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…

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18 days 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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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.

Disclosure: I am Scott Marsland, FNP-C, co-owner of Aurmina (the product discussed here), and may benefit financially from its promotion. This is not medical advice; consult your healthcare provider.

When I read Justus R. Hope’s Substack piece, “The Pancreatic Cancer Paradox: How One Hidden Population Achieved the Impossible,” it felt like a gift—not just to readers, but specifically to Pierre and me in our ongoing work on environmental toxins and patient recovery. Though I don’t know Justus personally, I admire his collaborations with Dr. Paul Marik and the way he fearlessly connects dots that many overlook. His spotlight on polluted water as a driver of pancreatic cancer aligns so closely with what we’ve seen clinically and written about—it’s a timely reinforcement that demands a response.

As a family nurse practitioner and co-founder of the Leading Edge Clinic with Dr. Pierre Kory, I’ve spent years connecting environmental dots to chronic illness—especially how our water, the most basic necessity, has become a vector for harm. Justus captures this starkly: pancreatic cancer defies medical progress, with rates rising (early-onset up ~2.4% annually since the mid-1990s) amid polluted river basins like the Mississippi-Ohio-Missouri, Danube, and Rhine. Industrial runoff, agricultural nitrates converting to N-nitroso carcinogens, and forever chemicals like PFAS drive inflammation, DNA alkylation, and elevated risks (odds ratios up to 3.2 in some studies; hazard ratios around 1.66 for nitrate exposure in certain analyses). Obesity compounds it, with each 5-point BMI increase adding ~13% risk. Hope’s “rivers of death” aren’t hyperbole—they’re documented environmental betrayal.

At the Leading Edge Clinic, patients arrive with fatigue, digestive complaints, or vague toxicities that they wouldn’t think to connect with their “safe” water sources. Pierre’s “Pierre Kory’s Medical Musings” series has dissected this rigorously, and as co-owners of Aurmina (with Lisa Kory), we’ve translated those insights into action. Here’s my response, drawing heavily from Pierre’s evidence-based breakdowns for depth.

The Personal Evolution: From Distilled Devotion to a Broader View

My wife Kerrie and I started distilling our home water in 1994, right after moving in together during my nursing school days in Philadelphia. The city was in the thick of the crack epidemic—even our garbage cans got stolen off the front steps—and the chlorinated tap water tasted undrinkable. A customer at the supermarket where I worked handed me a book on the health benefits of distilled water, and it made practical sense: no more lugging jugs home. We’ve stayed loyal ever since (though I have no financial interest in the company), now on our third Waterwise 4000 distiller—reliable workhorses that have followed us through moves and life changes, including decades of family summers in Ocean City, New Jersey, where the Marsland clan gathers thanks to my aunt Sue and uncle Bruce’s generosity. This distilled routine has been a quiet constant in our shared life.

I even recently posted a Lightning Bug video demonstrating the combo: distill tap water, add Aurmina ionic sulfated trace minerals, let it settle briefly, and drink. Simple, effective purity. Pierre ribs this in patient instructions as “The Marsland Method,” poking fun at my long-standing allegiance.

Yet recent conversations have shifted me toward his “ham hock” pragmatism: start with plain municipal tap (or well) water. Aurmina flocculates and precipitates pollutants, leveraging the baseline structure and ions (calcium, sodium, chloride) already present for better efficiency. Demineralized sources like distilled or RO can leach minerals long-term, per Frantisek Kozisek’s seminal 2004/2005 review for the WHO Guidelines on Drinking Water Quality. Kozisek documented risks including fatigue, weakness, headache, metabolic acidosis (especially in infants on low-mineral water), higher cardiovascular mortality (15-35% increased risk from soft/low-magnesium water in epidemiological data), hypertension, osteoporosis, cramps, and even links to motor neuron disease and pregnancy complications. Animals on demineralized water show stunted growth and poor reproduction; humans report 40-60% chronic dehydration worsening cognition and performance.

Having learned about how Aurmina’s ionic sulfated trace minerals purify and transform water, I now understand that Kerrie and I have likely been harming ourselves by drinking straight distilled water for the last thirty-odd years—missing those essential minerals and structure. My distilled + Aurmina routine still excels—adding bioavailable traces—but I’m appreciating tap-first for its mineral foundation, letting Aurmina handle the heavy contaminants before filtration.

While Pierre and Lisa were vacationing in Maui, kite surfing and relaxing, they decided to run their now-famous “sparkling water experiment”: picking up various commercial bottled sparkling water brands, adding Aurmina to each, and letting them sit overnight. The results were eye-opening (and alarming)—most turned cloudy or developed yellowish flecks and sediment precipitating out, revealing hidden contaminants even in supposedly premium brands; only one stayed crystal clear. Meanwhile, I was holding down the fort in Ithaca under overcast grey skies, covering his patients for a week—because I offered. No beach epiphanies for me, just steady clinical grind and growing respect for his practical water philosophy, sparked by that very Hawaiian vacation test.

Just as we’ve spent years shoring up our home’s foundation—me hand-excavating dirt, breaking down disintegrating cinder block, gathering stones while Kerrie designed and built the walls against chronic water seepage—I’ve come to see our drinking water as the body’s true foundation. Small, consistent fixes there prevent bigger breakdowns downstream.

The Bigger Picture: “Legally Clean” Isn’t Enough

Pierre’s posts expose the myth: treatment focuses on regulatory checkboxes, not biology. Plants coagulate, filter, and disinfect to remove ~85%+ solids and most pathogens, but prioritize pipe safety and EPA limits for only ~100 monitored pollutants—not the 100,000+ chemicals in use (adding ~1,000 yearly). Thousands slip through: pharmaceuticals (antibiotics, hormones), endocrine disruptors (BPA, phthalates), pesticides, microplastics, flame retardants, illicit drugs, and disinfection byproducts like trihalomethanes (THMs) from chlorine—known carcinogens “diluted” in risk models.”

Legally clean” meets standards, yet delivers a toxic brew. Justus Hope’s Iowa-linked studies align: nitrates above half the MCL (5 mg/L nitrate-N) raise pancreatic cancer hazard ratios ~1.66 in some cohorts; animal-source dietary nitrites show odds ratios up to 2.3-3.2. PFAS alone attribute ~6,800-6,864 U.S. cancer cases yearly (per recent ecological analyses of UCMR data and SEER incidence 2016-2021), with ties to digestive, endocrine, respiratory, thyroid, and rare cancers. Aging infrastructure (lead pipes, fracking fluids) and global wastewater dumping (80% untreated) amplify it.

Clinically, I’ve witnessed symptom relief after source changes and Aurmina treatment—no drama, just consistent gains in energy and gut function from these small, persistent adjustments, much like the steady progress we see in patients over time.

Aurmina: Bridging Purity and Vitality

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.

Aurmina’s volcanic-mineral complex (akin to Shimanishi’s original formulations and Adya Clarity) goes beyond removal—it lends coherence and mineral re-organization. In 2014 tests by water toxicologist Paul Rosenfeld, 1-2 tsp per gallon neutralized over 250 contaminants to undetectable levels via flocculation (precipitating into filterable clumps): heavy metals (lead, arsenic, mercury), PFAS relatives, phthalates, BPA, glyphosate, pharmaceuticals, and more. Residuals stayed minimal (aluminum <0.05 mg/L, iron trace). It adds balanced ions—calcium ~30-32 mg/L, magnesium ~12-13 mg/L, sodium, boron, strontium—mimicking pristine spring water.

Pierre’s “Water Quality, Structure, and the Biology of Performance” highlights structured (hexagonal-clustered) water’s benefits: improved cellular hydration, reduced oxidative stress, better glucose handling, and enhanced performance. Veterinary data shows racehorses with superior heart rate variability/recovery; livestock with faster growth and reproduction. Human parallels include sharper cognition and resilience against toxins—may support overall resilience against environmental toxins by reducing contaminant burden.

In practice: Tap/well—add Aurmina (1-2 tsp/gallon), settle 24-48 hours, filter (ceramic works well). Distilled/RO—quick 5-15 minute activation suffices. Either yields alive, vital water.

Closing Thoughts: Reclaiming What We Drink

Justus, thank you—your paradox boils down to systemic neglect, and shining light on it amplifies the urgency Pierre and I have felt for years. Pancreatic cancer’s rise tracks our toxic water exposures. Pierre’s series provides the roadmap: test your source, understand the flaws in “compliance,” and act. Aurmina helps restore what modern treatment strips away as a supportive tool for water purity and remineralization, based on our personal and clinical observations.

I’ve moved from purist to hybrid user, and patients benefit. Experiment, share results in comments, and, pardon the pun—let’s keep the conversation flowing.

Stay vigilant, stay hydrated.

How the Zinc Question Even Entered the Room

If you had told me four years ago that I would spend six months reading about zinc neurotoxicity, glutamate excitotoxicity, and copper deficiency myeloneuropathy in the context of post-COVID and post-vaccine syndromes, I would have politely smiled and changed the subject. Zinc was one of those “safe” nutrients—something we reflexively recommended for immune support, especially during the early pandemic waves when fear and misinformation were everywhere. Most patients were already taking it on their own anyway. The turning point came in the summer of 2025. I started noticing a pattern among a subset of patients who were making progress but then plateaued or even regressed. They were the ones who had been faithfully taking 30–50 mg of zinc daily (sometimes more) because “it helps with immunity” or “my functional medicine doctor said it’s good for long COVID.”

Sometimes I had to uncover their zinc use, because it wasn’t on their medication reconciliation (“It’s only zinc!”), or it was an accumulated dose from multiple supplements, buried on the back of the label. When I dug deeper, many had been on these doses for months or even years. At the same time, I was re-reading Russell Blaylock’s Excitotoxins: The Taste That Kills (1997) and came across his caution on page 125:

“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.”

That sentence stopped me cold. Here was a respected neurosurgeon warning—nearly three decades ago—that zinc could be a “two-edged sword” in the brain, protective at one receptor family (NMDA) but potentially harmful at another (AMPA/kainate). I began to wonder whether the very supplement we were tolerating as “harmless” might be contributing to the persistent brain fog, fatigue, dizziness, and emotional blunting we were seeing in some of our sickest patients. So I started asking. And tapering. And watching.

The responses were not universal, but they were dramatic enough in several cases that we could no longer ignore the signal. One man in his late 60s with intractable post-vaccine fog skipped his 50 mg morning dose one day and his wife told him the next morning, “I feel like I got my husband back.”

A young woman in her 20s stopped a 17 mg zinc-copper combo and her disabling dizziness and photophobia resolved in two weeks—enough to let her drive to university again.

These weren’t placebo-level changes; they were overnight or near-overnight shifts that demanded explanation. That is how we arrived at this conversation. Not from ideology or preconception, but from bedside observation, cross-referenced with historical warnings and modern mechanistic literature.

Zinc Supplementation in the United States: A Post-Pandemic Surge

The backdrop is important. Zinc use exploded during COVID. NHANES data show dietary supplement use overall among U.S. adults rose from 52% in 2011–2012 to 61.4% in 2021–2023, a 9.6 percentage point increase. Zinc-containing products were among the fastest-growing categories, with an 8.4 percentage point rise in specific zinc supplement use over the same period.In the 2011–2014 NHANES cycle, 34% of adults already reported consuming zinc from supplements (including multivitamins), with a mean intake of 24 mg/day among users. Dedicated single-ingredient zinc supplements were less common (~1–2% in earlier data), but zinc is ubiquitous in multivitamin-mineral formulations, taken by roughly 30–32% of adults.

Post-2020 sales trends and public health messaging about immune support almost certainly pushed total exposure higher, especially in the long-COVID and vaccine-injury communities where patients are often desperate for anything that might help.When average dietary zinc intake (9–13 mg/day) is added to supplements, a meaningful proportion of users likely exceed 25 mg/day chronically—and some push well past the NIH Office of Dietary Supplements (ODS) Tolerable Upper Intake Level (UL) of 40 mg/day. The UL is set based on the lowest observed adverse effect level for copper interference (~50–60 mg/day total intake), a threshold linked to real clinical pathology.

Mechanisms of Harm: Evaluating the Five Pillars

In the original drafts I wrote for this Substack series, I proposed five mechanistic pathways through which chronic high-dose zinc could contribute to neurological harm, particularly in the post-COVID and post-vaccine injury context. The evidence landscape is uneven, and it’s important to be precise about what is established versus what remains hypothesis-generating.

1. Copper Antagonism → Oxidative Stress & Impaired Myelin Synthesis
   This pillar is robust and clinically actionable. Chronic zinc intake >40–50 mg/day induces intestinal metallothionein, which sequesters copper and blocks its absorption, resulting in hypocupremia and copper-deficiency myeloneuropathy (CDM). CDM classically presents with sensory ataxia, dorsal column dysfunction, spastic gait, peripheral neuropathy, and dorsal column hyperintensities on MRI—mimicking subacute combined degeneration from vitamin B12 deficiency. Hematologic abnormalities (anemia, neutropenia, pancytopenia) often reverse rapidly with zinc cessation and copper repletion (2–8 mg/day elemental copper), but neurological deficits may only stabilize or partially improve if diagnosis is delayed. Case series document this pattern in patients taking high-dose zinc for immune support, macular degeneration, or denture cream use, with a noticeable increase reported after 2020.In the PASC and vaccine-injury population, the same inflammatory and metabolic stressors that drive long COVID may lower the threshold for copper depletion and make subclinical myeloneuropathy clinically manifest.

2–4. Th17/Treg Imbalance, PARP-1–Mediated Neuronal Apoptosis, and Mitochondrial ROS/Energy Failure
These three pillars are not a chimera—they have legitimate mechanistic roots in the literature—but they are far less directly supported as consequences of oral high-dose zinc in humans, especially at the intermittent levels we are discussing (>25 mg more than 2–3 times per week).

• Th17/Treg imbalance: Zinc deficiency promotes Th17 polarization and impairs Treg function, increasing autoimmune risk. Conversely, physiological and moderately high zinc supplementation suppresses Th17 cells and expands Treg populations, ameliorating experimental autoimmune encephalomyelitis (EAE, the animal model of multiple sclerosis). No studies show oral high-dose zinc driving Th17 dominance or worsening autoimmune neurological disease; the direction of effect is usually protective or neutral.

• PARP-1–mediated neuronal apoptosis: Excess free/synaptic zinc activates PARP-1, leading to DNA damage and apoptotic cell death in preclinical models of stroke, traumatic brain injury, and neurodegeneration. These effects are mediated by mitochondrial dysfunction and reactive oxygen species (ROS). However, this pathway is triggered by pathological intracellular zinc release during acute injury, not by systemic supplementation.

• Mitochondrial ROS & energy failure: Free Zn²⁺ catalyzes ROS generation and impairs ATP production in isolated mitochondria and neuronal cultures. Again, this is primarily a mechanism of acute excitotoxicity from synaptic zinc release, not from chronic oral intake.

That said, these mechanisms are not irrelevant. In patients with persistent neuroinflammation, blood-brain barrier permeability changes, and glutamate dysregulation—all documented features of PASC—these pathways could theoretically become more relevant at doses that would be well-tolerated in healthy individuals. The literature does not prove they are active at >25 mg 2–3×/week, but it does not rule them out either, especially when the CNS is already “primed” by spike protein exposure.

5. Molecular Mimicry Amplification
   This remains the weakest and most speculative pillar. No direct evidence connects zinc to amplification of SARS-CoV-2 cross-reactive autoantibodies or CNS auto-attack in PASC. CSF autoantibodies are documented in some neuro-COVID cases, but they correlate more with BBB leakage than with zinc status.

The Dual-Hit Hypothesis in Context

The proposed synergy between COVID-19–induced Th17-dominant immune skew and chronic (or even intermittent high) zinc remains a hypothesis-generating idea rather than an established causal pathway. Copper deficiency myeloneuropathy is the only pillar with strong, reproducible clinical evidence tied to oral zinc excess. The other mechanisms have roots in preclinical excitotoxicity and neuroinflammatory models but lack direct translation to the dosing and context we are discussing.

Still, in a population already experiencing persistent neuroinflammation, BBB permeability changes, hippocampal vulnerability, and glutamate dysregulation (all documented in PASC), the threshold for zinc-related harm may be meaningfully lower than in healthy individuals. The rapid clinical improvements we have seen after tapering zinc—even in patients taking balanced zinc-copper formulas—suggest that something beyond simple copper antagonism is at play. Whether that “something” is excitotoxicity, mitochondrial stress, BDNF signaling disruption, or another pathway remains an open question—but one worth pursuing.

Practical Dosing Thresholds and Safety Considerations in PASC / Vaccine Injury

References

1. Cowan AE, et al. Dietary Supplement Use in the United States, 2021–2023. J Nutr. 2024. DOI: 10.1016/j.tjnut.2024.08.001

2. Bailey RL, et al. Total and usual nutrient intakes from foods and supplements, NHANES 2011–2014. J Nutr. 2019. DOI: 10.1093/jn/nxz025

3. Gahche JJ, et al. Dietary supplement use among U.S. adults has increased since NHANES III (1988–1994). NCHS Data Brief. 2011;(61):1–8.

4. Office of Dietary Supplements, National Institutes of Health. Zinc Fact Sheet for Health Professionals. Updated January 6, 2026. https://ods.od.nih.gov/factsheets/Zinc-HealthProfessional/

5. 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

6. Duncan A, et al. Zinc-induced copper deficiency myeloneuropathy. Neurology. 2005. DOI: 10.1212/01.WNL.0000153542.02761.5F

7. Prodan CI, et al. Copper deficiency myeloneuropathy after bariatric surgery. Neurology. 2002. DOI: 10.1212/WNL.58.6.946

8. Kumar N. Copper deficiency myeloneuropathy. Continuum (Minneap Minn). 2023. DOI: 10.1212/CON.0000000000001278

9. Rosenkranz E, et al. Zinc supplementation induces regulatory T cells in experimental autoimmune encephalomyelitis. J Nutr Biochem. 2016. DOI: 10.1016/j.jnutbio.2015.12.005

10. Wessels I, et al. Zinc as a gatekeeper of immune function. Nutrients. 2017. DOI: 10.3390/nu9121286

11. Sensi SL, et al. Zinc in the physiology and pathology of the CNS. Nat Rev Neurosci. 2009. DOI: 10.1038/nrn2734

12. Morris DR, Levenson CW. Zinc in the developing brain. Adv Neurobiol. 2017. DOI: 10.1007/978-3-319-55769-4_3

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

Next in this series:

My Introduction to Mineral Therapy

As a family nurse practitioner treating over 1,000 patients with post-acute sequelae of COVID-19 (PASC) and vaccine-related injuries at the Leading Edge Clinic, my perspective on health has evolved dramatically. Months ago, I began exploring zinc’s role after noticing many patients took high doses daily, potentially harming neurons and myelin. This led to a broader investigation into trace minerals, guided by a patient’s generous translation of out-of-print Japanese books by Dr. Hisatake Nojima.

The cornerstone book was “Mineral Power: The Wonder of Healing Power Hidden in Trace Elements” (original title: “石の力”), a 2008 dialogue between Nojima and Dr. Hiroshi Shūtō. This book reframed my understanding: Modern diseases aren’t just lifestyle issues but stem from “living environment-related” deficiencies in trace elements, caused by depleted soils, pollution, and overconsumption. It advocates “Super Mineral Water”—granite dissolved in sulfuric acid—for ionized mineral repletion, emphasizing balance over isolation.This discovery resonated with my partner Dr. Pierre Kory’s research on ionized sulfated trace minerals, which we’ve used off-label to “reorganize” physiology.

Nojima’s work highlights how deficiencies disrupt genes, enzymes, and immunity, mirroring PASC symptoms like fatigue and brain fog. It critiques Western medicine’s symptom focus, promoting preventive integration—ideas that informed our zinc tapering protocols and synergies with therapies like lithium orotate and ketamine.

Detailed Overview of “Mineral Power”

Published around 2008, the book is structured as a conversation between Nojima (clinic director with U.S. research experience) and Shūtō (preventive medicine advocate). They argue trace minerals (zinc, selenium, vanadium, titanium, tungsten) are “gene minerals” vital for health, deficient in modern diets due to chemical fertilizers depleting soils. This causes “malnutrition despite overconsumption,” activating cancer genes and weakening defenses against “living environment-related diseases” (Shūtō’s term for metabolic syndrome, formerly “lifestyle diseases”).Super Mineral Water extracts ionized elements from granite for efficient absorption, normalizing cells without toxicity. Case studies show it shrinking tumors via “starvation tactics” (anti-angiogenesis), relieving pain, and treating intractable conditions. The authors blend Eastern (holistic) and Western medicine, with tools like bedrock bathing (mineral absorption via heat/magnetism), oxygen therapy, and stress reduction (e.g., enka singing for oxygenation).Critiques include overreliance on drugs causing iatrogenic harm and evidence-based medicine blocking innovations. They project mineral focus could cut Japan’s healthcare costs from ¥33 trillion to ¥10 trillion.

Key Themes and Arguments from the Book

• Mineral Deficiencies as Root Cause: Industrial agriculture prioritizes yield over nutrition, leading to deficiencies that disrupt autonomic, endocrine, and immune systems. Historical analogies: Scurvy/beriberi resolved by vitamins; modern equivalents solved by minerals.

• Environmental and Lifestyle Factors: Pollution accumulates toxins; overfed diets lack minerals. Shūtō on “body rust” from ROS; Nojima on avoiding harmful substances.

• Super Mineral Water’s Mechanism: Ionizes elements for gene activation, enzyme boosting, and cancer prevention. Safe, non-toxic; contrasts with drugs.

• Integrative Preventive Medicine: 21st century as preventive era; blend East/West. Early detection key.

• Book’s Relation to Zinc Discussions: Warns excess zinc inhibits copper (p. 13), aligning with copper antagonism pillar. Promotes balanced repletion, echoing my zinc tapering (e.g., symptoms resolved at <25 mg 2–3x/week).

Reflections and Criticisms

Shūtō’s reflections stress balance; Nojima’s afterword defends against critics, emphasizing reproducibility over strict EBM.

Strengths: Anecdotal + scientific; accessible.

Criticisms: Lacks large trials (hypothesis-generating); controversial claims. For me, it buttressed zinc risks—isolated high doses disrupt balance, worsened in PASC via spike/BBB leaks amplifying excitotoxicity.

References: Nojima & Shūtō (2008); Blaylock Excitotoxins (1997) for excitotoxicity ties.

(Hypothesis-Generating Note: Our mineral protocols show synergies with ketamine, potentially priming mitochondria—we have an upcoming paper with Dr. Mitch Liester and Dr Rachel Wilkenson.)

Strengths and Criticisms of the Book

The book blends anecdotes, science, and advocacy, making it accessible yet controversial. It challenges mainstream medicine but lacks large-scale trials, relying on case studies. Mineral Power is ideal for readers interested in alternative nutrition, but consult professionals for application.

Access to Mineral Power

It is not legally safe to upload a full PDF of Dr. Nojima’s book to my Substack, even though it appears to be out of print. Out-of-print status does not end copyright; most modern works remain protected for many decades, and posting a complete PDF online counts as reproducing and distributing the book, which normally requires permission from the rights holder. Substack’s own rules prohibit sharing material that infringes copyright, so instead of uploading the whole book, I will share brief quoted passages with commentary and clinical application, and focus on explaining and expanding on Nojima’s ideas in my own words. If we can secure permission or an avenue to share Nojima’s translated book in the future, I will happily inform Lightning Bug readers.

Coming next in this series: