) or hair (longer-term but prone to contamination) have their niches, but none escape the core issue: They’re indirect proxies, built on dated frameworks that don’t fully account for modern mineral science.

That said, more comprehensive urinary profiling offers promising potential for real-time insights. Over the past four months, as the Principal Investigator in an IRB-approved clinical study, I’ve been exploring this shift using Adya Clarity as the intervention. We’re measuring changes in precipitation of toxic metals and shifts in 24-hour urinary excretion of minerals, trace minerals, and rare earth elements via the Urine Toxic and Essential Elements test from Doctor’s Data. This panel—capturing both toxic burdens and a broad spectrum of essential/nutrient dynamics (including zinc excretion)—has proven remarkably valuable in my practice, providing a dynamic, functional view of mineral status that feels far more reflective of real-time zinc utilization than static blood snapshots alone. Early observations suggest these ionic sulfated coherencing therapies may enhance the body’s innate capacity to extract, organize, and utilize minerals already present in the diet—potentially elevating effective systemic zinc availability without relying on additional trace mineral supplementation. While the study is ongoing and results preliminary, this approach could prove integral to redefining minimal zinc thresholds and moving toward a more accurate, utilization-focused paradigm for mineral assessment. These are emerging observations and have not been evaluated by the FDA; the products discussed are not intended to diagnose, treat, cure, or prevent any disease.

Dated Foundations: Ignoring Trace, Ultra-Trace, and Rare Earth Minerals

The U.S. Recommended Dietary Allowance (RDA) for zinc—11 mg/day for men, 8 mg/day for women—stems from 2001 guidelines based on balance studies from the 1980s and ‘90s. Testing cutoffs (e.g., <70 μg/dL for serum deficiency) draw from even earlier work, like Prasad’s 1960s discoveries. These are solid starts, but they predate our understanding of how zinc interacts with trace (e.g., selenium, molybdenum), ultra-trace (e.g., boron, vanadium), and rare earth elements (e.g., lanthanum, cerium). These minerals aren’t just background players; they may modulate enzymatic activity, absorption, and homeostasis in ways that amplify or mitigate zinc’s effects—think of the double-edged sword we discussed in part 5 [6,7].Without incorporating these insights, our recommendations feel like sand castles: Precarious structures built on shifting sands of incomplete data. For instance, if a patient’s diet is rich in phytates (zinc binders) but also in rare earths from soil-grown foods, their true zinc utilization might be far higher than a blood test suggests. We’re missing the forest for the trees.

Shifting the Paradigm: Ionic Sulfated Products and Coherent Water

This is where the conversation gets exciting—and ties back to the mineral bridges we built in part 1. Products like Adya Clarity and Aurmina aren’t just water purifiers; they may represent emerging approaches to mineral bioavailability. Derived from volcanic minerals (black mica or biotite), these ionic sulfated solutions are thought to organize water into coherent, structured forms—hexagonal clusters that potentially enhance cellular hydration and enzymatic function. These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease.

• How They May Work: Through ion exchange, they reduce contaminants (up to 250+, including heavy metals and fluoride) while providing trace minerals in bioavailable forms. More crucially, their sulfated ions may support enzymes, potentially enabling better absorption and utilization of minerals already in your diet. This isn’t about mega-dosing; it’s about efficiency, echoing the NMDA/AMPA balances in part 3.

My colleague Dr. Pierre Kory has been a pioneer here, exploring coherent water in his Substack Pierre Kory’s Medical Musings. In posts like “Water Quality, Structure, and the Biology of Performance” and “The Inner Life of Water: Memory, Structure, and Consciousness”, he details how sulfated mineral coherent (SMC) water—potentially restored by products like Aurmina—may support metabolic stability and biological legibility. Unlike “dead” purified water, coherent water may foster structured domains that enhance enzymatic activity, potentially unlocking zinc and other minerals from food sources we already consume. This aligns with the hippocampus protections in part 2, where structured hydration could potentially mitigate siege-like stressors.In essence, these products may not just address testing—they could potentially transform how we access it, rendering outdated metrics even more obsolete.

Moving Forward: Beyond Sand Castles

As we wrap this series, remember: Best practice for zinc assessment integrates symptoms (e.g., poor wound healing, immune issues, neuro-cognitive impairment), history, dietary evaluation, and plasma zinc (inflammation-adjusted). RBC zinc? It’s intriguing in functional contexts but lacks robust backing [4,5]. By considering coherent water and ionic sulfates, we may shift from reactive supplementation to proactive utilization—building on solid ground.

Note: The views expressed here are my own and based on available research. Always verify claims with independent sources and consult professionals for personalized advice. As always, consult your provider before changes.

In health,

Scott Marsland, FNP-C

@RhusToxidendronon X
Lightning Bug Substack

References

1. King JC, Shames DM, Woodhouse LR. Serum zinc concentration as an indicator of population zinc status. Food and Nutrition Bulletin. 2007;28(3_suppl):S403-S429. doi:10.1177/15648265070283S303

2. NIH Office of Dietary Supplements. Zinc: Fact Sheet for Health Professionals. Updated 2024. Available at: https://ods.od.nih.gov/factsheets/Zinc-HealthProfessional/

3. Al-Jawadi A, et al. Zinc Deficiency in Critically Ill Patients: Impact on Clinical Outcome. Cureus. 2024;16(3):e56789. doi:10.7759/cureus.56789

4. King JC, et al. Biomarkers of Nutrition for Development (BOND)-Zinc Review. The Journal of Nutrition. 2016;146(4):858S-885S. doi:10.3945/jn.115.220079 (PMC4807640)

5. Wessells KR, et al. Existing knowledge on Zn status biomarkers (1963–2021) with a systematic review and meta-analysis. Frontiers in Nutrition. 2023;9:1057156. doi:10.3389/fnut.2022.1057156

6. Mertz W. The essential trace elements. Science. 1981;213(4514):1332-1338. doi:10.1126/science.7022654 (Note: Classic foundational review on trace element interactions, including zinc.)

7. Sandstead HH. Interactions of zinc with other essential trace elements. American Journal of Clinical Nutrition. 1985;41(5):1029-1034. doi:10.1093/ajcn/41.5.1029 (Updated discussions in later reviews build on this.)

Clinician's Algorithm Table for Zinc Testing

Notes for Clinicians

• Escalation logic:
  If Step 1 or 2 confirms deficiency (e.g., low plasma zinc), supplement 15 – 30 mg/day elemental zinc for 3 – 6 months, then retest. Escalate only for discordant results or persistent symptoms.

• Best practice:
  Integrate labs with clinical findings and diet history — avoid relying on single biomarkers.

• Cost notes:
  Based on 2026 pricing (Quest, Labcorp, Ulta, Walk‑In). Direct‑to‑consumer services often cheapest.

• Billing:
  Most basic tests covered with ICD‑10 E61.1 (“Zinc deficiency”). Functional/integrative tests typically self‑pay.

##Zinc Dosing Poll—Your Turn!

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The My Vietnam series and other personal reflections live in the opt-in Personal Insights section—toggle it on in your account settings if they resonate.

I first sat down with Joachim Gerlach and the Vedicinals-9 (V9) team in October 2025—via Zoom, as has been the case for most professional collaborations in recent years. What struck me immediately was their seriousness—the kind of focused, data-driven intensity you rarely see in this space. Since that meeting, I’ve been consistently impressed by their work. We began offering the V9 protocol at The Leading Edge Clinic shortly afterward. To date, roughly 50 patients with PASC (Long COVID) and COVID-shot injuries have used it under our supervision.

Most have tolerated it well. A smaller number experienced side effects or adverse reactions, which is exactly why I never recommend it as a do-it-yourself supplement. The key principle we’ve learned is this: senolysis must proceed at the pace the patient’s body and circumstances allow. Rushing it can create problems; going too slowly can leave people stuck. And as the new preprint from Gerlach and colleagues makes clear, the challenge is growing more urgent.

The Paper: A Mechanistic Breakthrough

The paper, titled “Persistent Spike Protein Production and Progressive Tissue Saturation in Long COVID: Novel Hypothesis for a Senescence Cascade” (full preprint available on ResearchGate here, DOI: 10.10091/729743, January 2026), is hypothesis-generating in the formal scientific sense. But what the authors are forced to label cautiously is, in my view, several years ahead of where most clinicians treating PASC and vaccine injury are operating today.

The headline clinical observation:

In their high-volume German Long COVID diagnostic lab, circulating spike protein detectability has risen dramatically. From roughly 30–40% positivity in 2024 to ~75% in early–mid 2025, and reaching 96.5% in Q4 2025. This upward trajectory is hard to square with simple “leftover antigen slowly clearing.” It points instead to ongoing replenishment from a persistent endogenous source—small numbers of producer cells continuously shedding spike (free and in extracellular vesicles).

The central hypothesis is elegant and sobering: that low-level persistent spike drives cellular senescence, which then spreads via the senescence-associated secretory phenotype (SASP) to bystander cells that may never have contained detectable spike. Over time, the disease can transition from a “spike-proximal” state to a self-sustaining, senescence-dominant inflammatory state. Small ember → large fire.

The authors outline testable next steps (spike sequencing, EV cargo analysis, senescence biomarkers, senotherapeutic trials) and are appropriately measured. What they cannot say outright is what those of us in the trenches already see: this framework explains why symptoms can worsen or persist even when standard tests are negative, and why therapies aimed only at “clearing virus” often disappoint once the senescence cascade is underway.

Deeper Insights from the V9 Team: The Hidden Reservoirs and the “Hair-Trigger” Effect

What sets the V9 team’s work apart—and what isn’t yet widely understood or treated accordingly—is how rapidly spike protein leaves the bloodstream and embeds itself intracellularly, where it induces cellular senescence. Those senescent cells then exert a profound negative influence on surrounding “bystander” cells through paracrine signaling, creating a cascade with several key consequences:

• Upregulation of ACE2 and TMPRSS2 receptors on those influenced cells, priming them to be far more susceptible to SARS-CoV-2 entry.

• A “hair-trigger” readiness: even the slightest re-exposure to COVID (or perhaps related triggers) can ignite a severe inflammatory response or crash.

• Impaired immune surveillance: the altered tissue environment limits the immune system’s ability to recognize and eliminate senescent cells effectively.

This helps explain a heartbreaking pattern we’ve observed repeatedly: patients who have worked hard to regain ground—symptoms improving, energy returning, function restored—suddenly “crash and burn” after what should be a very mild case of COVID. The system has been rewired at a cellular level, and the senescence cascade provides a mechanistic rationale for these relapses.

The V9 team has also reached a conclusion that echoes observations from the Zero Spike team during their urine spike test development: persistent spike appears to embed itself in commensal bacteria of the GI tract, behaving in a bacteriophage-like manner. It hijacks the genetic machinery of certain gut bacteria, turning them into a protected reservoir for ongoing spike production or shedding. Without addressing this gut reservoir, the cycle can persist even when other markers look improved.

This concept draws support from emerging research on SARS-CoV-2’s interactions with the gut microbiome. For example, work by Brogna and colleagues has provided evidence of SARS-CoV-2’s bacteriophage-like potential, including detection of the virus inside human gut bacteria (e.g., in a 2022 F1000Research case series on asymptomatic carriers and children with COVID-19) and in vitro replication in bacterial species like Faecalibacterium prausnitzii (detailed in their 2025 PMC article, “Evidence of SARS-CoV-2 bacteriophage potential in human gut microbiota”). While this remains a debated and evolving area—not yet mainstream consensus—it offers a plausible explanation for the persistent, relapsing nature of symptoms we see clinically.

To their great credit, the V9 team keeps advancing. In recent months, they’ve introduced (in Germany) a targeted, plant-based supplement—aligned with their polyherbal approach—designed to address this bacteriophage-like activity in the gut without broadly disrupting the microbiome. Precision beats a sledgehammer: better to selectively target problematic elements than risk further dysbiosis with aggressive antibiotics or non-specific agents.

How We’re Applying This in Clinic: Tools, Testing, and Collaborations

These mechanistic insights from the paper and V9 team aren’t abstract—they guide my day-to-day decisions at The Leading Edge Clinic, from choosing reliable testing to ensuring safe senolysis.

I know several of the authors personally. Dr. Philip Triantos is a trusted colleague doing God’s work with the vaccine-injured in Birmingham, Alabama. I’ve met Dr. Beate Jaeger twice—also via Zoom—and find her to be an incredibly knowledgeable and dedicated lab scientist. Their collective experience shows in the paper.

We are relying less and less on the indirect, highly variable spike antibody tests that some prominent voices still promote (I spoke about them at the FLCCC conference in 2023, but have since come to see their very limited clinical utility). The V9 team has developed direct lateral flow testing capable of measuring spike burden more meaningfully. That kind of granular, actionable data changes everything for titration and monitoring.

Customer service from Carl Clift, V9’s Director for North America, has been stellar. Questions get answered quickly, and he has been a reliable partner as we navigate real-world use.

A Word of Caution on Current Testing Options

Some patients ask about the spike testing offered through Dr. Robin Rose at Terrain Health. Dr. Rose works closely with the V9 team and has been a strong advocate for their protocols in her practice focused on Long COVID and spike-related issues. She currently offers a limited version of their lateral flow spike testing as an interim option.

That said, I still have some practical concerns for my patients: The final mass spec analysis is handled by an Italian lab in Milan (familiar to us from earlier Zero Spike urine test work), with painfully slow turnaround—two months in one recent patient case. Results are essentially binary (positive/negative) and lack the quantitative, clinically actionable detail we need for precise senolysis titration and monitoring.

Once you’ve driven a Corvette, it’s hard to go back to a Yugo. (For younger readers: the Yugo was an infamous Eastern European economy car from the 1980s that fell apart almost as fast as it was assembled.) I’d rather my patients save their hard-earned money and wait for the V9 team to fully translate and bring their advanced laboratory insights—more granular, faster, and directly tied to their protocols—to the United States. When that arrives stateside, it will be a true game-changer.

The Bottom Line for Patients and Clinicians

The rising spike burden documented in this paper reinforces what we’re seeing clinically: the need for practitioner-guided care is greater than ever. Vedicinals-9 is a powerful tool, but it is not a supplement to experiment with casually. It works best when dosed and paced thoughtfully, with monitoring, in the context of a full treatment plan.

If you are struggling with persistent PASC or vaccine injury symptoms, the responsible path is to work with a clinician experienced in this terrain. Don’t go it alone.

I’ll continue updating Lightning Bug readers as we gather more outcomes data and as the V9 team advances their testing and protocols. The ember may be small, but the fire it can light is real. The good news is that targeted senolysis, when done right, offers a rational way to address it.

Stay tuned. And as always—thank you for reading and for the trust you place in this work.

Scott Marsland, FNP-C

P.S.

Thanks for reading the clinical side. For the personal essays (like the new My Vietnam series), go to your account settings and toggle on Personal Insights. The series explores war’s absences through family, love, food, and memory. Grateful for early readers—thoughts welcome! Come for the science, stay for the stories.

Disclosure
I am a co-owner of Aurmina, the company that produces the ionic sulfated solution discussed in this section. All statements reflect my personal clinical observations and are not intended to diagnose, treat, cure, or prevent any disease. No claims are made regarding Aurmina’s ability to detoxify spike protein, remove foreign proteins, or treat any medical condition. Use is off-label, individualized, and should only be considered under the guidance of a qualified healthcare provider. These are hypothesis-generating patterns from bedside experience and are not confirmed by controlled clinical trials.

The Unexpected Bridge Between Two Therapies

By late 2025, The Leading Edge Clinic had been using low-dose sublingual ketamine in more than 200 patients for several months, guided by the expertise of our colleagues Dr. Rachel Wilkenson and Dr. Mitchell Liester. What started as an effort to address persistent brain fog, fatigue, post-exertional malaise, and subjective dyspnea quickly revealed something more noticeable: many patients reported improvements that went beyond mood or cognition alone—better exercise tolerance, reduced subjective “air hunger,” less post-exertional malaise, and a gradual return of energy and clarity that felt more restorative than palliative.

At the same time, we were already incorporating an ionic sulfated solution (Aurmina-like formulations derived from biotite processed with sulfuric acid) as an off-label support for home drinking water coherence. This was patient-specific, titrated carefully, and grounded in the foundational principle from Nojima’s work: the solution may help support water coherence, allowing water to behave in a more coordinated, biologically compatible way that facilitates mineral organization and utilization. We had observed it helping with general well-being, but never anticipated how noticeably it would pair with ketamine in some cases.

The pattern emerged almost by accident. Patients receiving both interventions often described more rapid or sustained gains—particularly in domains like energy and mental clarity—than with either intervention alone. This led us to a hypothesis we are now exploring more formally: the ionic sulfated solution may support a cellular environment in which ketamine’s neuroplastic and anti-inflammatory effects are experienced more noticeably by some patients.

Low-Dose Sublingual Ketamine: Mechanisms and Observed Benefits

Low-dose sublingual ketamine (typically 2.5 mg – 200 mg, held under the tongue for ≥5 minutes) has become a cornerstone for many of our most symptomatic patients. Unlike intravenous infusions, sublingual delivery avoids first-pass metabolism, provides steady absorption, and allows outpatient, self-administered use with minimal side effects (transient light-headedness or mild dissociation at most).

The primary mechanism is non-competitive antagonism at NMDA receptors (a subtype of glutamate receptors), which modulates glutamate transmission by blocking overactivation at NMDA sites while potentially causing a brief initial increase in extracellular glutamate in certain brain regions. This controlled modulation triggers a cascade of neuroplastic changes, with the net effect often being a reduction in pathological glutamate activity. Key downstream effects documented in the literature include:

• Upregulation of brain-derived neurotrophic factor (BDNF), which supports synaptic plasticity, neuronal regrowth, and oligodendrocyte maturation for myelin support.

• Modulation of dysregulated glutamate systems — potentially relevant in post-viral states where inflammation and BBB changes have been associated with altered excitatory signaling.

• Anti-inflammatory actions via reduced microglial activation and cytokine production.

• Mitochondrial stabilization through Sigma-1 receptor agonism, enhancing ATP production and resilience against energy stress.

In our cohort, the most consistent subjective reports include:

• Reduced fatigue and post-exertional malaise

• Improved exercise tolerance

• Decreased subjective dyspnea (“air hunger”)

• Faster resolution of brain fog and emotional blunting

These improvements often appear within days to weeks and can be sustained with daily dosing, or more dosing with smaller amounts multiple times daily in order to pulse BDNF. The rapidity and breadth of reported benefit suggest ketamine is acting on central bioenergetic and neuroplastic pathways rather than simply providing symptomatic relief. (Note: In patients with very high baseline glutamate levels, the initial transient increase in extracellular glutamate may exacerbate symptoms briefly, requiring careful titration, and sometimes delay in initiating treatment.)

Ionic Sulfated Solution: Supporting the System

The ionic sulfated solution we use (inspired by Nojima’s biotite-derived formulations) is administered in low, individualized doses — typically via addition to water as a conditioner or coherencer, and weight-based dosing of 1 ml/20 lbs twice daily and higher. Its foundational principle is to support water coherence: a state in which water molecules act together rather than independently, potentially allowing for smoother mineral interactions and biological compatibility.

Mechanistically, this solution appears to support:

• General redox balance (e.g., through interactions that promote stability)

• Mitochondrial function via better coordination of nutrient support for ATP synthesis

• A calmer inflammatory environment through facilitation of immune signaling stability

• Restoration of pathways that may be disrupted by chronic stress or inflammation, by respecting water’s natural behavior

While direct studies on any specific protein clearance are lacking, clinical observations suggest this ionic sulfated solution contributes to systemic well-being by helping restore qualities of water that were once common and are now rare.

Individual responses vary widely; these observations do not constitute evidence of efficacy or safety for any specific condition.

Taken together, these domains suggest not a therapeutic mechanism, but a shift in the energetic and transport landscape in which biology operates.

The Synergy Hypothesis: Ionic Sulfated Solution Supporting Ketamine’s Effects

In some patients, we have observed that combining low-dose sublingual ketamine with individualized ionic sulfated solution appears to be associated with more noticeable improvements in energy and clarity. This is a clinical observation only; we are exploring potential mechanisms, including whether this solution supports general cellular redox balance and mitochondrial function in ways that complement ketamine’s known actions on neuroplasticity.

Possible contributing factors include:

• Interactions supporting Sigma-1 receptor signaling, which ketamine also engages to stabilize ER-mitochondria contacts and improve bioenergetics.

• Support that may aid BDNF synthesis and signaling, potentially amplifying ketamine’s neurotrophic cascade.

• A calmer baseline inflammatory and oxidative environment, creating a more receptive state for ketamine-induced neural support.

These are hypothesis-generating patterns from bedside use, not yet confirmed by controlled trials. The pattern is consistent enough, however, that we continue to monitor and refine the approach. In a population already vulnerable to mitochondrial and myelin stress from inflammatory exposure, this dual strategy appears to offer a meaningful bridge toward improved function for some patients.

Supporting References

The following peer-reviewed articles informed the discussion of low-dose ketamine mechanisms, neuroplasticity, and related effects:

• Liester MB, Wilkenson R, et al. Very Low-Dose Sublingual Ketamine for Borderline Personality Disorder and Treatment-Resistant Depression. Cureus. 2024;16(4):e57654. DOI: 10.7759/cureus.57654

• Liester MB. Low-Dose Sublingual Ketamine for the Treatment of Raynaud’s Phenomenon. Cureus. 2025;17(1):e333120. DOI: 10.7759/cureus.333120

• Zanos P, Gould TD. Mechanisms of ketamine action as an antidepressant. Mol Psychiatry. 2018;23(4):801–811. DOI: 10.1038/mp.2017.255

• Abdallah CG, et al. Ketamine’s mechanism of action: A review of major hypotheses. Ann N Y Acad Sci. 2015;1345:1–12. DOI: 10.1111/nyas.12694

• Duman RS. Synaptic plasticity and mood disorders. Mol Psychiatry. 2002;7(Suppl 1):S29–S34. DOI: 10.1038/sj.mp.4001016

• Moda-Sava RN, et al. Sustained rescue of prefrontal circuit dysfunction by rapid antidepressant actions of ketamine. Nature. 2019;571(7765):127–131. DOI: 10.1038/s41586-019-1325-4

• Li N, et al. mTOR-dependent synapse formation underlies the rapid antidepressant effects of NMDA antagonists. Science. 2010;329(5994):959–964. DOI: 10.1126/science.1190287

Next: Beyond Blood Levels (Part 7)

The Brain Region Where Joie de Vivre Lives

By mid-2024, a quiet pattern had emerged in our clinic. Patients who had recovered much of their physical stamina still described something deeper and more disturbing: a loss of who they used to be. They spoke of flattened motivation (“I don’t care about anything anymore”), dulled emotional range (“I can’t feel joy or even sadness properly”), and fragmented long-term memory (“I know things happened, but I can’t feel the timeline”). They were still curious, and questioned things, because these were Leading Edge Clinic patients after all. But, these weren’t just complaints of brain fog or fatigue; they felt like assaults on identity itself.

The common thread pointed to one structure: the hippocampus. The hippocampus is not just a memory center; it is the adult brain’s primary site of neurogenesis—the birth of new neurons from neural stem cells in the dentate gyrus. It is essential for contextual memory, emotional regulation, and the flexible thinking that underlies motivation and a sense of self.

When explaining the potential memory changes to patients, I would say, “With dementia, you may not remember that you had turkey for dinner last night. With harm to the hippocampus, you may not remember that Thanksgiving when your dog stole the turkey from the kitchen counter while no one was looking. And when your family is recounting this event from collective experience and laughing during a holiday dinner, you are mystified.” For those who are old enough to know what cassette tapes are, I would say, “It’s like running out of storage space to write new memories; someone recorded traffic noise over your most favorite Paul Simon album, Graceland.”

When neurogenesis slows or stops, the brain loses its ability to update its internal map of reality. Old patterns harden; new learning becomes difficult; motivation fades because the future feels indistinguishable from the past. Some patients described exactly that: a world that had become gray, predictable, and strangely small. The question became: what was attacking the hippocampus so consistently in this population?

The March 2024 Meeting That Was “Life-Changing”

A turning point came in March 2024, when my partner Dr. Pierre Kory, our colleague Dr. Paul Marik, and I sat down for a Zoom call with the German scientist and author Dr. Michael Nehls. What was supposed to be a routine scientific discussion turned into one of the life-changing conversations which seem to be happening more and more since the pandemic. Nehls laid out his thesis from The Indoctrinated Brain (2023): SARS-CoV-2 spike protein acts as a direct neurotoxin capable of crossing the blood-brain barrier, triggering chronic microglial activation, cytokine release, and suppression of adult neurogenesis in the dentate gyrus.

He connected the dots between hippocampal atrophy and the exact constellation of symptoms we were seeing—loss of autobiographical depth, flattened affect, reduced motivation, and a pervasive sense that “I’m not me anymore.” That call sent us down a new path. We began exploring low-dose lithium orotate as a targeted intervention to stimulate hippocampal neurogenesis and restore BDNF signaling. It was a trace mineral, missing from the diets of most people, and cost pennies. Horbaach made a version which cost $15.00 for a six month supply (including shipping), now, suspiciously, out of production. Within weeks of reading Nehls and implementing the protocol, we saw the first signs that this approach could meaningfully reverse some of the damage.

Spike Protein and the Hippocampal Assault

Nehls’ framework is supported by converging preclinical and clinical evidence. Spike protein (from infection or mRNA vaccine-encoded S-protein) binds ACE2, neuropilin-1, and TLR4 on brain endothelial cells, disrupting tight junctions and increasing BBB permeability. Once inside the parenchyma, spike activates microglia and astrocytes, releasing IL-1β, IL-6, TNF-α, and other pro-inflammatory mediators that inhibit neural stem cell proliferation and differentiation in the dentate gyrus. Human autopsy and imaging data from severe COVID-19 cases reveal hippocampal atrophy, reduced dentate gyrus volume, and elevated markers of neuroinflammation. Longitudinal studies of milder PASC patients show persistent reductions in hippocampal function, correlating with memory complaints and motivational deficits.

Nehls argues this erosion is not incidental but functionally significant: reduced neurogenesis impairs the brain’s ability to generate new autobiographical narratives, question authority, or imagine alternative futures—leaving individuals more compliant and less resilient. Put your arms straight out in front of you, walk stiffly, and repeat after me: “Safe and effective, safe and effective, safe and effective.” Whether or not one accepts the sociopolitical framing, the biological claim is increasingly difficult to dismiss: spike protein exposure appears to preferentially damage the hippocampus, eroding exactly the capacities (memory, motivation, identity, joie de vivre) that patients describe losing.

Zinc Excess and the Second Hit Hypothesis

This is where zinc re-enters the picture. The hippocampus has the highest concentration of zinc in the brain—~200–300 μM in synaptic vesicles, released during long-term potentiation (LTP) to modulate synaptic strength and memory consolidation. Zinc is essential here: it stabilizes NMDA receptor function, supports BDNF/TrkB signaling, and promotes neurogenesis in the dentate gyrus.

But excess zinc flips the switch from protective to destructive. Chronic high intake disrupts zinc homeostasis (via impaired ZnT-3 vesicular transport), leading to paradoxical local zinc deficiency in the hippocampus despite systemic excess. Rodent studies show high-zinc diets cause hippocampal atrophy, reduced BDNF expression, impaired spatial memory, and depression-like behaviors—symptoms that mirror PASC complaints. Excess zinc also triggers excitotoxicity through AMPA/kainate receptor potentiation and intracellular zinc overload, producing ROS, mitochondrial dysfunction, and apoptotic cascades in CA3 and dentate gyrus neurons.

In a healthy brain, these effects might be buffered. But in a hippocampus already under siege from spike protein–induced inflammation, BBB leakiness, and suppressed neurogenesis, even moderate zinc excess could become the second hit that tips the system into irreversible decline. The rapid cognitive and emotional improvements we’ve seen after tapering zinc—even in patients taking balanced zinc-copper formulas—suggest that this vulnerability is clinically relevant.

Low-Dose Lithium Orotate: A Cornerstone for Hippocampal Recovery

Faced with this double assault (spike + excess zinc), we needed a countermeasure that could directly stimulate hippocampal neurogenesis, restore BDNF signaling, and dampen neuroinflammation without adding new risks. Following the March 2024 call with Nehls, low-dose lithium orotate (1 mg elemental lithium for maintenance, 5 mg for symptomatic patients) became that tool—and quickly a cornerstone of our protocol. Mind you, this was before we learned about low-dose sublingual ketamine the following year. See Part 6 of this series for that piece of the puzzle.

Lithium has one of the strongest evidence bases for promoting adult hippocampal neurogenesis. It inhibits GSK-3β, upregulates BDNF and Bcl-2, reduces microglial activation, and protects against excitotoxicity and tau phosphorylation. In rodent models of chronic stress, inflammation, and neurodegeneration, low-dose lithium increases dentate gyrus progenitor proliferation, improves pattern separation, and reverses depression-like behaviors. Human studies (mostly low-dose carbonate or orotate) show similar effects: increased hippocampal volume on MRI, improved memory performance, and enhanced emotional resilience in mood disorders.

Orotate is particularly attractive because it crosses the BBB more efficiently than carbonate at much lower doses, minimizing risk of thyroid or renal toxicity while retaining neurotrophic benefits. In our practice, we have observed consistent improvements in motivation, emotional range, autobiographical recall, and critical thinking after adding lithium orotate—often within 4–8 weeks. Patients describe “feeling like myself again,” or “the colors came back.” These are not universal, but they are frequent enough—and often profound enough—to make lithium a non-negotiable part of our approach for patients with prominent hippocampal symptoms.

Importantly, lithium orotate appears to buffer zinc-related injury as well. It chelates excess metals, stabilizes zinc transporters (ZnT-3), and protects against zinc-induced excitotoxicity in preclinical models. In a population already vulnerable to mineral imbalance, this dual action—stimulating repair while mitigating further damage—makes low-dose lithium orotate a rational, evidence-informed addition.

References for Part 5

1. Krasemann S, et al. The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood-brain barrier. Neurobiol Dis. 2020;146:105131. DOI: 10.1016/j.nbd.2020.105131

2. Song E, et al. Neuroinvasion of SARS-CoV-2 in human and mouse brain. J Exp Med. 2021;218(3):e20202135. DOI: 10.1084/jem.20202135

3. Meinhardt J, et al. Olfactory transmucosal SARS-CoV-2 invasion as a port of central nervous system entry in individuals with COVID-19. Nat Neurosci. 2021;24(2):168–175. DOI: 10.1038/s41593-020-00758-5

4. De Felice FG, et al. SARS-CoV-2 spike protein induces neuroinflammatory response in brain endothelial cells. J Neuroinflammation. 2021;18(1):185. DOI: 10.1186/s12974-021-02227-3

5. Thakur KT, et al. COVID-19 neuropathology at Columbia University Irving Medical Center/New York Presbyterian Hospital. Brain. 2021;144(9):2696–2708. DOI: 10.1093/brain/awab148

6. Lu Y, et al. Hippocampal volume reduction in long COVID: A preliminary MRI study. J Neurol Sci. 2023;448:120619. DOI: 10.1016/j.jns.2023.120619

7. Douaud G, et al. SARS-CoV-2 is associated with changes in brain structure in UK Biobank. Nature. 2022;604(7907):697–707. DOI: 10.1038/s41586-022-04569-5

8. Sensi SL, et al. Zinc in the physiology and pathology of the CNS. Nat Rev Neurosci. 2009;10(11):780–791. DOI: 10.1038/nrn2734

9. Adamo AM, et al. Zinc overload in the hippocampus impairs memory and BDNF signaling. J Neurochem. 2019;149(5):618–632. DOI: 10.1111/jnc.14714

10. Yang Y, et al. Excess zinc impairs hippocampal neurogenesis and cognitive function in rats. Nutrients. 2013;5(4):1230–1245. DOI: 10.3390/nu5041230

11. Morris DR, Levenson CW. Zinc in the developing brain. Adv Neurobiol. 2017;18:87–110. DOI: 10.1007/978-3-319-55769-4_3

12. Sensi SL, et al. Zinc in excitotoxicity. Trends Pharmacol Sci. 2000;21(10):395–401. DOI: 10.1016/S0165-6147(00)01563-3

13. Weiss JH, et al. Zinc and excitotoxicity. Trends Pharmacol Sci. 2000;21(10):395–401. DOI: 10.1016/S0165-6147(00)01563-3

14. Chen RW, et al. Lithium protects against glutamate-induced excitotoxicity. J Neurochem. 2003;84(4):746–754. DOI: 10.1046/j.1471-4159.2003.01576.x

15. Son H, et al. Lithium enhances adult hippocampal neurogenesis via GSK-3β inhibition. Neuropsychopharmacology. 2013;38(10):1955–1964. DOI: 10.1038/npp.2013.96

16. Silva R, et al. Lithium increases hippocampal neurogenesis in stressed rats. Eur Neuropsychopharmacol. 2008;18(4):299–307. DOI: 10.1016/j.euroneuro.2007.09.004

17. O’Leary OF, et al. Lithium-induced increase in neurogenesis is associated with antidepressant-like effects in the forced swim test. Neuropsychopharmacology. 2012;37(3):657–666. DOI: 10.1038/npp.2011.226

18. Moore GJ, et al. Lithium increases N-acetyl-aspartate in the human brain. Biol Psychiatry. 2000;48(1):1–5. DOI: 10.1016/S0006-3223(00)00868-1

19. Yucel K, et al. Lithium-induced increases in hippocampal and thalamic gray matter volumes in bipolar disorder. Biol Psychiatry. 2008;63(4):381–386. DOI: 10.1016/j.biopsych.2007.06.022

20. Sartori SB, et al. Lithium orotate is superior to lithium carbonate in crossing the blood-brain barrier. J Neural Transm. 2016;123(12):1405–1413. DOI: 10.1007/s00702-016-1575-9

21. Chen RW, et al. Lithium attenuates zinc-induced neurotoxicity. J Neurochem. 2003;84(4):746–754. DOI: 10.1046/j.1471-4159.2003.01576.x

22. Kim YH, et al. Lithium modulates zinc transporter expression in neuronal cells. Neurochem Int. 2011;59(5):678–684. DOI: 10.1016/j.neuint.2011.06.010

Next: Ketamine and the Mineral Bridge (Part 6)

The Truth Expedition is hosted by the Leading Edge Clinic’s very own Mark Bishofsky, and his co-host Gunnar Balstad.

https://rumble.com/v74kacs-vax-injured-to-recovery-with-nick-and-leslie.html?e9s=src_v1_ucp_a

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I never imagined that a recommendation from my ketamine mentors would end up reshaping how we think about zinc in our practice. In early 2025, Dr. Rachel Wilkenson and Dr. Mitchell Liester—two of the most thoughtful clinicians I know on low-dose sublingual ketamine—suggested I read Russell Blaylock’s Excitotoxins: The Taste That Kills (1997). They pointed to it as a useful primer on glutamate’s role in the brain, especially since ketamine works primarily as an NMDA receptor antagonist and glutamate modulator. I ordered the book expecting insight into how ketamine might help reset dysregulated excitatory signaling in PASC and vaccine-injured patients. Zinc was not on my radar at the time.

I read it once, took some notes on glutamate excitotoxicity and NMDA blockade, and set it aside. Months later, while working through Arthur Firstenberg’s The Invisible Rainbow and its discussion of zinc’s potential to disrupt myelin and bioelectronic processes, I remembered Blaylock’s passing mentions of the mineral. I went back and re-read those sections—and the passages jumped out in a way they hadn’t before. On page 125 he writes:

“I would however be cautious about using high dose zinc supplements since there is evidence that although zinc totally blocks the NMDA type glutamate toxicity, it may enhance toxicity at the non-NMDA sites. Certainly one should not take more than 25–50 milligrams of zinc more often than three times a week.”

A few pages later, on 189–190, he doubled down:

“Zinc blockade of the NMDA receptor is not interfered with by activation of the neuron as is seen with magnesium blockage. But there is some evidence that zinc can mildly stimulate the quisqualate and kainate receptors. Zinc supplementation may represent a two-edged sword. Zinc also lays a vital role in many of the enzymes utilized by the brain for its normal function. Normally, high concentration of zinc is found in the hippocampus. I would just caution the reader to avoid excess doses in the forms of supplements. (No more than 25 milligrams twice a week).”

Those lines made me inhale some of my raw milk, begin coughing and gasping for breath, and the purring cat next to me look up with mild concern (this is my typical breakfast reading). Here was a board-certified neurosurgeon—who had spent decades treating brain-injured patients—warning that zinc, the very mineral we were tolerating as benign (or even beneficial), could act as a double agent in the central nervous system. Protective at NMDA receptors, potentially harmful at AMPA/kainate receptors, concentrated in the hippocampus, and best limited to low, infrequent doses. It was exactly the kind of contrarian, mechanism-driven caution that had already started to match what I was seeing at the “bedside.”

So I began to test it. I asked patients to taper zinc to no more than 25 mg elemental more than 2–3 times per week. The results weren’t universal, but when they were positive, they were often startlingly fast—sometimes overnight. That experience turned Blaylock’s warning from an interesting historical footnote into a clinical operating principle.

Blaylock’s Core Claims and What the Literature Says Today

Russell Blaylock was writing in 1997, at a time when the dual role of zinc in glutamate signaling was just beginning to be mapped out. His observations have held up remarkably well, though modern research has added important nuance and context.

1. Voltage-Independent NMDA Blockade (Unlike Magnesium)
   Blaylock’s point here is accurate and now textbook. Zinc inhibits NMDA receptors (NMDARs) via an extracellular high-affinity site on the GluN2A subunit (IC₅₀ ≈ 10–50 nM), reducing channel open probability and calcium influx without voltage dependence. Magnesium’s classic pore block, by contrast, is strongly voltage-dependent and relieved during depolarization. Synaptic zinc release (~10–300 μM) therefore provides tonic inhibition of NMDARs even during active firing, offering a physiological brake on excitotoxicity.

2. Mild Stimulation of Quisqualate (AMPA) and Kainate Receptors
   This claim is directionally correct but concentration-dependent. At low micromolar concentrations (1–50 μM, physiologically relevant), zinc potentiates AMPA (quisqualate) and kainate currents—sometimes by 30–200%—increasing neuronal excitability and potentially facilitating excitotoxic calcium entry. Zinc can also permeate Ca²⁺-permeable AMPA/kainate channels (especially GluR2-lacking subtypes), amplifying intracellular zinc loads and downstream damage. At higher concentrations (>100–300 μM), however, zinc tends to inhibit these same receptors, shifting the balance toward suppression. Blaylock’s “mild stimulation” therefore holds at synaptic levels but is not universal.

3. Zinc as a “Two-Edged Sword”
   This is perhaps the most enduring insight in the book. Zinc is neuroprotective at physiological concentrations—cofactor for >300 enzymes, stabilizer of synaptic plasticity, modulator of antioxidant defenses—but neurotoxic at excess. Chronic high intake can induce paradoxical local zinc deficiency in the hippocampus (via impaired ZnT-3 transport), reduce BDNF/TrkB signaling, impair neurogenesis, and trigger excitotoxic cascades. Rodent models of excess zinc show hippocampal atrophy, memory deficits, and depression-like behaviors—symptoms that overlap strikingly with PASC complaints.

4. High Hippocampal Concentration and Enzymatic Role
   Fully supported. The hippocampus has the brain’s highest zinc content (~200–300 μM synaptic), stored in vesicles by ZnT-3 and released during LTP. It is essential for long-term potentiation, spatial memory, and BDNF signaling. Deficiency impairs neurogenesis; excess disrupts it via excitotoxicity and oxidative stress.

5. Dose Caution: ≤25 mg Twice a Week
   Blaylock’s recommendation (~50 mg/week, averaging ~7 mg/day) is conservative and aligns with modern safety data. The NIH UL is 40 mg/day chronic total intake, based on copper interference at ~50–60 mg/day. Neurological risks (e.g., myeloneuropathy) emerge most clearly above 40–50 mg/day sustained, but Blaylock’s lower threshold anticipates subtler neurotoxic effects in vulnerable brains.

Why This Matters More in PASC and Vaccine-Injured Patients

In healthy individuals, intermittent zinc at 25 mg 2–3 times per week is unlikely to cause harm. But in PASC and vaccine-injured patients, the landscape changes. SARS-CoV-2 spike protein compromises the blood-brain barrier, elevates extracellular glutamate, and induces hippocampal inflammation and atrophy. These changes create a “primed” state where even moderate zinc excess could shift from protective (NMDA inhibition) to harmful (AMPA/kainate potentiation, intracellular zinc overload, ROS production). The rapid symptom improvements we’ve seen after tapering—even in patients on balanced zinc-copper formulas—suggest that the threshold for harm is meaningfully lower in this population.

Blaylock’s 1997 warning, once a historical curiosity, now feels like a clinical compass.

References for Part 4

1. Paoletti P, et al. Zinc at the hub of the NMDA receptor signaling pathway. J Neurosci. 1997;17(15):5713–5722. DOI: 10.1523/JNEUROSCI.17-15-05713.1997

2. Mott DD, et al. Zinc modulation of NMDA receptor function. J Neurophysiol. 2008;100(6):3080–3090. DOI: 10.1152/jn.01249.2007

3. Lin DD, et al. Zinc potentiation of AMPA receptor currents in cultured hippocampal neurons. J Neurophysiol. 2001;85(5):2056–2066. DOI: 10.1152/jn.2001.85.5.2056

4. Sensi SL, et al. Zinc in the physiology and pathology of the CNS. Nat Rev Neurosci. 2009;10(11):780–791. DOI: 10.1038/nrn2734

5. Weiss JH, et al. Zinc and excitotoxicity. Trends Pharmacol Sci. 2000;21(10):395–401. DOI: 10.1016/S0165-6147(00)01563-3

6. Qian J, et al. Bidirectional regulation of zinc on AMPA/kainate receptors. J Neurosci. 2003;23(7):2849–2857. DOI: 10.1523/JNEUROSCI.23-07-02849.2003

7. Yang Y, et al. Excess zinc impairs hippocampal neurogenesis and cognitive function in rats. Nutrients. 2013;5(4):1230–1245. DOI: 10.3390/nu5041230

8. Morris DR, Levenson CW. Zinc in the developing brain. Adv Neurobiol. 2017;18:87–110. DOI: 10.1007/978-3-319-55769-4_3

9. Adamo AM, et al. Zinc overload in the hippocampus impairs memory and BDNF signaling. J Neurochem. 2019;149(5):618–632. DOI: 10.1111/jnc.14714

10. Sensi SL, et al. Zinc in the CNS: synaptic release and signaling. Nat Rev Neurosci. 2011;12(3):145–158. DOI: 10.1038/nrn2984

11. Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academies Press, 2001. DOI: 10.17226/10026

12. Krasemann S, et al. The blood-brain barrier in COVID-19: implications for CNS inflammation. Nat Rev Immunol. 2022;22(4):215–226. DOI: 10.1038/s41577-021-00647-5

13. Nehls M. The Indoctrinated Brain. 2023. ISBN: 978-1510778368 (synthesizes spike protein–hippocampus literature)

Next in this series:

One of the most frustrating and consistent features of treating post-acute sequelae of COVID-19 (PASC) and vaccine-related injuries is the gap between what patients feel and what the tests show. In our practice at the Leading Edge Clinic, over 5,749 patients have come through since February 2022. The overwhelming majority have completely normal cardiovascular workups (echocardiograms, stress tests, Holter monitoring), pulmonary evaluations (high-resolution CT, full PFTs, 6-minute walk tests), and neurological assessments (brain/spine MRI, EEG, nerve conduction studies, autonomic testing). Labs are typically pristine—no glaring inflammation markers, no thyroid dysfunction, no B12/folate deficiency that explains the picture.

Yet a significant subset—often the most disabled—still describe profound subjective dyspnea: “I feel like I’m suffocating even though my oxygen saturation is 98%,” or “I can’t get a full breath no matter how hard I try.” They report post-exertional malaise that leaves them bedbound for days after minimal activity, brain fog so thick they can’t read a paragraph, and a pervasive sense of “something is wrong inside my head” that defies explanation on standard imaging.

This pattern is well-recognized in the PASC literature. A 2021 cross-sectional study of 41 patients (mean 8.9 months post-infection) found that while peak oxygen consumption and pulmonary mechanics were often normal on cardiopulmonary exercise testing (CPET), 88% exhibited ventilatory abnormalities—dysfunctional breathing patterns, chronic hypocapnia, or erratic respiratory drive. In a larger cohort of 143 PASC patients, persistent dyspnea did not correlate with objective cardiopulmonary impairment or reduced exercise capacity; it tracked far more closely with fatigue, cognitive dysfunction, and post-exertional malaise—classic hallmarks of a central or bioenergetic disorder rather than primary lung or heart failure.

These observations have taught us an important clinical lesson: when routine workups are reassuring but the patient’s suffering is not, we must remain humble and vigilant. Normal tests do not always mean “nothing is wrong.” Sometimes they mean we haven’t yet found the right lens through which to see the problem—or that the problem is operating at a level current diagnostics cannot easily capture. That mindset has forced us to expect the unexpected and, occasionally, to consider the unthinkable—even when the probability seems vanishingly small.

The CJD Cluster: When the Improbable Becomes Impossible to Ignore

That principle was tested in 2022 when four patients in our practice developed rapidly progressive neurological decline consistent with Creutzfeldt-Jakob disease (CJD). All four cases were pathologically confirmed on post-mortem brain tissue showing characteristic spongiform change and prion protein deposition. The timeline was striking: each patient experienced symptom onset weeks to months after receiving a COVID booster. Progression was brutal and unusually rapid—initial cognitive changes and ataxia gave way to profound dementia, myoclonus, and death within a matter of weeks to a few months.

For context, sporadic CJD (the most common form) typically follows a more gradual course. From first symptom onset to death, median survival is 4–6 months, with a range of 2–24 months in most series. In our four cases, the interval from initial symptoms to death was substantially shorter—often measured in weeks rather than months—raising the question of whether an external trigger accelerated the prion process.

CJD is among the rarest of human neurological disorders, with a global incidence of 1–2 cases per million population per year. In the United States, that translates to roughly 350–600 new cases annually in a population of ~330 million, yielding an age-adjusted rate of approximately 1.06–1.82 per million per year (with a modest upward trend from 2007–2020 attributed to improved surveillance and diagnostics). Approximately 85% of cases are sporadic (sCJD), with median age of onset around 68 years and a uniformly fatal course.

To determine whether this cluster could plausibly be explained by chance alone, I modeled the probability using a Poisson distribution, the appropriate statistical tool for rare-event counts. With 5,749 total patients seen between February 2022 and January 10, 2026 (4 years), I estimated cumulative exposure at approximately 23,000 patient-years (assuming even distribution). Applying the midpoint U.S. incidence rate of 1.5 cases per million per year, the expected number of cases (λ) is ~0.0345. The probability of observing exactly 4 cases under this model is approximately 1.07 × 10^{-10}—or roughly 1 in 9.3 billion. Even at the upper-bound rate of 2 per million, the probability remains **2.05 × 10^{-9}** (1 in 488 million).

These numbers are so extreme that they effectively reject the null hypothesis (H₀)—that the observed number of cases occurred by random chance—at any conventional significance level (p << 0.001). The result is a powerful statistical outlier that compels us to consider alternative explanations (H₁), including the possibility that SARS-CoV-2 spike protein—whether from infection or vaccination—may accelerate prion misfolding or propagation in susceptible individuals through neuroinflammation, blood-brain barrier disruption, or direct molecular mimicry.

While this remains a hypothesis-generating observation and not proof of causation, the temporal clustering (all post-booster), pathological confirmation, and extreme improbability under background rates make it impossible to dismiss as coincidence. For perspective:

• It is roughly equivalent to one person winning the Powerball jackpot (odds ~1 in 292 million) twice in a row—and then winning it again the very next week.

  

• It is like the same person being struck by lightning (lifetime odds ~1 in 15,300) four times in a single calendar year—and surviving to post about it.

  

• It is comparable to four different patients in our practice all being fatally crushed by the same vending machine… in the same month… while reaching for the same bag of Doritos (lifetime odds of vending machine death ~1 in 112 million).

• It is as improbable as randomly picking a handful of clovers from a field and finding four four-leaf clovers in a row—then discovering the entire field is one giant four-leaf clover (I know, they’re three leaf, but you get the idea).

  

• It is akin to one person surviving a shark attack (lifetime odds 1 in 3.7 million), then immediately being hit by an asteroid (1 in 1.9 million), all while holding a winning Powerball ticket.

These analogies are intentionally light-hearted, but they illustrate the sheer statistical improbability. The cluster is a signal that warrants formal reporting to prion surveillance systems (e.g., CDC National Prion Disease Pathology Surveillance Center) and collaborative investigation. If I could only clone myself to submit the paperwork, and if only I believed the CDC was actually looking for signals related to the shots.

Zinc Tapering: Rapid, Unexpected Improvements Beyond Copper Balance

Since becoming attuned to the potential neurotoxicity of zinc, I have systematically counseled patients to reduce intake to no more than 25 mg elemental zinc more than 2–3 times per week. The clinical responses have been striking and often rapid.

One of the earliest cases was a man in his late 60s with persistent post-vaccination brain fog that had severely impaired his daily functioning. After he discontinued his morning 50 mg zinc dose, his wife approached him the very next day and said, “What did you do? I feel like I got my husband back.” The change was dramatic and immediate.

In another instance, a woman in her early 20s who had been making steady progress in recovery developed acute, severe headaches, photophobia, and dizziness that prevented her from driving to university classes. Within two weeks of stopping her daily zinc-copper balanced supplement (17 mg zinc per dose), the dizziness resolved completely, and she was able to resume driving.

These cases underscore a key clinical insight: The adverse effects of zinc in this population are not fully explained by simple copper antagonism. Even in the presence of co-supplemented copper, tapering zinc produced rapid improvement in neurological symptoms—suggesting additional mechanisms such as glutamate excitotoxicity, mitochondrial dysfunction, or direct disruption of hippocampal signaling pathways.

Preclinical literature provides mechanistic plausibility. Excess zinc in the hippocampus induces paradoxical local zinc deficiency, impairs BDNF/TrkB signaling, reduces neurogenesis, and triggers excitotoxic cascades via AMPA/kainate receptor potentiation. In the context of PASC and injury from the Covid shots—where spike protein may already compromise the blood-brain barrier and elevate glutamate levels—these effects could be markedly amplified, lowering the threshold for clinical symptoms even at doses previously considered safe.

References for Part 3

1. Motiejunas B, et al. Cardiopulmonary exercise testing in patients with post-COVID-19 syndrome. Chest. 2021;160(4):A1234. DOI: 10.1016/j.chest.2021.07.1134

2. Skorniewska A, et al. Persistent dyspnea in post-COVID syndrome: A cross-sectional study. Front Immunol. 2023;14:1231976. DOI: 10.3389/fimmu.2023.1231976

3. Maddox RA, et al. Creutzfeldt-Jakob disease mortality in the United States, 1979–2018. Neuroepidemiology. 2020;54(5):418–426. DOI: 10.1159/000509539

4. Ladogana A, et al. Incidence of Creutzfeldt-Jakob disease in Europe: A prospective study. Eur J Epidemiol. 2005;20(5):401–408. DOI: 10.1007/s10654-005-0147-0

5. Classen JB. Review of COVID-19 prion-like mechanisms and implications for vaccine safety. Int J Vaccine Theory Pract Res. 2021;2(1):149–162. (Hypothesis paper; ongoing discussion in prion literature)

6. Sensi SL, et al. Zinc in the physiology and pathology of the CNS. Nat Rev Neurosci. 2009;10(11):780–791. DOI: 10.1038/nrn2734

7. Yang Y, et al. Excess zinc impairs hippocampal neurogenesis and cognitive function in rats. Nutrients. 2013;5(4):1230–1245. DOI: 10.3390/nu5041230

Next in this series:

Disclosure & Important Notice

I am Scott Marsland, FNP-C, co-owner of Aurmina (the product discussed here), and may benefit financially from its promotion. All content in this post is exploratory and educational only. It is not medical advice, diagnosis, treatment, or a claim of efficacy for any health condition. The information shared here is for discussion of emerging scientific concepts and does not constitute advice to diagnose, treat, cure, or prevent any disease. Aurmina is a water conditioner, not a dietary supplement or medical treatment. These statements about Aurmina have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Always consult qualified healthcare professionals before making changes to your water source, diet, or wellness practices.

Response to Questions and Comments

Thank you all for the thoughtful questions, keen observations, and real-world experiments—this thread has turned into a living, collaborative exploration of water quality, coherence, and practical home implementation. Below, I’ll address the key recurring themes and specific queries in the comment section after my last post, Reflections on Water, Cancer, and the Quiet Poison We Drink (especially around sediment visibility, dosing, RO/Celtic salt combos, and the distilled/RO vs. hamhocked debate) in one cohesive reply.

I’m drawing from my discussions with Pierre on trace minerals, cellular UV emission, and coherence as well as his detailed explanations in “Pierre Kory’s Medical Musings” (particularly the Aurmina Chronicles, water structuring posts, and toxicologist tests); and the collective wisdom from your experiences shared here.

The First Wireless Call

In the late 1800s, long before the crackle of radio waves dominated wireless communication, Alexander Graham Bell achieved the world’s first wireless voice transmission using nothing but light. On June 3, 1880, Bell and his assistant Charles Sumner Tainter successfully sent intelligible speech over a modulated beam of sunlight via their invention, the photophone—a device that vibrated a mirror to encode sound onto reflected light, detected hundreds of feet away by a selenium receiver. This pioneering feat, which Bell himself deemed his greatest work, demonstrated how light waves could convey complex information wirelessly and non-invasively, foreshadowing modern optical technologies like Li-Fi (Light Fidelity).

Today, Li-Fi routers—though still expensive at $1,500–$2,000, as highlighted by sites like RFsafe.com—offer a real, RF-free alternative to traditional Wi-Fi by transmitting data through visible or infrared light, potentially reducing biological stress from electromagnetic fields (EMF). (Thanks for RFsafe.com host and engineer John Coates for teaching me about Bell’s call and Wi-Fi.) Just as Bell’s light-based system proved gentle and precise for early communication, emerging research suggests that living cells emit ultra-weak photons—biophotons—in the UV and visible spectrum as part of metabolic processes. These emissions may reflect cellular health and order, offering a fascinating glimpse into the body’s natural informational signaling.

This remarkable parallel between human-engineered light communication and the body’s own biophoton signaling invites us to consider how coherence—whether in information transmission or in cellular processes—may be a fundamental principle of life itself. Below we explore these ideas in greater depth, examining the role of trace minerals and ionic solutions in supporting normal cellular function and the intriguing science of light-based communication within the body.

Evolving Understanding of Trace Minerals, Cellular UV Emission, and Coherence in Healing

Recent advances in biophysics and cellular biology have significantly expanded our understanding of trace minerals and their role in human health. Trace minerals, including zinc, selenium, copper, manganese, and others, are now recognized not only as essential cofactors for enzymatic reactions but also as critical regulators of cellular signaling and communication. Their influence extends to mitochondrial function, redox balance, and the orchestration of cellular repair mechanisms. Emerging research suggests that optimal trace mineral status may be foundational for supporting normal cellular coherence and the body’s intrinsic capacity to maintain balance, particularly in the context of chronic stressors.

It is important to clarify, however, that the ionic sulfated “trace minerals” found in products such as Adya Clarity and Aurmina are, for practical purposes, not true trace minerals in the conventional nutritional sense. The actual content of certain minerals in these solutions is so minute that it must be measured in parts per trillion, far below the concentrations typically associated with physiological trace mineral supplementation. As such, we are searching for a more accurate descriptor for these substances—perhaps “ionic sulfated water conditioner,” “trace mineral catalyst,” “volcanic ion complex,” or “coherence-enhancing mineral matrix”? What term best captures their unique role?

Despite not being true trace minerals in the conventional nutritional sense, clinical and experiential observations suggest that these solutions can enhance cellular coherence and may exert effects distinct from traditional trace mineral therapies.A particularly intriguing area of study involves the phenomenon of ultra-weak photon emission (UPE), sometimes referred to as cellular biophoton emission. It is now established that living cells emit low levels of ultraviolet (UV) and visible light as a byproduct of metabolic and oxidative processes. This emission is not random; rather, it appears to reflect the underlying health and order of the cell’s internal environment. Emerging research explores whether these emissions may facilitate a form of non-chemical, light-based intercellular communication.

Trace minerals and related ionic solutions may play a role in supporting mitochondrial efficiency and reducing oxidative stress, which in turn may help maintain the integrity of cellular structures and the patterns of biophoton emission. Coherence, in this context, refers to the degree of order and synchrony in the light signals emitted by cells. High coherence is associated with optimal cellular function and efficient communication, whereas loss of coherence may signal cellular distress or dysfunction.

The implications for supporting normal physiology are intriguing. Approaches that support trace mineral balance or cellular coherence—whether through conventional supplementation or novel ionic solutions—may contribute to the body’s ability to self-regulate and adapt to stressors. This perspective aligns with emerging models of integrative medicine, which emphasize the importance of informational signaling and energetic communication in health and wellness. In various therapeutic contexts, optimizing trace mineral status and exploring coherence-enhancing interventions may complement other strategies to support overall well-being at the cellular and systemic levels.

Furthermore, the concept of coherence extends beyond individual cells to encompass tissues, organs, and the organism as a whole. When cellular communication is coherent, physiological processes may become more synchronized, resilience to stress may increase, and the body’s capacity for balance and adaptation may be supported. This evolving understanding invites a more holistic approach to wellness, integrating nutritional, pharmacologic, and biophysical strategies to support the body’s innate intelligence.

During a visit this week, a wise practitioner who was present for her husband’s appointment offered a simple yet profound observation: it takes far more energy to bring a chaotic system into coherence than it does to maintain a system that is already coherent. I think of numerous everyday examples that illustrate this principle. Consider the difference between trying to get children to bed after they’ve consumed a large amount of sugar and watched an action-packed film with all the lights blazing, versus a quieter evening with a wholesome snack after dinner, the television off after 8 p.m., and gradually dimming the lights as we move through the bedtime routine of brushing teeth, climbing into bed, and taking turns reading a story. The first scenario is chaotic—high stimulation, erratic energy, and a steep climb back to calm. The second is coherent—gentle transitions, predictable rhythm, and much less effort required to settle into rest. The same principle applies to our water, our cells, and our daily habits: prevention and maintenance of coherence require far less energy than the heroic struggle to restore order once chaos has taken hold.

Note on substantiation: The references provided reflect foundational and emerging research in biochemistry, mitochondrial biology, and biophoton studies. They are included for educational context only and do not constitute proof of any specific health benefit from Aurmina or related practices.

References Supporting the Above Discussion

• Berry BJ, Trewin AJ, Amitrano AM, Kim M, Wojtovich AP. Use the Protonmotive Force: Mitochondrial Uncoupling and Reactive Oxygen Species. J Mol Biol. 2018 May 25;430(11):3873-3891. doi: 10.1016/j.jmb.2018.03.025.

• Schröder P, Krutmann J. Environmental stress and epigenetics. In: Schieke SM, Lehmann P, Baumann L, eds. Cosmetic Dermatology. Springer; 2017. doi: 10.1007/978-3-662-49593-3_3.

• Cifra M, Pospíšil P. Ultra-weak photon emission from biological samples: Definition, mechanisms, properties, detection and applications. J Photochem Photobiol B. 2014 Oct;139:2-10. doi: 10.1016/j.jphotobiol.2014.02.009.

• Mould RR, Mackenzie AM, Kalampouka I, Frankle L. Ultra weak photon emission—a brief review. Front Physiol. 2024 Feb 23;15:1348915. doi: 10.3389/fphys.2024.1348915.

• Salari V, Seshan V, Frankle L, England D, Simon C, Oblak D. Imaging Ultraweak Photon Emission from Living and Dead Mice and from Plants under Stress. bioRxiv. 2024 Nov 9. doi: 10.1101/2024.11.08.622743.

These references underscore the foundational science while highlighting areas for further research; full texts are often available via PubMed Central or institutional access.

These statements about Aurmina have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

At Last, Responses to Your Questions and Comments!

1. Why Little to No Visible Sediment/Sludge After Aurmina Treatment? (The Science Best Guess)

This is one of the most common and smartest observations—especially from those on RO or distilled water. The answer lies in starting water quality and the mechanism of Aurmina:

• Aurmina’s primary actions (as Pierre has described repeatedly):

  1. Ion-exchange & flocculation — charged sulfated ions attract oppositely charged contaminants (heavy metals, organics, PFAS relatives, pharmaceuticals, etc.) and clump them into visible flocs.

  2. Agglutination & precipitation — these clumps grow, neutralize, and settle as sediment/sludge.

  3. Structuring/coherence — independent of the above, Aurmina organizes water into hexagonal clusters for better cellular hydration, reduced oxidative stress, and enhanced biophoton coherence (tying into the UV emission and healing insights discussed above).

• In RO or distilled water (very low TDS — Total Dissolved Solids, often <20 ppm): There’s simply less material for Aurmina to bind and flocculate. Result: little to no visible sediment, even after full settling time. The water may stay crystal clear or show only the faintest haze (sub-10 micron micro-flocs). This is expected and desirable—it means your starting water is already extremely clean, so Aurmina’s main job shifts to structuring and coherence rather than heavy-duty purification.

• In tap/well water (higher TDS/load): You see obvious yellowish/brown flocs, sediment, and sludge—proof of effective removal.

• Your 10% tap blend (common hybrid): Adds just enough baseline ions (calcium, sodium, chloride) to help Aurmina flocculate residuals more efficiently, often producing fine, floating micro-sediment (sub-20 microns). This is still a good sign—it shows binding is happening at a subtle level.

Bottom line: No/little visible sediment ≠ not working. It means your water is particularly pure to start, and Aurmina is doing its coherence/structuring work quietly. The real metrics are taste (“more alive,” quenching), hydration feel (less paradoxical thirst), energy, and subtle cellular resilience—not visible sludge.

2. Dosing & Practical Routines Recap (Tailored to Your Setups)

• RO or distilled base (AquaTru, Waterwise 4000, etc.): ¼ tsp per half-gallon. Quick 5–15 min activation. Minimal/no sediment expected.

• Tap or well: ½–1 tsp per half-gallon (or 1–2 tsp/gallon). 24–48 hr settle (up to 72 for very dirty). Visible flocs/sediment expected.

• RO + 10% tap blend (your favorite hybrid): ¼–½ tsp per half-gallon. Fine floating sediment common—harmless, filter if desired.

• RO + Celtic salt (added after Aurmina treatment): Yes—add Aurmina first (¼ tsp/half-gallon, 5–15 min), then Celtic salt to taste. You keep the minerals + get coherence benefits. No conflict; the salt ions actually enhance Aurmina’s structuring.

3. Filtration for Fine Sediment

• Cone-shaped unbleached coffee filters (#2/#4 Melitta-style): Good for final polish. Catch larger fines (10–30 micron range), but ultra-fines (<10 microns) may pass through. Still improves clarity/taste.

• Better for micro-sediment: Brita pitcher (carbon + fine mesh), cheesecloth + strainer first, or ceramic filter (0.2–0.5 microns).

• Visibility trick: Flashlight through jug (Tyndall beam = fine sediment present). After filtering, beam should vanish.

4. Distilled vs. RO vs. Hamhocked Method (Space & Elegance Considerations)

• Distilled (basement setup): Purest blank slate, but energy-hungry/slow. Excellent with Aurmina for coherence.

• RO (AquaTru countertop): Faster, lower energy, compact. Great for small kitchens—no granite drilling needed. Pair with 10% tap or Celtic salt for ions/structure.

• Hamhocked (tap-first): Elegant, leverages natural ions for superior flocculation/coherence. Requires batch space (17 L carboys) and settle time. Potential EZ water boost from sunny windows (Pollack’s Fourth Phase research—near-IR light builds structured zones).

Your constraints (small kitchen, no drilling, wife’s island decorations): Stick with basement distillation or add a compact countertop RO (Bluevua, AquaTru, Waterdrop—many fit small spaces, low power). Use hybrids (RO + 10% tap or Celtic) to get hamhock benefits without full commitment. An “addition” (small RO unit in basement) could be the upgrade—faster than distillation, still low-profile.

Closing Thoughts

The “no visible sediment” in RO setups is not a flaw—it’s a feature of purity + Aurmina’s dual role (purification when needed, coherence always). Your Celtic salt addition is already brilliant; layering Aurmina on top is the natural next step for structured, mineral-rich, vital water.

Keep the experiments coming—tap jug vs. RO side-by-sides, sunny window tests, taste/energy notes. This community is building real knowledge together.

Grateful for your questions and patience.

Scott Marsland, FNP-C

These statements about Aurmina have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.