Part 1 — Verbatim Record with Audio Testimony

“There’s some people that’s never believed my testimonies. So I decided to post some pics of me before MMS and now. ..Top left is when I was bedridden and had parathyroid surgery. The inflammation was insane. The top right, I was still so sick, I never thought I was going to live, I was so sick with so many ailments. Look at the dark circles. I swear I was dying. The bottom 2 pics are me now...I couldn’t work for 3 years, I never thought I’d ever work again. When I did walk, I had to use a cane. Now I’m back to work full time. I feel amazing. Thanks to chlorine dioxide, I got my life back....

I really don’t even look like the same person. It’s miraculous!”

“I started mms with an agressive approach. I was so very sick and had so many problems I had been bedridden for a year, 2 surgeries and completely had not worked in 3 years. I began mms 3 activated drops every hour, 8x a day. I did mms baths, I did Andreas Kalcker’s Protocol E, then moved on to his 3 month Protocol P (parasite cleanse). I continued with mms 3 activated drops 3x a day and I saw immediate results in my health. I did foot baths, I weaned off so many meds. My labs started all coming back normal. My body healed itself. I had even forgotten about my plantar fasciitis until someone mentioned it, and I realized it was completely gone. All the calcifications that had accumulated in my body causing spurs, they were around the aorta of my heart, my calcium stabilized, my vitamin D stabilized, my blood pressure stabilized, everything that was causing me to have to give up my passion profession as a hairdresser, completely left. All my swelling gone, all my inflammation, gone, if you haven’t heard my testimonies, I can definitely post the audio or send to you. I never thought I was going to live, much less ever work again. I have lost over 40lbs and working as a hairdresser full time again! Yes plantar fasciitis gone! But my worst ailments gone too. The key is consistency. Aggressively attack the bad cells in your body. Take out the trash! Then the body has the ability to heal itself. The show of me on The Bob the Plumber show is in the pinned section but I’m the second half of the show. It was a lot to condense into 20 min. My audio is much longer and detailed. I need to make an updated audio. I don’t even look like the same person in that video now.”

Link to original message

Part 2 — Applicable Protocols

Starting Procedure

Protocol 1000

Bath Protocol

Foot-bath Protocol

Protocol C

The testimonial describes an aggressive, escalating hourly dosing schedule combined with full-body baths, foot baths, and a multi-month parasite cleanse — this maps most closely onto a general, non-specific “cure everything” approach (Protocol 1000/Protocol C) layered with the bath and foot-bath adjuncts rather than any single condition-specific protocol.

Part 3 — Mechanistic Critique

Inflammation and swelling. There is a plausible theoretical mechanism: low-dose chlorine dioxide-induced ROS can neutralize the reactive species associated with the body’s stress/infection response, drawing an explicit parallel to the anti-inflammatory effects reported for medical ozone therapy (citing Tartari et al.’s rheumatoid arthritis model). [1]

Chronic fatigue, “bedridden,” feeling amazing after resuming activity. As previously discussed, mitochondrial hormesis (mitohormesis) offers a mechanistic frame for generalized “getting my life back” claims: low-dose ROS exposure is proposed to upregulate antioxidant defenses and improve mitochondrial quality control in cells with baseline mitochondrial dysfunction. This is the strongest theoretical candidate for explaining a broad, non-specific return of energy and function. [2]

Calcification, aortic calcium deposits, bone spurs, calcium/vitamin D “stabilization,” and blood pressure normalization. I do not have a mechanistic explanation for these improvements; any effect of chlorine dioxide would seem to me to be secondary, resulting from the body’s improved metabolic state.

Plantar fasciitis resolution and 40-lb weight loss. The general anti-inflammatory/ROS mechanism of action could theoretically account for reduced local soft-tissue inflammation, but the source text does not make this extension explicitly, so applying it here is speculative even within the bounds of the provided literature.

Hormesis In More Detail and How it Could Theoretically Improve Things.

The concept: a small, non-harmful dose of oxidative stress makes cells “stronger and better prepared for future challenges” by temporarily boosting antioxidant enzyme activity and triggering production of new protective proteins, rather than simply damaging tissue the way a high dose would. Chlorine dioxide is theorized to work along this dose-response curve, showing a “beneficial dose” sitting within a “Hormetic region,” distinct from higher doses that cause “oxidative damage” and “harm” relative to a reference risk line. This hormetic process is associated with three specific downstream adaptive effects: enhanced mitochondrial biogenesis (more cellular energy output), upregulated antioxidant defense systems (greater resilience to future oxidative or infectious stress), and stimulated autophagy/mitophagy (clearance of damaged mitochondria and dysfunctional cells). [2] Applied to this testimonial, mitohormesis is the best-fitting theoretical candidate for the general recovery of energy, workability, and “labs coming back normal” — it doesn’t require a condition-specific pathway, just a systemic upgrade in cellular resilience.

Overall Assessment

The inflammation/swelling reduction and the generalized “restored energy” narrative have the most explicit theoretical scaffolding based upon the understood mechanisms of chlorine dioxide — ROS-mediated anti-inflammatory action and mitohormesis, respectively — both of which currently rest on anecdotal compilations and cross-therapy analogy (to ozone and to WF10) rather than controlled clinical evidence in humans given this specific compound and dosing regimen. The calcification reversal, parathyroid-related recovery, calcium/vitamin D/blood pressure “stabilization,” parasite elimination, and weight loss cannot be directly attributed to chlorine dioxide but rather to a comprehensive improvement in health that is secondary. [3]

References

1. Tartari APS, et al. Anti-inflammatory Effect of Ozone Therapy in an Experimental Model of Rheumatoid Arthritis. Inflammation. 2020 Jun;43(3):985-993. https://pubmed.ncbi.nlm.nih.gov/32382842/

2. Curious Human Productions. How chlorine dioxide can reverse and prevent diabetes, chronic fatigue, cancer, and more. The Curious Substack. Retrieved August 18, 2026, from https://curioushumanproductions.substack.com/p/how-chlorine-dioxide-can-reverse

3. Curious Human Productions. (2026, July 21). How chlorine dioxide reverses diabetes (technical report). The Curious Substack. https://curioushumanproductions.substack.com/p/how-chlorine-dioxide-reverses-diabetes

Earlier this year, while researching borax (sodium tetraborate decahydrate), I discovered that 20 Mule Team Borax appears to have removed purity information from its website sometime in 2016. From the website’s launch through 2015, purity information was readily available.

Below are screenshots from Archive.org, with the relevant information outlined in red. I also saved the URLs for the archived pages; however, when I checked most recently, those links were no longer working.

The Dial Corporation. (2010). 20 Mule Team® Borax: About [Archived web page]. Wayback Machine. (2012 Archive Webpage Snapshot showing borax purity info)

https://web.archive.org/web/20120107084327/https://www.20muleteamlaundry.com/about

(2014 Archive Webpage Snapshot showing borax purity info)

https://web.archive.org/web/20140520151814/http://www.20muleteamlaundry.com/about/what-is-borax/

Note: This is for educational purposes. This is not medical advice, and I am not telling you what you should do. Every person is or should be in control of their own health in spite of what the current medical establishment would like you to believe.

Curious note: I have now been performing remote ischemic conditioning on myself daily for just over a year. What started as a curiosity born from my research into oxidative therapies has become one of the most consistent, evidence based habits in my entire health routine. I am not alone in this. A growing number of readers of this Substack have written in to tell me they have picked up the same simple, five cycle cuff protocol and stuck with it for weeks, months, and now, for some, over a year. We are, in a very real sense, a small self experimenting community, testing a low cost intervention that mainstream medicine has been sitting on for decades. What we are about to explore today may be the single most important reason yet to keep doing it.

Where This Series Has Taken Us So Far

If you are new here, a quick recap will help. I first introduced remote ischemic conditioning (RIC) as the no cost, simple home therapy that medical and biohacking experts ignore. That article covered how brief, repeated cuff based blood flow restriction triggers systemic protective signaling, boosts endurance and antioxidant defenses, and conditions the cardiovascular system in ways that mimic exercise. From there, I laid out the exact home protocol I use daily: five cycles of five minute cuff inflation at 200 mmHg followed by five minutes of release.

I then went deeper into specific applications. I explained how RIC acts as natural miracle grow for the brain by driving BDNF production. I showed how it functions as a workout and recovery solution for athletes and everyday movers. I also described how it can serve as a surgery shield that protects the heart, brain, kidneys, and other organs before and after operations. I explored more provocative territory too, including a theoretical case for RIC as a natural approach to erectile dysfunction rooted in nitric oxide and endothelial function, and even a mechanistic idea connecting RIC to your body’s own structured water production at the vessel wall. Across every article, one theme keeps coming back. RIC does not just protect the vascular system. It actively reshapes it making it better. Today, we take that theme to one of its most important points so far.

Why Building New Circulation Is So Important

Here is the idea I want you to think about. What if your body could grow its own detour around a blocked or narrowed blood vessel, without a surgeon, a stent, or a scalpel? This is not science fiction. It is called collateral circulation, and it is one of the most underappreciated survival mechanisms built into human physiology.

Collateral vessels are small, pre existing connections between nearby arteries that normally carry very little blood. A recent, comprehensive review describes them as “unique, naturally occurring endogenous bypass vessels that provide alternative pathways for oxygen delivery in obstructive arterial conditions and diseases.” [1] When a main artery narrows or closes off, whether from plaque buildup, a clot, or an old injury, these dormant channels can enlarge and take over. They slowly reroute blood around the blockage to keep the downstream tissue alive.

The clinical evidence for this protective effect is strong and growing. A 2025 meta-analysis pooling 41 studies and more than 10,000 stroke patients found that good collateral circulation was significantly associated with a favorable outcome, with a pooled odds ratio of 1.67. [2] In the heart, a large nomogram based study of patients with acute ST elevation heart attacks confirmed that a well developed coronary collateral network is a “crucial protective mechanism,” and identified factors such as prior coronary disease and blockage location as strong predictors of who develops these lifesaving vessels. [3] Older but still foundational data back this up further. Patients with well developed coronary collaterals tend to have smaller heart attacks, better long term survival, and fewer complications than patients whose collateral networks never developed. [4] The same holds true in the brain, where a person with strong collateral flow can experience a major arterial blockage and still walk away with minimal damage, while someone with poor collaterals suffers a devastating stroke from the exact same blockage.

This is exactly why the question of whether RIC can build new collateral circulation is not a minor technical detail buried in a journal. It may be one of the most important discoveries in preventive vascular medicine of our time. It suggests that a person with an existing, silent narrowing somewhere in their coronary or cerebral arteries, something many people carry for years without knowing it, might be able to grow a natural bypass around that narrowing before it ever causes a heart attack or a stroke. Instead of waiting for the crisis and then reacting with a stent or a clot busting drug, RIC raises the possibility of getting ahead of the crisis by upgrading your circulation while you still have time.

What the Science Actually Shows

Let’s look at what has been studied, what is being studied right now, and how strong the evidence is.

Cerebral collateral growth is the most established finding for RIC specifically. In a middle cerebral artery occlusion model, researchers found that RIC “enhanced collateral circulation, diminished early ischemic lesions, enlarged pial collaterals, and mitigated infarct volume.” It worked through the Akt-eNOS signaling pathway acting on the brain’s leptomeningeal anastomoses, the natural backup vessels that connect neighboring artery territories. [5] A related study found that limb RIC increases Notch signaling activity and directly promotes new vessel growth in the ischemic rat brain, meaning it does not just improve blood flow for a short time. It stimulates the structural growth of new vessel connections. [6]

Chronic, repeated RIC appears to drive real structural remodeling, not just a short lived boost in flow. A review of chronic RIC protocols found it capable of improving cerebral blood flow in chronic cerebral ischemia, likely by promoting angiogenesis, vascular remodeling, and collateral formation. This was backed by measurable increases in vascular markers and actual increases in vessel number and volume on advanced imaging. [7] A separate animal model of chronic reduced brain blood flow found that repeated RIC increased angiogenesis and increased circulating endothelial progenitor cells, the cells that help build new vessels, resulting in more vessels and less space between them. [8]

Human trials are now testing this idea directly. The ongoing RICAS trial is evaluating whether chronic RIC improves collateral status in stroke patients whose blockages come from large artery atherosclerosis. The trial explicitly frames RIC as a candidate for collateral augmentation as a secondary stroke prevention strategy, especially for people whose existing collaterals are poor to moderate. [9] This is no longer just a theory. It is being tested in real patients as a way to actively upgrade the brain backup circulation.

The heart shows encouraging, earlier stage, findings. A clinical study using cuff based RIC in patients undergoing cardiac catheterization found it “improved distal coronary perfusion pressure and rapidly increased distal coronary occlusive pressure thereby improving coronary collateral blood flow” within a single session. [10] Researchers studying coronary collateral growth broadly point to sustained shear stress, physical exercise, and repeated stimulus as the strongest known triggers for true vessel remodeling. [4] RIC fits squarely into that category of repeated shear stress stimulus, which is exactly why the chronic, daily practice matters far more than a single isolated session.

The mechanism ties it all together. Repeated restriction and release of blood flow triggers a systemic release of protective chemical signals. It activates endothelial pathways, especially Akt-eNOS and Notch, that over time promote both new capillary growth and the enlargement of pre existing collateral channels . [5, 6, 7] Because true vessel remodeling depends heavily on sustained, repeated shear stress rather than one exposure, this explains why chronic, day after day practice, such as a daily RIC session, shows far more structural benefit than a one time exposure ever could.

Why This Should Change How You Think About RIC

Step back and look at the full picture. Most people think of prevention in terms of avoiding damage: eat better, do not smoke, keep your blood pressure down. Those things matter enormously, but they are fundamentally defensive. What the collateral circulation research on RIC points to is something offensive. It is about actively building redundant infrastructure into your own circulatory system before you ever need it. It is the physiological version of digging a second well before the first one runs dry.

If you already carry risk factors for coronary or cerebral artery narrowing, and most people over 40 do, whether they know it or not, this may be the single most compelling reason yet to make RIC a permanent daily habit rather than an occasional biohack. The vessels you build today may be the exact ones that save your heart or your brain tissue on the day you least expect it.

The Protocol I Use Every Day

If you want to start doing this, here is the evidence based home protocol I laid out in detail in The Perfect Home Protocol for Remote Ischemic Conditioning. It is the same one I have personally followed for over a year.

• Place a blood pressure cuff, manual or automatic, securely around your upper arm.

• Inflate the cuff to at least 200 mmHg, or 50 mmHg above your systolic blood pressure, to fully restrict blood flow.

• After five minutes, deflate the cuff completely and leave it deflated for another five minutes.

• Repeat this cycle for a total of five sets.

• Alternate arms daily, and avoid the protocol if you have peripheral vascular disease, a history of blood clots, severe hypertension, or poor limb sensation. (or proceed with caution and your own discretion)

That is it. Five sets, five minutes on, five minutes off, one cuff, no cost. RIC offers a way to trigger the same kind of protective vessel remodeling that has kept so many patients with strong natural collaterals alive through their worst cardiac and neurological events, and it offers a way to trigger it on purpose, safely, and for free, without waiting for a crisis to force your hand. The only question left is whether you are willing to make it part of your daily routine building the circulation that might one day save your life.

References

1. Faber, J. E. (2025). Collateral blood vessels in stroke and ischemic disease: Formation, physiology, rarefaction, remodeling. Journal of Cerebral Blood Flow & Metabolism. Advance online publication. https://pmc.ncbi.nlm.nih.gov/articles/PMC11904929/

2. Liu, H., et al. (2025). Collateral circulation significantly improves prognosis in cerebral infarction: A meta-analysis. American Journal of Translational Research, 17(6), 4546–4561. https://e-century.us/files/ajtr/17/6/ajtr0163891.pdf

3. Shao, H., et al. (2025). Predictors of coronary collateral circulation in patients with acute ST-segment elevation myocardial infarction: A nomogram-based approach. Reviews in Cardiovascular Medicine, 26(4), Article 26477. https://pmc.ncbi.nlm.nih.gov/articles/PMC12059742/

4. Meier, P., et al. (2013). The collateral circulation of the heart. BMC Medicine, 11, 143. https://pmc.ncbi.nlm.nih.gov/articles/PMC3689049/

5. Saito, M., Hoshino, T., Ishizuka, K. . Remote Ischemic Conditioning Enhances Collateral Circulation Through Leptomeningeal Anastomosis and Diminishes Early Ischemic Lesions and Infarct Volume in Middle Cerebral Artery Occlusion. Transl. Stroke Res. 15, 41–52 (2024). https://doi.org/10.1007/s12975-022-01108-2

6. Qin L, et al. Beyond Pharmacology: The Biological Mechanisms of Remote Ischemic Conditioning in Cerebrovascular Disease. Biomolecules. 2024 Nov 5;14(11):1408. https://pmc.ncbi.nlm.nih.gov/articles/PMC11592304/

7. Chong J, Bulluck H, Fw Ho A, Boisvert WA, Hausenloy DJ. Chronic remote ischemic conditioning for cardiovascular protection. Cond Med. 2019 Aug;2(4):164-169. https://pmc.ncbi.nlm.nih.gov/articles/PMC7169952/

8. Khan, M. B., et al. (2017). Chronic remote ischemic conditioning is cerebroprotective and induces vascular remodeling in a VCID model. Translational Stroke Research, 9(1), 51–63. https://pmc.ncbi.nlm.nih.gov/articles/PMC5750336/

9. Zhao ZA, Lv Y, Chen HS. Effect of RICAS (Remote Ischemic Preconditioning on Collaterals of Atherosclerosis Stroke): Rationale and Design. J Am Heart Assoc. 2025 Mar 18;14(6):e038570. https://pmc.ncbi.nlm.nih.gov/articles/PMC12132773/

10. Xu Y, Yu Q, Yang J, Yuan F, Zhong Y, Zhou Z, Wang N. Acute Hemodynamic Effects of Remote Ischemic Preconditioning on Coronary Perfusion Pressure and Coronary Collateral Blood Flow in Coronary Heart Disease. Acta Cardiol Sin. 2018 Jul;34(4):299-306. https://pmc.ncbi.nlm.nih.gov/articles/PMC6066945/

Part 1 — Testimonial

After 6 months of uncontrollable growth of the pappilomas and the veterinarian giving up on the dog, she is cured.

“1 week after beginning a CDS protocol of 3 application methods! Wow!!!! After 6 months of uncontrollable growth, the pappilomas are drying up and falling off! We have been giving her 1 Activated MMS drop 3x/day in her mouth with 10ml water (approx 1 Tbl) and then more drinking water after, with CDS 3000 ppm full i diluted spray directly on thr external and gum-line growths 5x/day, and 1 Tbl Activated MMS in a full bath for 20 minutes 3x/week. It is the 1st time in 6 months that we have seen these pappilomas shrink and dry up and some have fallen off!”

This person kept posting updates with pictures for the approximately 40 days that it took to clear the infection.

Here’s what they did:

• 1 Activated MMS drop 3x/day in her mouth with 10ml water (approx 1 Tbl) and then more drinking water after

• CDS 3000 ppm full undiluted spray directly on the external and gum-line growths 5x/day

• 1 Tbl Activated MMS in a full bath for 20 minutes 3x/week.

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Full Image Gallery

Part 2 — Protocol Links

Protocol 1000 for the oral drop-in-water dosing)

Spray Protocol for the undiluted CDS spray on external growths

Bath Protocol for the full-body MMS bath

Part 3 — Mechanistic Critique

ClO₂ inactivates viruses by oxidizing viral proteins and nucleic acids, thereby preventing viral replication, and specifically it disrupts the viral capsid and RNA, impairing the virus’s ability to infect host cells. Papillomaviruses are non-enveloped, capsid-protected DNA viruses, so a direct oxidative attack on capsid proteins at the site of undiluted 3000 ppm topical spray application is mechanistically consistent with the general antiviral mode of action described. [1]

A second mechanism that may be relevant to why the papilloma lesions might resolve: low-dose ROS acting as an immune-modulating signal rather than purely destructive agent. The reversal and resolution of the papillomavirus could result from ROS-induced mitochondrial hormesis, where low, non-cytotoxic ROS doses trigger adaptive cellular responses. For example, NP001 (a purified, pH-adjusted sodium chlorite/chlorine-dioxide-precursor drug) appears to work as a macrophage-targeted immune regulator that shifts macrophages from a pro-inflammatory M1 state toward a reparative M2 state. [2] This is mechanistically important because independent veterinary literature establishes that canine papilloma regression is fundamentally immune-mediated — CD4+ and CD8+ T-cell infiltration drives spontaneous wart clearance in dogs. [3]

If low-dose systemic ClO₂ absorbed orally and via bath immersion modestly shifts macrophage polarization and immune signaling this would align with the dog’s own immune-clearance pathway that is already documented as the natural resolution mechanism for canine papillomas.

Final Analysis

This six-month, veterinarian-unresponsive case of papillomavirus, with extensive cauliflower-like coalescing growths shown across the Day 0 to Day 42 photos, exceeds the typical timeframe for spontaneous regression. Notably, the growths began regressing immediately after the chlorine dioxide protocols were implemented, making spontaneous regression less likely, though not entirely ruled out.

References

1. Ge Y, Zhang X, Shu L, Yang X. Kinetics and Mechanisms of Virus Inactivation by Chlorine Dioxide in Water Treatment: A Review. Bull Environ Contam Toxicol. 2021 Apr;106(4):560-567. https://pmc.ncbi.nlm.nih.gov/articles/PMC7904506/

2. Miller RG, Zhang R, Block G, Katz J, Barohn R, Kasarskis E, Forshew D, Gopalakrishnan V, McGrath MS. NP001 regulation of macrophage activation markers in ALS: a phase I clinical and biomarker study. Amyotroph Lateral Scler Frontotemporal Degener. 2014 Dec;15(7-8):601-9. https://pmc.ncbi.nlm.nih.gov/articles/PMC5524125/

3. Nicholls PK, Moore PF, Anderson DM, Moore RA, Parry NR, Gough GW, Stanley MA. Regression of canine oral papillomas is associated with infiltration of CD4+ and CD8+ lymphocytes. Virology. 2001 Apr 25;283(1):31-9. Full Article

This archive, and all of The Curious Substack, remains open and free for anyone who needs it. Thank you to all the generous paid subscribers who support this ongoing work and ministry to our fellow humans. This work will always stay free and open for as long as the Curious Substack exists. If you’d like to support it, becoming a paid subscriber is one way to do that, but please don’t feel obligated if you can’t afford it. Jesus said, “Freely you have received, freely give.” This is a ministry to you, my fellow humans.

Note: This is for educational purposes. This is not medical advice, and I am not telling you what you should do. Every person is or should be in control of their own health in spite of what the current medical establishment would like you to believe.

Curious Note: This archive contains two sections. Section 1 covers MMS protocols and Section 2 covers CDS protocols.

If you’ve been following along but weren’t sure where to find all protocols in one place, this archive is for you. Below is a walkthrough of every article in the Curious Substack Chlorine Dioxide Protocol Archive, organized so you can quickly find the method that fits your situation—whether that’s getting started, treating an acute illness, or addressing a specific condition.

Getting Started

The Guide to Buying Chlorine Dioxide: Where to Find Reliable Premade Solutions breaks down where to source reliable, ready-to-use chlorine dioxide solutions since these can only legally be sold for water purification. It explains the two-bottle kit system (sodium chlorite “Part A” and an acid activator “Part B”), how to verify a kit is genuine by the amber color change and pool-water smell when the drops combine, and profiles three long-standing suppliers (KV Lab, WaterPureWorld, and All One Wellness). It also covers proper storage, shelf life (12 months to several years if kept cool and dark), and the amber glass bottles needed for diluted skin and eye solutions.

Chlorine Dioxide for Beginners is the foundational primer that explains what chlorine dioxide is, how MMS (sodium chlorite) and an acid activator combine to form MMS1, and the core philosophy every new user needs: the Low and Slow Principle and the Three Golden Rules (No Change, Reduce, and Increase Rules). It walks through the basic starting regimen, how to build an all-day dosing bottle, and where to find water purification kits that meet the correct concentration specifications.

(Part 1) How to Use Chlorine Dioxide — The Starting Procedure introduces the Starting Procedure, the essential first step before using any other protocol. This gradual, day-by-day dosing schedule (starting at a quarter drop hourly and building up over four to five days) is designed to acclimate the body and minimize Herxheimer detox reactions—especially important for people with poor detox pathways or chemical sensitivities. It’s the on-ramp everyone should complete before moving to Protocol 1000.

(Part 2) How to Use Chlorine Dioxide — Protocol 1000 picks up where the Starting Procedure leaves off. This is the workhorse protocol for most illnesses and general detoxification: one activated drop of MMS1 every hour for eight hours a day, prepared as an all-day bottle. It can be run anywhere from a single day to three weeks depending on the goal, always governed by the Three Golden Rules.

(Part 3) How to Use Chlorine Dioxide — Protocol 1000-F covers the “Frequent” variation used specifically for rapid-onset acute illness. Dosing intensifies to one drop every 15 minutes for the first two hours before transitioning into standard Protocol 1000. This frequent early dosing is intended to maintain a higher initial level of chlorine dioxide in the body while a fast-moving bacterial or viral illness is taking hold.

Protocol 1 (Unactivated MMS for Taste-Sensitive Users) offers a simple, virtually tasteless alternative for people who can’t tolerate the flavor of activated chlorine dioxide drops. Instead of pre-activating MMS with an acid, 1–5 drops of plain sodium chlorite are added directly to a liter of drinking water and consumed throughout the day, relying on the body’s own stomach acid (HCl) to generate ClO₂ internally—this was the original method Jim Humble used to treat his mining team for malaria. The article walks through appropriate starting doses for beginners (1–2 drops), how to scale up gradually while watching for Herxheimer reactions, and an important caution: this method should be avoided by anyone on acid-suppressing medications like Prilosec or Omeprazole, since low stomach acid prevents proper conversion to chlorine dioxide.

Topical and Localized Applications

Chlorine Dioxide for Skin Diseases and Skin Conditions details the simple spray protocol (10 activated drops per ounce of water) for superficial wounds, cuts, insect bites, and skin conditions like psoriasis, eczema, and ringworm, plus a stronger CDS-based “Protocol D” for deeper wounds and ulcers. The article is packed with testimonials and photos covering antibiotic-resistant infections, diabetic ulcers, autoimmune skin conditions, and more, alongside a review of the proposed oxidative, immune-modulating, and antimicrobial mechanisms behind these results.

Chlorine Dioxide Nasal Spray Procedure (DIY or Commercial) shows how to build a simple saline-and-MMS1 nasal spray or rinse to address stuffy noses, allergy symptoms, and chronic sinus infections. It compares the DIY version to commercial options like Snoot Spray and includes multiple testimonials of people resolving long-standing sinus and allergy issues within days to weeks.

Respiratory Nebulizer Protocol lays out three separate nebulizing methods—unactivated sodium chlorite, activated MMS1, and pure CDS—each with specific dilution ratios and timing, for treating respiratory infections and conditions. It draws on animal and human studies (including an influenza mouse model and a Japanese classroom study) to support inhaled low-concentration chlorine dioxide as a safe respiratory intervention.

CLO2 Gas and Cup Procedure explains the “cup method,” where activated drops are trapped in a glass and the gas (not the liquid) is applied directly to skin for one to two minutes. This approach is highlighted for ear infections, small skin cancers, spider bites, and abscesses, with testimonials describing rapid resolution of ear pain, shrinking of a suspected melanoma, and clearing of long-standing abscesses.

Chlorine Dioxide Eye Protocol (also covered under CDS as **Protocol O**) provides a full recipe and instructions for treating eye infections, styes, conjunctivitis, corneal issues, and even reports of improved vision, using either MMS1 diluted in saline or a CDS-and-saline eye drop/spray formula. It includes over 20 testimonials ranging from cured pink eye and cleared corneal opacity to reported drops in eye pressure for glaucoma and resolved macular symptoms.

Oral and Dental Health

Oral Infection & Restoring Oral Health Protocol (Part 1) focuses on eliminating active oral infections—abscesses, gingivitis, periodontitis—using MMS1 or CDS-based brushing and rinsing procedures, with an optional DMSO addition for deeper penetration into gum and tooth tissue. Numerous first-person testimonials describe abscesses and tooth infections resolving within days without antibiotics or root canals.

Oral Infection & Restoring Oral Health Protocol (Part 2) shifts from treating infection to long-term restoration, outlining the Weston A. Price Foundation’s nutrient-based approach to remineralizing teeth using vitamins K2, D, and A alongside supporting minerals like magnesium and zinc. It includes a personal supplement regimen and dietary guidelines aimed at reversing early tooth decay and supporting gum health.

Maintenance and General Wellness

Maintenance Protocol (How Can Chlorine Dioxide Benefit a Healthy Person?) addresses how chlorine dioxide can support a healthy person, not just someone actively ill. It frames ClO2 as a mild oxidative stressor that triggers beneficial mitochondrial hormesis (similar to exercise), and offers two simple maintenance approaches—either a twice-weekly higher dose or a smaller twice-daily dose—for ongoing mitochondrial and general health support without overtaxing the body.

Alternative Systemic Delivery Methods

Enema Protocol covers how to deliver chlorine dioxide directly into the lower gastrointestinal tract for conditions affecting the bowel, liver, prostate, and urinary system, including a slow overnight infusion variation (Protocol EC) for more serious illness. The article shares dramatic testimonials involving inflammatory bowel disease remission, cancer regression, autism symptom improvement, and parasite elimination.

Bath Protocol (MMS1 Bath, Part 1) explains how to introduce chlorine dioxide through a full-body soak, exposing a large surface area of skin to the solution as an alternative for people who can’t tolerate oral dosing. It details water preparation (including an optional borax step to bind chlorine and fluoride), a graduated dosing schedule up to 60 activated drops per bath, and how to safely add DMSO for enhanced absorption in later sessions.

Foot Bath Protocol (MMS1 Bath, Part 2) adapts the same bathing principle for people without access to a full tub, limited mobility, or higher sensitivity, using a small basin at ankle height instead. It follows the same drop-count progression and DMSO ratio guidelines as the full bath, plus variations like a low-water compress method or a deeper calf-level soak for more coverage.

Bag Protocol offers an unconventional but powerful alternative for people who cannot tolerate chlorine dioxide orally due to severe Herxheimer reactions or gastrointestinal issues. By sealing the body inside a large plastic bag with a small dish of activated MMS1, the gas is absorbed through the skin for systemic effect. The article includes a striking testimonial of significant cognitive recovery following a traumatic brain injury attributed to consistent use of this method.

The Humidifier Protocol describes a simpler, passive alternative to nebulizing—adding MMS1 drops or CDS to a cool-mist humidifier for overnight respiratory and sinus exposure. It walks through dosing ranges (roughly 15–25 activated drops per liter of water) and includes testimonials of resolved chronic coughs, cleared sinus congestion, and reduced fever symptoms in a child.

Specialized Protocols

Mold & Fungus Protocol addresses a specific roadblock some people hit: mold and fungus that Jim Humble believed can “shield” other pathogens from chlorine dioxide’s effects, stalling recovery on standard protocols. The article details an internal bentonite clay-and-CD alternating and combined dosing sequence, plus an external clay-and-Vaseline salve for skin fungus, and flags conditions—like Candida, Lyme disease, asthma, and herpes—where this protocol should be run before starting Protocol 1000.

There are 2 methods for the vaginal douche protocol. Two chlorine dioxide pioneers, Jim Humble and Andreas Kalcker, each developed a vaginal douche method for infections and reproductive support. Humble’s MMS1 uses a reusable douche bag paired with oral protocols; Kalcker’s Protocol V favors CDS for its gentler pH, delivered via a vaginal irrigator or long-necked bottle. Both stress low starting doses and purified, body-temperature water as a supporting therapy and typically not a standalone.

Pet Protocol provides a simplified, “dummy-proof” method for treating animals with unactivated sodium chlorite added to drinking water, taking advantage of a pet’s own stomach acid to generate chlorine dioxide internally. The included testimonials cover recoveries from respiratory infections, neurological issues, tumors, giardia, and post-surgical infections in dogs and cats.

CDS Protocols

Understanding and Using CDS (Chlorine Dioxide Solution)

Archive of Chlorine Dioxide Protocols using CDS — Intro to CDS explains the difference between MMS1 (acidified in sodium chlorite) and CDS, a purer chlorine dioxide gas dissolved directly in water or saline, popularized in part by Andreas Kalcker. It covers why CDS is often better tolerated for sensitive applications like enemas, eye treatments, and intravenous use, along with its main drawback: needing refrigeration to prevent the gas from evaporating out of solution.

CDS Protocol C and Protocol S introduce the two foundational CDS dosing approaches: Protocol C (Classic), the standard daily regimen of diluted CDS taken hourly for most illnesses and detoxification, and Protocol S (Sensitive), a much slower, day-by-day dose escalation designed for people with chemical sensitivities or poor detox capacity—effectively the CDS equivalent of the Starting Procedure.

Protocol F (Frequent) is the CDS-based emergency protocol for sudden illness, food poisoning, or unknown infections, using an intensive schedule of doses every 15 minutes for two hours (with F10 through F30 concentration tiers based on severity and body weight) before transitioning into standard Protocol C.

CDS Protocol D (Dermatological) is the CDS equivalent of the topical spray protocol, using undiluted 3000 ppm CDS sprayed directly onto skin infections, ulcers, psoriasis, and even MRSA-affected areas. Because pure CDS typically doesn’t cause the stinging associated with MMS1 sprays, it’s often preferred for sensitive or painful wounds, applied as frequently as hourly until the condition improves.

CDS Protocol O (Ophthalmic/Eye) is the CDS-specific eye protocol, combining saline, a measured amount of CDS, and optional DMSO into eye drops for treating infections, inflammation, and vision-related complaints—covered in detail alongside the MMS1-based eye protocol above, complete with over a dozen testimonials of resolved eye conditions.

Where to Go Next

If you haven’t yet watched The Universal Antidote documentary, that’s the best place to start for the full background on what chlorine dioxide is, how it works, and my three-year investigation behind it. You can find it at theuniversalantidote.com

For a deeper, structured understanding of everything covered in this archive, the completely free training course is available at theuniversalantidote.com/the-universal-antidote-course

Part 1 — Testimonial

54 days to cure what the doctor said was incurable. Here is an image of the full sequence with the dates. The doctor said, “Think of it as a barnacle on a ship and just deal with it.”

Part 2 — Relevant Protocol

Twice a day he would activate three drops of Sodium Chlorite (MMS). He would then add 10 mL of water and three drops of DMSO to this and then he would use a small paint brush to paint the liquid onto the affected area of his ear.

This was a modification of the skin and spray protocol. The gas protocol could've also been used.

Part 3 — Mechanistic Critique

Plausible mechanism for the CD and DMSO. Chlorine dioxide (ClO₂) is a broad-spectrum oxidizing antimicrobial that acts by oxidizing membrane lipids and proteins, denaturing aromatic amino acids, and generating reactive oxygen species (ROS) that damage pathogen structures and nucleic acids. ClO₂ has been described as a “size-selective antimicrobial agent,” with low-concentration ClO₂ oxidatively destroying micron-scale pathogens (bacteria, biofilms, fungi) while sparing larger host cells because of the host’s antioxidant defenses. If the ear condition described was bacterial of fungal

This oxidative/antimicrobial mechanism for ClO₂ provides a plausible rationale for why chlorine dioxide might disrupt bacterial or fungal pathogens if present on the ear. The DMSO used in the protocol provided a penetration component aiding the ClO2 to penetrate deeper into the lesion. This testimonial provides an anecdote consistent with the literature concerning the selective and oxidative nature of chlorine dioxide.

Curious Note: A few months ago, comments on one of my earlier boron articles caught my attention. One reader mentioned borax’s long history as a welding and metalworking flux. Another brought up its role in glassmaking, the same chemistry behind shatter-resistant Pyrex and laboratory glassware. That got me wondering whether the chemistry behind these industrial uses might mirror how boron behaves biochemically inside the human body. What I found surprised me. Along the way, my research also led me to an unexpected third field: nuclear reactor engineering.

What follows is the result of that investigation: three very different fields, one mineral, and a set of parallels that run far deeper than I expected.

Picture a steel foundry at full roar. The furnace blazes at over 2,900 degrees Fahrenheit. A worker ladles molten iron into a casting mold, then sprinkles a fine white powder across the glowing surface. Within seconds, the powder melts, flows, and begins pulling a dark film of contaminating oxides away from the metal. The worker knows what will happen without it: a weak, brittle casting riddled with flaws. The white powder is borax, and it has been doing this job for centuries.

Walk into a glass manufacturing plant and you find something equally remarkable. Glass engineers add boron compounds to the molten silica batch, not as a filler or a colorant, but as a structural participant that weaves itself into the molecular architecture of the finished glass. The result is Pyrex cookware that does not shatter when you pour cold water into a hot pan, laboratory glassware that resists the most corrosive chemicals, and fiber optic cables that carry data across continents.

Now walk into the control room of a nuclear power plant. The reactor operators carefully monitor the concentration of boric acid dissolved in the coolant water that flows around the uranium fuel rods. Too little boron, and the chain reaction accelerates beyond safe limits. Too much, and it slows to a halt. The boric acid is also doing something else, something less obvious: managing the hydroxyl radicals generated when intense radiation splits the coolant water molecules apart.

Three industries. Three very different processes. One mineral doing essential work in all of them. Now ask yourself this: what if the same chemistry that stabilizes your borosilicate cookware, cleans forged steel joints, and controls radical damage inside nuclear reactors is also working inside every cell of your body? The evidence says it is, and the parallel runs deeper than metaphor.

Section 1: Borax in Glassmaking — The Structural Former

When glassmakers add borax to a silica melt, the borax breaks down and contributes boron trioxide (B₂O₃) to the batch. This compound does not simply dissolve into the glass the way a pinch of salt dissolves into water. It participates structurally. At the atomic level, boron atoms form covalent bonds with oxygen atoms inside the silica lattice, creating a hybrid structure in which boron and silicon share the load of holding the material together. [1] Chemists call this role a structural “network former” because boron does not sit passively within the glass structure. It becomes part of the architecture itself.

This structural integration produces a cascade of improved properties. First, it lowers the viscosity of the molten glass, making it easier and cheaper to work at lower furnace temperatures. [1] Second, it dramatically reduces the coefficient of thermal expansion, which is the tendency of a material to expand when heated and contract when cooled. Ordinary soda-lime glass expands and contracts significantly with temperature swings, which is why it cracks so easily. Borosilicate glass, containing roughly 12 to 13 percent B₂O₃ by weight, expands and contracts at about one-third the rate of regular glass. [1] A Pyrex baking dish can go from a cold refrigerator to a hot oven without fracturing because boron has fundamentally changed how the silica structure responds to thermal stress.

Third, boron’s presence in the glass structure inhibits devitrification, which is the spontaneous tendency of glass to crystallize and become cloudy and brittle over time. [1] Without boron, glass under thermal or chemical stress can begin reverting toward a crystalline structure, losing its transparency and mechanical strength. Boron disrupts this process by occupying structural positions that would otherwise allow crystalline order to develop.

These properties explain why borosilicate glass shows up in heat resist vials, laboratory beakers and flasks, fiber optic cables, and telescope mirror substrates. [1] In every case, the lesson is the same: boron does not merely improve glass. It transforms the fundamental nature of the material from the inside out by becoming part of its molecular framework.

Section 2: Borax as Flux — The Purifier

A forge weld is one of the oldest metalworking techniques known to humanity. A blacksmith heats two pieces of iron or steel to near-melting temperature, then hammers them together. At those temperatures, the metal surface oxidizes almost instantly. Iron oxides are chemically incompatible with iron metal, so if the oxide film is not removed, the weld will contain contamination layers that prevent true metallurgical bonding. The joint will look solid but will fail under stress.

This is where borax earns its place in the forge. When sprinkled onto hot metal, borax melts at approximately 1,400 degrees Fahrenheit, well below iron’s welding temperature. [2] The molten borax flows across the metal surface and immediately begins reacting with the iron oxides. The mechanism that drives this reaction is boron’s identity as a Lewis acid, meaning it possesses an electron-deficient orbital that aggressively attracts electron-pair donors. Metal oxides are electron-rich at their oxygen atoms, so borate ions strip those oxides away from the metal surface by forming low-melting borate-oxide complexes. [2] Those complexes are fluid at forge temperatures and float away from the weld zone as slag when the pieces are hammered together. The result is a clean, oxide-free metal interface that bonds completely.

This principle extends far beyond the blacksmith’s shop. In brazing and soldering, borax-based flux pastes prevent oxide formation on copper, brass, and silver components during torch work, allowing filler metals to flow freely into clean joints. [2] In precious metal refining, anhydrous borax flux is added to crucibles melting gold, silver, and platinum to pull dissolved gases and metal oxides out of the melt before the metal is poured into molds. [2] In industrial steel production, borate fluxes are poured over molten steel surfaces to prevent atmospheric oxidation during solidification, and they are increasingly replacing fluorspar because fluorine emissions face growing environmental regulation. [2]

The governing principle is elegant and straight forward: flux does not add strength. It removes what prevents bonding. The metal already contains the ability to form a strong joint. The flux clears the contamination that was standing in the way.

Section 3: Boric Acid in Nuclear Reactors — The Radical Manager

The use of boric acid in nuclear reactors is well known in the context of neutron absorption and reactivity control. But there is a second, less publicized role that boric acid plays inside reactor coolant systems, one that connects directly to the biochemical story we are building.

In light-water reactors, the uranium fuel rods are surrounded by circulating water that serves as both coolant and neutron moderator. The intense ionizing radiation from fission continuously strikes the coolant water molecules, splitting them apart in a process called radiolysis. [3]

The hydroxyl radical (- OH) produced by this reaction is one of the most chemically aggressive species in existence. Inside a reactor, it drives oxidative corrosion and stress cracking in the metal pipes and pressure vessels of the coolant circuit. Managing this radical chemistry is a significant engineering concern for reactor safety and longevity. [3]

Boric acid is dissolved in the reactor coolant at precisely controlled concentrations. At the alkaline pH maintained in reactor coolant water, boric acid deprotonates to the borate ion B(OH)₄⁻, which reacts with hydroxyl radicals and effectively intercepts the - OH radical before it can attack metal surfaces, converting it to a less reactive species and protecting the system’s structural integrity.

This is boron functioning as a radical buffer: a chemical agent whose job is to absorb and neutralize the damaging byproducts of high-energy processes. The reactor cannot eliminate radical production, because radical production is an unavoidable consequence of the energy extraction process itself. What it can do is manage those radicals with the right chemistry. Boric acid is part of that chemistry.

Section 4: The Biochemical Mirror — Borate as a Biological Structure Former

Now we step inside the human cell, and the parallels become striking.

At physiological pH, approximately 98 percent of boron circulates in the body as boric acid B(OH)₃, a neutral, trigonal molecule. But in alkaline microenvironments such as the mitochondrial matrix (pH approximately 8.0), the intestinal lumen, and inflamed tissue, boric acid gains a hydroxyl group and converts to the borate ion B(OH)₄⁻. [3] This tetrahedral, negatively charged form is biochemically active in a specific and important way: it forms reversible covalent bonds with molecules that contain adjacent hydroxyl groups, called cis-diol configurations. [4]

The list of biomolecules containing cis-diol configurations includes ribose and deoxyribose sugars (the structural backbone of RNA and DNA), the coenzymes NAD⁺, NADH, NADP⁺, and NADPH (the cell’s primary hydrogen-carrying electron transfer molecules), catechol neurotransmitters including dopamine and epinephrine, and the polysaccharide chains of glycoproteins and proteoglycans that coat the surface of every cell in the glycocalyx. [5, 6]

Just as boron’s B–O bonds knit together the silica structural network in glass, borate’s B–O bonds knit together the sugar-protein mesh of the glycocalyx, though in the glycocalyx the linkage is a reversible, dynamic diester bond rather than a permanent covalent lattice. [6]

Research has confirmed that boronic acids form borate esters with the 1,2-diol and 1,3-diol saccharide groups that are abundant in the glycocalyx, and this esterification is the basis for targeted drug delivery systems that use boron chemistry to anchor therapeutic agents to cell surfaces . [6]

Importantly, this cross-linking is reversible. Borate ester bonds can form and release based on local pH, competing ligands, and boron concentration, which means the system is dynamic and self-regulating. This mirrors the glass analogy in one more respect: just as the borosilicate structural properties can be tuned by adjusting the boron content of the batch, the degree of borate cross-linking in biological matrices is tunable by boron availability.

When boron is deficient, this structural stabilization is lost. Animal deprivation studies show that boron-deficient organisms exhibit reduced osteoblast activity, impaired membrane integrity, and disrupted cell signaling. [7] The biological parallel to removing boron from borosilicate glass is precise: without it, the structure loses its resistance to stress and begins to degrade.

Section 5: The Biochemical Mirror — Borate as a Biological Flux

The flux analogy translates into cellular biochemistry with equal precision.

Recall that metallurgical flux works by using boron’s Lewis acid character to dissolve and remove electron-rich oxide contaminants from metal surfaces, clearing the way for clean bonding. Inside cells, reactive oxygen species (ROS) play a role analogous to oxide scale. They form constantly as byproducts of mitochondrial respiration, immune activity, and xenobiotic metabolism, and they contaminate enzyme active sites and membrane structures, interfering with normal function. Borate’s Lewis acid affinity for electron-rich oxygen species makes it a potent interceptor of these biological “oxides.”

At alkaline pH, the borate ion scavenges hydroxyl radicals (- OH) with a Gibbs free energy of -36.9 kJ/mol, making the reaction thermodynamically favorable. [3] A 2025 study confirmed that boric acid supplementation significantly increases reduced glutathione (GSH) levels and reduces oxidative damage markers in animals under oxidative stress, demonstrating that the radical-scavenging effect is not merely theoretical but functionally relevant in living systems. [8]

Borate also acts as a flux specifically on the cell’s most critical hydrogen-carrying molecule, NAD⁺. Because NAD⁺ contains a ribose sugar with a cis-diol configuration, borate can reversibly bind to it, temporarily withdrawing it from the dehydrogenase enzymes that use it in metabolic pathways. [9] This is a precise molecular flux action: boron pulls the substrate away from the reaction surface in a controlled, reversible manner, modulating the rate of energy metabolism.

Perhaps the most striking biological flux action involves bone formation. Research published in Communications Biology demonstrated that borax directly stimulates the NaBC1 borate membrane transporter, which activates the bone morphogenetic protein receptor BMPR1A and triggers a downstream cascade through ERK1/2, Akt, and Smad1 kinases, all essential for osteogenic differentiation of stem cells. [10] Critically, this osteogenic activation occurred without any added growth factors. Boron alone cleared the way for bone-building signals to flow, parallel to how forge flux clears the oxide scale before filler metal can bond.

Section 6: The Mitochondria as a Biological Nuclear Reactor

This is where all three industrial analogies converge on a single biological system: the mitochondrion.

Your mitochondria are not just energy factories in a vague, textbook sense. Their operating principles mirror nuclear reactor engineering with a precision that is worth examining carefully, because this is exactly where boric acid’s role as a radical manager becomes most biologically relevant.

Controlled Energy Release

A nuclear reactor extracts energy from uranium through a carefully regulated chain reaction rather than a single explosive detonation. Mitochondria do the same with chemical energy. The electron transport chain (ETC) strips high-energy electrons from NADH and FADH₂ and passes them through Complexes I, III, and IV in the inner mitochondrial membrane, releasing energy in precise, stepwise increments rather than all at once. [11] Uncontrolled release of that energy at any single point would destroy the system. The engineering principle in both cases is the same: managed, staged energy extraction.

The Proton Gradient as the Turbine

In a nuclear plant, heat from fission converts water to pressurized steam that spins a turbine to generate electricity. In mitochondria, the energy from electron flow pumps protons (H⁺) across the inner membrane into the intermembrane space, building a proton-motive force. This gradient then drives ATP synthase, a physically rotating molecular turbine, to synthesize ATP. [12] This process, called chemiosmosis, is functionally identical in its engineering logic to steam-driven electricity generation. The fuel changes. The turbine principle does not.

Double Membrane as the Containment Vessel

Nuclear reactors use containment vessels to confine dangerous reactions. Mitochondria use a double-membrane system, with an outer membrane and a highly folded inner membrane called the cristae, to compartmentalize the chemistry and maximize the surface area available for energy conversion [13]. The geometry in both cases serves the same engineering purpose: contain the reaction, concentrate the output, and protect the surrounding environment from the byproducts.

Reactive Oxygen Species as Radiation Leakage

When electrons occasionally slip off the ETC and react with oxygen, they generate superoxide (O₂⁻), the mitochondrial equivalent of radiation leakage from a reactor. [14] Superoxide is converted to hydrogen peroxide (H₂O₂) by superoxide dismutase (SOD). When H₂O₂ encounters free iron in the iron-rich mitochondrial matrix, the Fenton reaction produces the hydroxyl radical (- OH), the most reactive and damaging ROS in biology. [15, 16]

Because mitochondrial DNA (mtDNA) sits directly adjacent to this reaction zone without the protection of histone proteins, it suffers disproportionate oxidative damage. This is a leading molecular mechanism of mitochondrial aging and age-related disease. [14, 15]

This is precisely the same problem that nuclear engineers face with radiolysis. In both systems, the energy extraction process inevitably generates - OH radicals. In both systems, those radicals must be chemically managed or they will degrade structural integrity. And in both systems, borate chemistry is part of the management solution.

When boric acid is present within the mitochondrial matrix, the alkaline pH modestly favors its conversion to active borate and increased - OH scavenging activity. [17, 18] The mitochondrion, like the reactor coolant, creates the precise chemical environment in which borate is reactive against hydroxyl radicals. This is not coincidence. It reflects the pH-gating of borate chemistry responding to the same engineering problem in two very different contexts.

Section 7: What Happens When the Systems Run Without Protection

A forge without flux produces welds that appear solid on the surface but contain buried oxide contamination layers. Under load, those joints fail at a fraction of their intended strength. Glass produced without adequate boron devitrifies under heat cycling, developing crystalline regions that scatter light and create stress fracture points. A nuclear reactor whose coolant chemistry is poorly managed suffers accelerating corrosion damage in its pressure vessels and piping, ultimately threatening the integrity of the entire system.

Boron deficiency produces analogous failures in the human body, and the evidence for this has been accumulating steadily since the early 1980s when Forrest Nielsen and colleagues at the USDA Grand Forks Human Nutrition Research Center began systematically studying boron deprivation in humans and animals. [7, 19]

The documented consequences of low boron status include impaired bone mineralization and reduced osteoblast activity [7, 12], elevated inflammatory markers consistent with increased oxidative stress [8], disrupted steroid hormone metabolism including reduced estrogen and testosterone levels [20], dysregulated vitamin D activation (a 49-day repletion trial with 3 mg/day sodium borate raised 25(OH)D₃ levels by 39%) [20], elevated plasma homocysteine and reduced S-adenosylmethionine, biomarkers implicated in arthritis, osteoporosis, cognitive decline, and cardiovascular disease [20], and cognitive impairment reflected in EEG studies showing that low boron intake shifts brain electrical activity toward low-frequency patterns associated with reduced alertness and mental performance. [20]

The modern dietary reality sharpens the concern. Boron is richest in raisins, prunes, avocados, almonds, chickpeas, lentils, and dark leafy greens. [20] These are precisely the foods most displaced by ultra-processed food consumption in Western diets. Intensive monoculture agriculture and the widespread use of boron-poor synthetic fertilizers have further depleted soil boron levels in many regions, reducing the boron content of even whole plant foods. [7] Estimated optimal intake based on human deprivation studies and clinical data falls in the range of 3 to 10 mg per day. [19] Average Western dietary intake is approximately 1 to 2 mg per day. [19] The gap between what the body needs and what modern diets typically provide is not trivial.

Section 8: Optimizing Boron — Practical Considerations

Curious note: I do not have any financial interest in any of these companies or products for sale. I make no commissions or profits from the sale any supplement. The only way I am compensated for my work is through the support of generous paid subscribers on Substack.

Addressing suboptimal boron intake does not require exotic interventions. A diet intentionally built around boron-dense whole foods goes a long way. Among the best dietary sources are raisins and prunes (2 to 4 mg per 100g), avocados (approximately 2 mg per fruit), almonds (approximately 2.5 mg per ounce), chickpeas and lentils, and broccoli and other cruciferous vegetables. [20]

For those who supplement, four forms are commonly available: borax (sodium tetraborate), potassium borate, boron citrate, or boron glycinate. All four are well absorbed orally and converted to boric acid in the gastrointestinal tract before entering systemic circulation. Pay attention to the amount of elemental boron in whichever you choose. I personally use 20 Mule Team Borax which I take based upon my own research on purity, bioavailability, and cost. [20] The debate over relative bioavailability is ongoing, but current evidence does not show clinically meaningful differences between forms at equivalent boron doses.

Boron’s biological actions are also deeply synergistic with magnesium, vitamin D, and calcium. Boron deprivation worsens magnesium deficiency outcomes, impairs vitamin D activation, and dysregulates calcium metabolism. [19, 20] These minerals work as an integrated network, and optimizing one without the others produces incomplete results.

As discussed previously, there is a therapeutic window for boron which should be respected. The target is optimization, not maximization. This subject was covered thoroughly in this article.

Closing: The Ancient Chemistry in Every Cell

The glassmakers of ancient Rome, the blacksmiths of medieval Europe, and the nuclear engineers of the twentieth century each discovered, through the logic of their respective crafts, that a particular boron compound could solve a specific and difficult problem. Stabilize the network structure. Clear the contaminants. Manage the radicals.

They did not know they were converging on the same chemistry that had already been intelligently embedded in the biological machinery of life. The mitochondrion in your cells runs on the same engineering principles as a nuclear reactor, extracts energy through the same gradient-turbine logic, and generates the same dangerous radical byproducts. The cell surface glycocalyx is stabilized by the same cross-linking chemistry that makes borosilicate glass resistant to thermal shock. The enzyme active sites are protected from oxidative contamination by the same Lewis acid mechanism that keeps forged steel joints clean.

Boron is not a pharmacological intervention. It is a structural and purifying element that biological systems appear to depend on at the deepest level of their operation. The forge needs its flux. The glass melt needs its structural network former. The reactor needs its radical buffer. So, evidently, do we. Ensuring that boron intake meets the body’s biological requirements is not alternative medicine. It is applied biochemistry, written in the same chemical language that built some of humanity’s most durable and reliable technologies.

References

1. Zeng L, Sun H, Peng T. Effect of Borax On Sintering Kinetics, Microstructure and Mechanical Properties of Porous Glass-Ceramics From Coal Fly Ash by Direct Overfiring. Front Chem. 2022 Mar 17;10:839680. https://pmc.ncbi.nlm.nih.gov/articles/PMC8968146/

2. Rio Tinto Borax. (2019). Borates in metallurgical applications [Technical bulletin]. Borax.com. https://www.borax.com/resources/technical-bulletin/borates-in-metallurgical-applications

3. Bhatt, D. L., Bhattacharya, S., & colleagues. (2024). The reactivity of hydroxyl radicals toward boric acid as a function of pH. Journal of Physical Chemistry A 128(35), 7321-7330. https://doi.org/10.1021/acs.jpca.4c03933

4. Springsteen, G., & Wang, B. (2002). A detailed examination of boronic acid-diol complexation. Tetrahedron, 58(26), 5291-5300. https://doi.org/10.1016/S0040-4020(02)00489-1

5. Hunt, C. D. (2003). Dietary boron: An overview of the evidence for its role in immune function. Journal of Trace Elements in Experimental Medicine, 16(4), 261-271. https://scispace.com/pdf/dietary-boron-an-overview-of-the-evidence-for-its-role-in-130v40hhur.pdf

6. Ellis GA, Palte MJ, Raines RT. Boronate-mediated biologic delivery. J Am Chem Soc. 2012 Feb 29;134(8):3631-4. https://pmc.ncbi.nlm.nih.gov/articles/PMC3304437/

7. Nielsen, F. H. (2008). Is boron nutritionally relevant? Nutrition Reviews, 66(4), 183–191. https://doi.org/10.1111/j.1753-4887.2008.00023.x

8. Serdaroglu Kasikci E, et al. Protective Effect of Boric Acid on Oxidative Damage and Cognitive Function in Aging Modeled Rats. Medeni Med J. 2025 Mar 28;40(1):18-25. https://pmc.ncbi.nlm.nih.gov/articles/PMC11974467/

9. Paties Montagner G, et al. Redox Mechanisms Underlying the Cytostatic Effects of Boric Acid on Cancer Cells-An Issue Still Open. Antioxidants (Basel). 2023 Jun 19;12(6):1302. https://pmc.ncbi.nlm.nih.gov/articles/PMC10294879/

10. Rico P, et al. Borax induces osteogenesis by stimulating NaBC1 transporter via activation of BMP pathway. Commun Biol. 2020 Nov 27;3(1):717. https://pmc.ncbi.nlm.nih.gov/articles/PMC7695834/

11. Wilson DF. Oxidative phosphorylation: regulation and role in cellular and tissue metabolism. J Physiol. 2017 Dec 1;595(23):7023-7038. https://pmc.ncbi.nlm.nih.gov/articles/PMC5709332/

12. Junge, Wolfgang & Nelson, Nathan. (2015). ATP Synthase. Annual Review of Biochemistry. 84. 631-657. 10.1146/annurev-biochem-060614-034124. Full article

13. Joubert F, Puff N. Mitochondrial Cristae Architecture and Functions: Lessons from Minimal Model Systems. Membranes (Basel). 2021 Jun 23;11(7):465. https://pmc.ncbi.nlm.nih.gov/articles/PMC8306996/

14. Turrens, J. F. (2003). Mitochondrial formation of reactive oxygen species. The Journal of Physiology, 552(2), 335–344. https://doi.org/10.1113/jphysiol.2003.049478

15. Cadenas, E., & Davies, K. J. A. (2000). Mitochondrial free radical generation, oxidative stress, and aging. Free Radical Biology and Medicine, 29(3-4), 222–230. https://doi.org/10.1016/S0891-5849(00)00317-8

16. Murphy, M. P. (2009). How mitochondria produce reactive oxygen species. Biochemical Journal, 417(1), 1–13. https://doi.org/10.1042/BJ20081386

17. Petersson F, Jonsson M. The Reactivity of Hydroxyl Radicals toward Boric Acid as a Function of pH. J Phys Chem A. 2024 Sep 12;128(36):7593-7600. https://pmc.ncbi.nlm.nih.gov/articles/PMC11403659/

18. Poburko D, Santo-Domingo J, Demaurex N. Dynamic regulation of the mitochondrial proton gradient during cytosolic calcium elevations. J Biol Chem. 2011 Apr 1;286(13):11672-84. https://pmc.ncbi.nlm.nih.gov/articles/PMC3064219/

19. Nielsen FH, Eckhert CD. Boron. Adv Nutr. 2020 Mar 1;11(2):461-462. https://pmc.ncbi.nlm.nih.gov/articles/PMC7442337/

20. Pizzorno L. Nothing Boring About Boron. Integr Med (Encinitas). 2015 Aug;14(4):35-48. https://pmc.ncbi.nlm.nih.gov/articles/PMC4712861/

Part 1 — Skin Cancer Testimonial

A young woman in Latin America.

(Translated from Spanish)

Experimental treatment for 3 carcinomas:

“I had 3 hard, very heavy tumours, so big that they almost prevented me from breathing. At night, while sleeping, I had blood that would get me into my nose and choked me.

After 2 weeks of CDS [protocols C and D], I felt that the tumours were drying up more and more. After 3 days, my tumours were gone like sand and my new nose appeared.

I had an appointment with the doctor who told me that my tumours should be reduced before I intervened on my nose (no details of what the doctor had planned). I went to my appointment at the medical office to do a biopsy and the secretary, who had seen the pictures of my sick nose, after I removed my mask screamed - it was a miracle, it’s a miracle! - Fortunately, my aunt who accompanied me was able to confirm my remarks by testifying.”

Part 2 — Protocol Link

Given the reported use of “protocols C and D” for cutaneous carcinomas on the nose:

Protocol C

Protocol D

Part 3 — Possible Mechanisms of Action

The mechanisms of action of ClO2 for this reported carcinoma likely converge on reactive oxygen species (ROS)-mediated cytotoxicity and apoptosis as chlorine dioxide’s proposed anticancer mechanism. Kim et al. showed ClO₂ induces significant, dose-dependent cytotoxicity in breast and colorectal cancer cell lines, with vitamin E (an antioxidant) partially rescuing cell viability — indicating ROS as the causal cytotoxic agent, since cancer cells reportedly carry a higher baseline ROS burden than normal cells and are therefore more vulnerable to further oxidative push. [1] Yıldız et al. extended this to small-cell lung cancer cells, showing ClO₂ triggers apoptosis via nuclear blebbing, vacuolar formation, and G2/M cell-cycle arrest, with markedly less toxicity toward normal endothelial (HUVEC) cells. [2] A separate patent document proposes ClO₂-based formulations (topical, injectable, or oral) as apoptosis inducers for a long list of cancers, including skin cancer, squamous cell carcinoma, and basal cell carcinoma, framing the mechanism as selective induction of programmed cell death in aberrant/senescent cells while sparing normal tissue. Chlorine dioxide’s “size-selective” oxidative action is proposed to destroy microorganisms and abnormal cells more readily than large, antioxidant-defended human cells, and separately notes ClO₂ can accelerate wound healing via cGMP/guanylate cyclase induction. [3, 4]

References

1. Kim, Yonggyun & Kumar, Sunil & Cheon, Wonsu & Eo, Hyun & Kwon, Hyeok & Jeon, Yongho & Jung, Jinboo & Kim, Wook. (2016). Anticancer and Antiviral Activity of Chlorine Dioxide by Its Induction of the Reactive Oxygen Species. Journal of Applied Biological Chemistry. 59. 31-36. Full Article

2. Yıldız SZ, Bilir C, Eskiler GG, Bilir F. The Anticancer Potential of Chlorine Dioxide in Small-Cell Lung Cancer Cells. Cureus. 2022 Oct 6;14(10):e29989. Retraction in: Cureus. 2025 Oct 16;17(10):r194. https://pmc.ncbi.nlm.nih.gov/articles/PMC9636887/

3. Cell apoptosis inducer containing chlorine dioxide and application thereof to preparation of cosmetics, or anti-aging or antineoplastic drugs (China Patent No. CN103720709A). (2013, December 12). China National Intellectual Property Administration. https://patents.google.com/patent/CN103720709A/en

4. Alliger, H. (2019, November 5). Method and compositions for treating cancerous tumors (U.S. Patent No. 10,463,690 B2). U.S. Patent and Trademark Office. https://patents.google.com/patent/US10463690B2/en

Welcome to Module 4.2 of Magnesium Mastery. In the previous module, we established the broad scope of magnesium’s role in cellular and metabolic function. In this module, we focus on the most foundational of those roles: magnesium’s indispensable position at the center of ATP production and bioenergetics. Without understanding this relationship, it is difficult to fully appreciate why magnesium deficiency can produce such a wide and seemingly unrelated constellation of symptoms. By the end of this module, you will understand exactly how magnesium enables the cell to produce, transfer, and utilize energy and what happens at the molecular and clinical level when it does not.

This article continues the building of a comprehensive course on magnesium which will be part of a much larger project: a free, fully open-access mega-course covering all vitamins and minerals.

If it has been a while since you’ve followed the series, or if you are new, here are the previous units to review:

Unit 1: Introduction to Magnesium

Unit 2: Magnesium and the Cardiovascular System

Unit 3: Magnesium and the Endocrine System

All of these units will eventually be organized into structured free courses hosted on a dedicated platform (TheVitaminCourse.com), which is currently under development. The long-term goal is to provide high-quality, comprehensive education—completely free—to professionals, laypeople, and even younger learners.

This work is offered freely as part of a larger mission. If you would like to support and help sustain this effort, maintaining a paid subscription is one of the most direct ways to do so and enables continued research, writing, and course development.

Section 1: The Mg-ATP Complex — Why Free ATP Is Not Enough

Every cell in the human body runs on adenosine triphosphate (ATP), the universal energy currency of life. Students and clinicians alike are taught that ATP provides the energy for muscle contraction, ion transport, biosynthesis, and signaling. What is far less commonly taught is that free ATP, on its own, is not the biologically active form.

To be used as a substrate by the vast majority of ATP-dependent enzymes, ATP must first bind a magnesium ion. The resulting complex, Mg-ATP, is the true substrate for hundreds of enzymatic reactions, including those central to mitochondrial energy metabolism. The magnesium ion coordinates with the beta and gamma phosphate groups of ATP, stabilizing the molecule’s highly charged triphosphate tail and positioning it correctly within enzyme active sites. Without this coordination, ATP is geometrically and electrostatically unable to engage the catalytic machinery of most ATP-dependent enzymes efficiently. [1, 2, 3]

This distinction has profound clinical implications. A patient may have a serum ATP level that appears adequate and yet still be functionally energy-depleted at the cellular level if intracellular free magnesium is insufficient to generate adequate Mg-ATP. The cell’s energetic problem in magnesium deficiency is not simply that ATP is made in lower quantities, it is that the ATP available cannot be fully utilized. [2, 4, 5]

The specificity of the Mg-ATP requirement extends across metabolic pathways. Hexokinase, phosphofructokinase, pyruvate kinase, and adenylate kinase, all key enzymes in glycolysis, use Mg-ATP as their substrate. ATP synthase, the enzyme responsible for producing the majority of cellular ATP via mitochondrial oxidative phosphorylation, requires magnesium both as a substrate component and as a direct activator. This means magnesium sits at both ends of the energy cycle: it is needed to make ATP via the mitochondrial machinery, and it is needed to use ATP once it has been made. [3, 6]

Section 2: Magnesium Inside the Mitochondria

Mitochondria are not passive recipients of cytosolic magnesium. They maintain their own regulated pool of Mg²⁺, and the dynamics of this intramitochondrial magnesium are increasingly recognized as critical determinants of cellular energy status and metabolic resilience. [4, 7]

The primary gateway for magnesium entry into the mitochondrial matrix is MRS2 (Mitochondria RNA Splicing 2 protein), a magnesium-selective channel embedded in the inner mitochondrial membrane. MRS2 is the mammalian homolog of a yeast splicing factor that was found to be structurally similar to bacterial CorA magnesium channels. [4, 8]

Landmark research using fluorescence imaging and metabolomic analysis in MRS2 knockdown cells demonstrated that disruption of mitochondrial Mg²⁺ homeostasis fundamentally alters energy metabolism. Cells with reduced MRS2 activity showed: [4, 8]

• A shift in mitochondrial energy metabolism away from oxidative phosphorylation

• Altered mitochondrial morphology consistent with dysfunction

• Reduced ATP production

• Increased vulnerability to cellular stress

These findings established that it is not simply the presence of magnesium in the cytosol that matters; it is whether mitochondria can maintain their own adequate magnesium concentration via regulated uptake. Intramitochondrial Mg²⁺ is a semi-independent variable that responds to physiological stimuli and cannot simply be inferred from serum or even cytosolic magnesium levels. [4, 7, 8]

A June 2026 landmark review in Aging Cell articulated this position most forcefully, describing magnesium as a “bioenergetic checkpoint” that orchestrates mitochondrial function and metabolic resilience across a range of conditions including metabolic disease and aging. This framing captures an important truth: magnesium does not simply participate in mitochondrial reactions as one cofactor among many, it exercises regulatory control over the rate and efficiency of the entire mitochondrial energy-producing apparatus. [5]

Section 3: Magnesium and the Electron Transport Chain

The electron transport chain (ETC) is the heart of mitochondrial ATP production, comprising four major protein complexes (Complex I through IV) embedded in the inner mitochondrial membrane. Electron flow through these complexes drives proton pumping across the membrane, generating the proton motive force that powers ATP synthase. Magnesium is involved at multiple levels of this system.

Complex I (NADH:ubiquinone oxidoreductase) is the largest and most complex entry point into the ETC. Its assembly, structural stability, and catalytic activity are supported by magnesium-dependent processes, including the Mg-ATP-driven protein folding and chaperone functions required for its correct assembly. Dysfunction of Complex I is one of the most common mitochondrial defects associated with clinical disease, and magnesium deficiency has been shown to reduce Complex I activity in experimental models. [4, 7, 9]

Complex V (ATP synthase) is where magnesium’s role is most directly characterized. This molecular motor, which rotates to synthesize ATP from ADP and inorganic phosphate, requires Mg²⁺ both as a structural component and as part of the catalytic mechanism. MgADP, not free ADP, is the true substrate transported into the F₁ catalytic head, and MgATP is the product released. Disruption of intramitochondrial Mg²⁺ concentrations therefore directly impairs the final and most productive step of cellular energy generation. [2, 6]

The ADP/ATP translocator (ANT), which exchanges newly synthesized ATP for cytosolic ADP across the inner mitochondrial membrane, also demonstrates magnesium-dependent kinetics. Early kinetic work in plant mitochondria demonstrated that higher magnesium concentrations increase ADP import and accelerate ATP synthesis via ATP synthase, a regulatory pattern subsequently confirmed for the mammalian ANT using direct kinetic assays of ATP-ADP exchange, establishing magnesium as a positive regulator of net ATP flux across the inner mitochondrial membrane. [10, 11]

Section 4: Magnesium, Mitochondrial Membrane Potential, and ROS

The mitochondrial membrane potential, the electrical gradient maintained across the inner mitochondrial membrane, is the immediate driving force for ATP synthesis and a sensitive indicator of mitochondrial health. Adequate Mg²⁺ is required to maintain the mitochondria membrane potential. When intracellular magnesium is depleted, mitochondrial membrane potential falls, ATP synthesis slows, and the electron transport chain becomes inefficient, leading to premature electron leak and the generation of reactive oxygen species (ROS). [7, 12]

This relationship between magnesium depletion, membrane potential disruption, and ROS overproduction is one of the most important mechanistic links between magnesium status and chronic disease. ROS generated by a dysfunctional ETC damage mitochondrial membranes, oxidize mitochondrial DNA (which has limited repair capacity compared to nuclear DNA), and inactivate key ETC proteins, creating a self-amplifying cycle of mitochondrial deterioration. [12, 13, 14]

Research in Communications Biology has specifically demonstrated that intracellular Mg²⁺ protects mitochondria from oxidative stress by preserving membrane potential under oxidative challenge and reducing the amplitude of ROS bursts. When Mg²⁺ levels are experimentally reduced, cells become measurably more vulnerable to oxidant-induced mitochondrial damage and ATP loss. [12]

A complementary line of evidence comes from studies on the TRPM7 channel (Transient Receptor Potential Melastatin 7), a bifunctional ion channel-kinase that regulates cellular and mitochondrial Mg²⁺ uptake. Research has shown that hypomagnesemia driven by TRPM7 dysfunction impairs mitochondrial function, reduces ATP output, and amplifies inflammatory signaling which connects the cellular magnesium entry mechanism directly to mitochondrial bioenergetics and to inflammatory disease states. [15]

Section 5: Magnesium and the Krebs Cycle

Before electrons can enter the ETC, the cell must generate the electron carriers NADH and FADH₂ through the citric acid cycle (Krebs cycle). Magnesium is a required cofactor for five of the eight Krebs cycle enzymes, including:

• Isocitrate dehydrogenase: catalyzes the first oxidative decarboxylation step and is directly activated by Mg²⁺

• α-Ketoglutarate dehydrogenase complex: another key decarboxylation step; requires Mg²⁺ for CoA-binding activity

• Succinyl-CoA synthetase: generates GTP (equivalent to ATP) directly within the cycle

• Malate dehydrogenase and citrate synthase: activities are modulated by intramitochondrial Mg²⁺ concentration. [3, 7]

• The cumulative consequence of magnesium’s role across these enzymes is that the entire throughput of the Krebs cycle is sensitive to intramitochondrial Mg²⁺ status. Inadequate magnesium does not simply slow one step, it reduces the rate of NADH and FADH₂ generation simultaneously across multiple checkpoints, starving the ETC of electron donors and reducing ATP yield per unit of substrate consumed. [4, 7]

Section 6: The Bioenergetic Checkpoint Model

The most integrative framework for understanding magnesium’s mitochondrial role comes from a 2026 review in Aging Cell, which positions magnesium as a bioenergetic checkpoint; a regulatory node that links mitochondrial performance to whole-body metabolic resilience. This model proposes that magnesium’s simultaneous influence over substrate metabolism (Krebs cycle), electron transport (Complex I, Complex V), ATP export (ANT), ROS management, and membrane potential maintenance means it functions as a master coordinator of mitochondrial output rather than simply a passive cofactor. [5, 7]

In practical terms, this framework predicts that states of chronic low magnesium create a metabolically constrained mitochondria phenotype: cells produce less ATP per unit of substrate, generate more ROS per unit of oxygen consumed, maintain lower mitochondrial membrane potential, and are more vulnerable to additional stressors. This constrained phenotype is a mechanistic driver of conditions including metabolic syndrome, type 2 diabetes, cardiovascular disease, and accelerated aging. [5]

Supporting this model, a study in EMBO Molecular Medicine used a mouse model of Hutchinson-Gilford progeria syndrome, a disease of accelerated aging, and found that dietary magnesium supplementation improved ATP availability, reduced oxidative stress, and extended lifespan in these animals. These findings suggest that magnesium’s mitochondrial role is not limited to day-to-day cellular housekeeping but is relevant to the deeper biology of aging and age-related disease. [16]

Section 7: Animal Studies

Controlled animal studies have provided consistent and reproducible evidence for the consequences of magnesium deficiency on mitochondrial function. Research conducted across multiple species — including rats, mice, and guinea pigs — has demonstrated that dietary magnesium deprivation leads to measurable reductions in mitochondrial ATP output, decreased Krebs cycle enzyme activity, increased mitochondrial ROS production, and reduced Complex I function. Importantly, these defects are reversed upon magnesium repletion, establishing a clear causal relationship rather than mere correlation. [7, 9]

Studies using MRS2 knockdown models have further confirmed that it is specifically mitochondrial magnesium, not just systemic or cytosolic magnesium, that determines cellular energy status and stress vulnerability. These experiments demonstrated that even under conditions of normal cytosolic magnesium, selective depletion of mitochondrial Mg²⁺ was sufficient to impair oxidative phosphorylation, alter mitochondrial morphology, and increase susceptibility to apoptotic stimuli. [4, 8]

Section 8: Cellular & Human Studies

Study 1: Intracellular Mg²⁺, ADP, and ATP Dynamics (Gout et al., PNAS 2014)

A foundational study published in the Proceedings of the National Academy of Sciences used ³¹P-NMR spectroscopy in plant cell cultures to directly measure free Mg²⁺, ADP, and ATP concentrations simultaneously within a living cell, one of the first demonstrations of this kind of real-time, compartment-specific measurement. Although the study used plant cells rather than human tissue, its central finding, that cytosolic free Mg²⁺ concentration dynamically regulates the ratio of free ADP to Mg-ATP in both the cytosol and mitochondria, and that fluctuations in cellular Mg²⁺ directly modulate the rate of mitochondrial respiration, describes a conserved biochemical mechanism. The same Mg-ADP-ATP relationship has since been confirmed in mammalian systems by subsequent research cited throughout this module, including Yamanaka et al. [4] and Fujita et al. [12] This makes the Gout et al. findings a mechanistic foundation for the human and animal evidence discussed in the remainder of this section. [2]

Study 2: Magnesium, Fatigue, and Mitochondrial Function in Clinical Populations

Clinical studies in populations with chronic fatigue and unexplained energy impairment have found associations between low intracellular magnesium status and reduced mitochondrial ATP production capacity. The landmark case-control and clinical trial in patients with chronic fatigue syndrome found that patients had significantly lower red blood cell magnesium levels than matched controls, and that magnesium sulfate supplementation improved energy levels, emotional state, and functional capacity compared with placebo — findings consistent with the mitochondrial mechanism outlined above. [13, 17]

Study 3: Magnesium Supplementation and Mitochondrial ROS (Zheltova et al., 2016)

A study examining the relationship between magnesium status and oxidative stress markers in humans found that magnesium deficiency was consistently associated with elevated malondialdehyde (MDA) — a marker of lipid peroxidation — and reduced antioxidant enzyme activity. Magnesium supplementation reversed these markers, consistent with the restoration of mitochondrial ROS management. [13]

Study 4: TRPM7, Hypomagnesemia, and Mitochondrial Dysfunction

Clinical and mechanistic investigations into TRPM7 channel function have linked acquired hypomagnesemia to impaired mitochondrial ATP production and amplified inflammatory signaling in cardiac and hepatic tissues. These human data reinforce the concept that maintaining adequate cellular Mg²⁺ uptake via TRPM7 and MRS2 is a prerequisite for sustained mitochondrial performance. [15]

Section 9: Case Study

Case Study: A 47-Year-Old Woman With Persistent Fatigue and Exercise Intolerance

Patient Background

A 47-year-old female nurse presents with a six-month history of persistent fatigue, difficulty completing her usual exercise routine, and a general sense of “running on empty” despite adequate sleep. She reports muscle heaviness after exertion that takes longer than expected to resolve. Her medical history is notable for type 2 diabetes managed with metformin (1,000 mg twice daily) and a diagnosis of GERD for which she has been taking omeprazole (20 mg daily) for three years. She eats a diet high in convenience foods and consumes minimal fruits, nuts, or leafy greens. Routine labs show a serum magnesium of 1.8 mg/dL — at the lower boundary of the normal reference range — along with mildly elevated fasting glucose despite metformin adherence.

Clinical Management

Her physician notes several converging risk factors for functional magnesium depletion: chronic proton pump inhibitor (PPI) use, which impairs intestinal magnesium absorption; metformin, which is associated with increased renal magnesium wasting in some patients; a magnesium-poor diet; and type 2 diabetes, itself associated with increased renal magnesium excretion. A red blood cell (RBC) magnesium level is ordered as a more sensitive indicator of intracellular magnesium status and returns at the lower end of the reference range, consistent with subclinical intracellular depletion.

The physician explains that the Mg-ATP complex is the biologically active form of ATP, and that even modestly low intracellular magnesium can impair mitochondrial oxidative phosphorylation, reduce ATP synthesis efficiency, and increase mitochondrial ROS production — mechanisms directly consistent with her symptoms of fatigue and post-exertional heaviness. Magnesium glycinate 200 mg is initiated twice daily with meals to minimize gastrointestinal side effects and maximize absorption. Dietary counseling is provided, emphasizing magnesium-rich foods including almonds, pumpkin seeds, spinach, and whole grains. The PPI dose is reviewed and a proton pump inhibitor deprescribing trial is considered given her GERD has been stable.

Outcome and Follow-Up

At eight weeks, the patient reports meaningful improvement in her energy levels and reduced post-exertional fatigue. She has resumed her exercise routine without the prolonged recovery she previously experienced. A repeat RBC magnesium level shows improvement into the mid-normal range. Her fasting glucose has also modestly improved, consistent with magnesium’s role in insulin signaling and glucose metabolism — which will be covered in greater depth in Module 4.3. She is advised to continue magnesium supplementation and to maintain dietary vigilance, given her ongoing PPI use and metabolic risk factors.

Section 10: Clinical Implications

The mechanisms reviewed in this module have direct relevance to everyday clinical practice. Consider the following key takeaways:

• Fatigue is the most common and underrecognized consequence of impaired Mg-ATP production. Patients with chronic fatigue, reduced exercise tolerance, or unexplained “energy poverty” — especially those with risk factors for magnesium depletion such as PPI use, diuretics, diabetes, or a processed-food diet — warrant assessment of magnesium status beyond the standard serum level.

• Serum magnesium is a poor proxy for mitochondrial and cellular magnesium status. The mitochondrial Mg²⁺ pool is regulated independently of cytosolic levels, and MRS2-mediated uptake into mitochondria represents a distinct variable that is not captured by any standard clinical test. RBC magnesium or 24-hour urinary magnesium provide modestly better insight, but no perfect clinical test currently exists. Clinical judgment, dietary history, and the totality of symptoms remain essential.

• Polypharmacy is a significant and underappreciated driver of functional magnesium depletion. PPIs, loop diuretics, thiazide diuretics, metformin, and certain immunosuppressants all contribute to magnesium depletion by impairing absorption or increasing renal excretion. Patients on multiple such agents may experience compounding mitochondrial effects.

• Magnesium depletion and mitochondrial dysfunction are mutually reinforcing. Increased mitochondrial ROS production caused by magnesium deficiency damages mitochondrial membranes and enzymes, further impairing the cell’s ability to maintain its magnesium gradients — a self-amplifying cycle that makes early intervention more effective than late correction.

• Supplementation form matters for bioavailability. Magnesium glycinate and magnesium citrate are well-tolerated and bioavailable forms suitable for addressing acute cellular and mitochondrial depletion. Magnesium oxide — the most widely available over-the-counter form — has poor bioavailability and is less appropriate when cellular repletion is the goal.

Conclusion

In this module, we have examined magnesium’s role as a foundational requirement for mitochondrial ATP production. From the Mg-ATP complex — the biologically active form of ATP — to magnesium’s direct regulatory functions in F₀F₁-ATP synthase, the Krebs cycle, Complex I of the electron transport chain, ADP/ATP translocator activity, and mitochondrial ROS management, it is clear that magnesium is not merely a participant in bioenergetics. It is a central checkpoint through which the cell coordinates the rate, efficiency, and safety of energy production. When that checkpoint fails due to inadequate magnesium, the consequences ripple outward — impairing every system that depends on adequate ATP supply, which is ultimately every system in the body. [5]

In Module 4.3, we will build on this foundation by examining magnesium’s role as a cofactor across the broader landscape of cellular enzymes — including those governing glycolysis, the insulin signaling cascade, and core biosynthetic pathways — and connect these functions to clinical metabolic disease.

References

1. Dunn J, Grider MH. Physiology, Adenosine Triphosphate. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023. https://www.ncbi.nlm.nih.gov/books/NBK553175/

2. Gout E, Rébeillé F, Douce R, Bligny R. Interplay of Mg2+, ADP, and ATP in the cytosol and mitochondria: unravelling the role of Mg2+ in cell respiration. Proc Natl Acad Sci U S A. 2014 Oct 28;111(43):E4560-7. https://pmc.ncbi.nlm.nih.gov/articles/PMC4217410/

3. de Baaij JH, Hoenderop JG, Bindels RJ. Magnesium in man: implications for health and disease. Physiol Rev. 2015;95(1):1-46. https://journals.physiology.org/doi/full/10.1152/physrev.00012.2014

4. Yamanaka R, Tabata S, Shindo Y, Hotta K, Suzuki K, Soga T, Oka K. Mitochondrial Mg(2+) homeostasis decides cellular energy metabolism and vulnerability to stress. Sci Rep. 2016 Jul 26;6:30027. https://pmc.ncbi.nlm.nih.gov/articles/PMC4960558/

5. Huang CW, Wen CY, Tsai AP, Wang B, Tsui KH, Hsu YJ, Li CJ. Magnesium as a Bioenergetic Checkpoint Linking Mitochondrial Function, Metabolic Disease, and Aging. Aging Cell. 2026 Jun;25(6):e70578. https://pmc.ncbi.nlm.nih.gov/articles/PMC13238608/

6. Ko Y, Hong S, Pedersen P. Chemical Mechanism of ATP Synthase. Journal of Biological Chemistry, 1999; 274, 28853-28856. https://www.jbc.org/article/S0021-9258(19)51912-3/fulltext

7. Pilchova I, Klacanova K, Tatarkova Z, Kaplan P, Racay P. The Involvement of Mg2+ in Regulation of Cellular and Mitochondrial Functions. Oxid Med Cell Longev. 2017;2017:6797460. https://pmc.ncbi.nlm.nih.gov/articles/PMC5516748/

8. Piskacek M, Zotova L, Zsurka G, Schweyen RJ. Conditional knockdown of hMRS2 results in loss of mitochondrial Mg(2+) uptake and cell death. J Cell Mol Med. 2009 Apr;13(4):693-700. https://pmc.ncbi.nlm.nih.gov/articles/PMC3822876/

9. Arancibia-Hernández, Y. L., Hernández-Cruz, E. Y., & Pedraza-Chaverri, J. (2023). Magnesium (Mg2+) deficiency, not well-recognized non-infectious pandemic: Origin and consequence of chronic inflammatory and oxidative stress-associated diseases. Cellular Physiology and Biochemistry, 57(S1), 1–23. https://www.cellphysiolbiochem.com/Articles/000603/index.html

10. Busch, K., & Ninnemann, H. (1997). The controlling influence of ADP, ATP and magnesium on the activities of adenylate kinase, ATP synthase, ADP/ATP translocator and the mitochondrial respiration in plants. Plant Science, 128(1), 85–95. https://doi.org/10.1016/S0168-9452(97)00117-9

11. Chinopoulos, C., Vajda, S., Csanády, L., Mándi, M., Máthé, K., & Adam-Vizi, V. (2009). A novel kinetic assay of mitochondrial ATP-ADP exchange rate mediated by the ANT. Biophysical Journal, 96(6), 2490–2504. https://pmc.ncbi.nlm.nih.gov/articles/PMC2907717/

12. Fujita K, Shindo Y, Katsuta Y, Goto M, Hotta K, Oka K. Intracellular Mg2+ protects mitochondria from oxidative stress in human keratinocytes. Commun Biol. 2023 Aug 24;6(1):868. https://pmc.ncbi.nlm.nih.gov/articles/PMC10449934/

13. Zheltova AA, Kharitonova MV, Iezhitsa IN, Spasov AA. Magnesium deficiency and oxidative stress: an update. Biomedicine (Taipei). 2016 Dec;6(4):20. https://pmc.ncbi.nlm.nih.gov/articles/PMC5112180/

14. Nadalutti CA, Ayala-Peña S, Santos JH. Mitochondrial DNA damage as driver of cellular outcomes. Am J Physiol Cell Physiol. 2021 Dec 22;322(2):C136-C150. https://pmc.ncbi.nlm.nih.gov/articles/PMC8799395/

15. Liu M, Dudley SC Jr. Beyond Ion Homeostasis: Hypomagnesemia, Transient Receptor Potential Melastatin Channel 7, Mitochondrial Function, and Inflammation. Nutrients. 2023 Sep 9;15(18):3920. https://pmc.ncbi.nlm.nih.gov/articles/PMC10536927/

16. Villa-Bellosta R. Dietary magnesium supplementation improves lifespan in a mouse model of progeria. EMBO Mol Med. 2020 Oct 7;12(10):e12423. https://pmc.ncbi.nlm.nih.gov/articles/PMC7539193/

17. Cox IM, Campbell MJ, Dowson D. Red blood cell magnesium and chronic fatigue syndrome. Lancet. 1991 Mar 30;337(8744):757-760. https://pubmed.ncbi.nlm.nih.gov/1672392/

Part 1 — Testimonial

...I got sick, with what the doctors assumed was Covid. They said this because after the week of me being ill I suddenly developed extreme anxiety out of nowhere...

I also developed GI issues which the doctors said is caused by anxiety...Doctors gave me a bunch of meds and basically said “this is your new life”.

I knew of MMS before because I had really bad psoriasis and I was messaged by quite a few people with information on it...After my anxiety issues I decided I’d put full commitment into it...

...overtime my anxiety and GI symptoms got less and less...

...going from a point of being terrified to go into a store or being away from my car to feeling fine most the time, is something that I didn’t think would happen again.

...Also, my psoriasis has also been pretty much gone too. And this is winter so usually this is when it’s at its worst.

Part 2 — Relevant Protocols

Starting Procedure

Protocol 1000

Protocol D

The general oral protocols (Starting Procedure, Protocol 1000) align with the “full commitment” internal use described, while Protocol D addresses the topical/skin dimension of the psoriasis.

Part 3 — Mechanistic Critique

In my previous articles on the Mechanisms of Action of Chlorine Dioxide Series, I review all of the known and theoretical mechanisms of action of chlorine dioxide. Those articles are fully referenced. I will be using this body of work to help provide an explanation regarding the mechanisms of action for the outcomes of the testimonial above.

Psoriasis — anti-inflammatory ROS effects — The anti-inflammatory effects reactive oxygen species, such as ozone, have been researched in psoriasis and other inflammatory conditions. The proposed mechanism is cytokine modulation: in an experimental rheumatoid arthritis model, ozone reduced pro-inflammatory cytokines IL-12 and TNF-alpha while increasing the anti-inflammatory cytokine IL-10. Since psoriasis is a TNF-alpha and IL-driven inflammatory skin condition, this is a plausible pathway. This same ROS exposure can result in NRF2 activation by mild oxidative stress, which upregulates antioxidant defense enzymes (SOD, catalase, glutathione peroxidase) and could theoretically dampen the oxidative component of psoriatic inflammation.

Anxiety — I have received quite a few other testimonials regarding improvement in anxiety while taking chlorine dioxide, but the literature provides no mechanism connecting chlorine dioxide to central nervous system function, neurotransmitter activity, HPA-axis regulation, or anxiety symptoms specifically. There are quite a few environmental toxins which can be involved in psoriasis conditions like this, I have a hunch that their elimination from the body using chlorine dioxide could potentially improve anxiety symptoms. Also, I think that some underlying undiagnosed infections can cause anxiety, and perhaps an underlying infection was eliminated, resulting in the elimination of anxiety.

GI symptoms — The antimicrobial and biofilm-disruption mechanisms of chlorine dioxide (effective against E. coli, Streptococcus, and biofilm-associated bacteria) could theoretically be invoked if the person’s GI symptoms stemmed from bacterial dysbiosis, since ClO2’s size-selective oxidative action is described as capable of killing micron-scale pathogens while sparing host tissue via the body’s antioxidant defenses.

For a full review of the mechanisms of action of Chlorine Dioxide, please access the Mechanisms of Action of Chlorine Dioxide Series

To review all of the protocols for Chlorine Dioxide please visit the CLO2 Protocol Archive

The European Union classifies boric acid and borax as Category 1B reproductive toxins, placing them in the same regulatory tier as thalidomide-class hazards. Yet a substantial body of animal research spanning goats, rams, rabbits, swine, cattle, poultry, and fish shows that low-to-moderate boron doses actually support or improve fertility parameters. Multiple human epidemiological studies have also clearly demonstrated no reproductive harm, even among workers with high, borax-mining-related occupational exposure. And if that isn’t enough to raise an eyebrow, wait until you see where the EU itself quietly allows borax back into the food supply, a detail that exposes just how selective this “ban” really is. [1, 2]

The Hormetic Pattern Regulators Overlook

Boron does not behave like a linear toxin. Across nearly every species studied, it follows a hormetic, or biphasic, dose-response curve: deficiency and excess both cause harm, while a broad middle range supports reproductive function. [3] The EU’s Category 1B classification stems almost entirely from high-dose rodent studies — particularly the Weir and Fisher two-year rat feeding trial that identified testicular atrophy only above roughly 52 mg B/kg body weight per day, with a robust no-observed-adverse-effect level (NOAEL) around 17.5 mg B/kg bw/day sustained through three generations. Extrapolating that ceiling effect to every boron-containing product, at every dose, misrepresents the actual shape of the data. [4]

What the Animal Literature Actually Shows

Goats: The most thoroughly documented benefit

Dietary borax at roughly 1.1–1.3 mg Boron/kg bw/day significantly raised sperm concentration and total sperm output in adult male goats, correlating with blood and seminal boron levels and upregulating key testicular immune and antioxidant genes. A companion trial at 70 mg boron per kg diet over six months raised serum testosterone and boosted expression of CYP17A1, a core steroidogenesis gene, with histology confirming healthier testicular structure. Boron-enriched semen extenders also produced the highest post-thaw sperm motility in Angora goat cryopreservation trials. [5, 6, 7]

Rams: Testosterone and semen quality rise together

At an estimated 14.0 mg B/kg bw/day using borax-derived boric acid in the diet, rams showed significantly increased testosterone, greater sperm concentration, larger seminal volume, and fewer abnormal sperm over a four-month trial. In Merino ram semen extenders, a modest 0.25 mM boron concentration produced the best post-thaw motility, mitochondrial activity, and viability, while higher concentrations began impairing antioxidant gene expression, illustrating the hormetic effect within a single study. [8, 9]

Rabbits: Every tested dose improved semen quality

Borax supplementation in adult male rabbits significantly increased sperm concentration, total output, motility, live sperm percentage, and normal morphology at every dose level tested, alongside improved antioxidant capacity and testosterone. [10]

Swine: Better piglets, not more piglets

Weanling gilts fed roughly 0.125 mg B/kg bw/day (from borax (sodium borate)) over a long-term trial produced heavier, more viable piglets at weaning and showed improved bone strength in sows without any negative effect on litter size. [11]

Cattle: Metabolic support for postpartum reproduction

Peripartum dairy cows given boron supplementation showed reduced negative energy balance markers, supporting the metabolic readiness needed for postpartum reproductive cycling. Boric acid added to Jersey bull semen extenders at microgram concentrations also protected sperm motility and mitochondrial function during cryopreservation. [12, 13]

Poultry: Hormones, follicles, and hatchability improve at low doses

Wanxi white geese fed 57 and 114 mg boron per kg diet showed significantly increased reproductive hormones, better follicular development, and improved egg qualification and hatchability rates, with the higher dose showing the strongest benefit. Japanese quail fed 25 mg nano-boron per kg diet showed the best yolk index, while higher doses reduced hatchability — again demonstrating the hormetic ceiling directly in a female reproductive outcome. Layer hens fed 75–150 mg boron per kg diet improved bone strength and mineral retention, and an in-ovo sodium borate injection at 0.5 mg increased hatching power in broiler chicks compared to higher doses. [14, 15, 16, 17]

Fish and cryopreservation studies across species

Brown trout sperm treated with 0.4 mM boron in cryopreservation extender showed significantly higher fertilization and eyeing rates with less DNA damage. Ankara buck semen extenders containing boron at 0.25 mM and 1 mM improved post-thaw motility from 66% in untreated controls to over 76%, while also reducing DNA damage after thawing. [18, 19]

Rats: Safety within a wide range, protection against damage

Rat data are the backbone of the EU’s toxic classification, yet the data actually supports a much more favorable picture of borax on fertility when looking at low to moderate doses which are far below what has shown reproductive it harm. The Weir and Fisher multigeneration study found completely normal litter size, progeny weight, and reproduction through three generations at 5.9 and 17.5 mg B/kg bw/day, with testicular atrophy appearing only far above that range. Separately, boron protected against high-fat-diet-induced sperm damage, histopathological injury, and DNA damage in Wistar rats, showing no harm within its tested dose range. A systematic review of other animal studies (rabbits, rams, goats) similarly found that dietary boron at 17.5–70 mg per kg of feed improved spermatogenesis quality in some trials. [3, 4, 20, 21]

(Curious note: using standard feed-intake conversion factors, 17.5–70 mg per kg of diet translates to an estimated 0.5–3.5 mg B/kg body weight per day, a range well below the 17.5 mg B/kg bw/day no-adverse-effect level established in the Weir and Fisher rat study.)

Female Fertility: The U-Shaped Curve on the Other Side of the Equation

Nearly all of the article above concerns male reproductive parameters, but a parallel body of research on female fertility — implantation, embryo viability, ovulation, egg quality, and pregnancy outcomes — shows the same biphasic pattern.

The same Weir and Fisher multigeneration study anchoring the male rat data above also tracked female outcomes directly. At 5.9 and 17.5 mg B/kg bw/day, female Sprague-Dawley rats showed completely normal litter size and reproductive performance through three generations, with a NOAEL for female fertility separately confirmed at 17.5 mg B/kg bw/day in later toxicological reviews. Only at much higher doses — around 52–58.5 mg B/kg bw/day — did females show decreased ovulation, and only above roughly 116 mg B/kg/day did outright failure to conceive appear, mirroring the male testicular-atrophy threshold in the same strain. [22, 23]

Dedicated embryo-level research pushes the female-side evidence further toward true essentiality. A landmark series of in vitro and in vivo studies found that low-boron diets reduced the number of implantation sites in pregnant rats and separately impaired blastocyst formation, blastocyst cell number, and increased embryo degeneration in cultured mouse preimplantation embryos — demonstrating that the female reproductive system responds to boron deficiency, not only to excess. A parallel study in Xenopus laevis found that chronic feeding of a low-boron diet adversely affected reproduction and development, reinforcing that the U-shaped curve on the female side spans amphibians as well as mammals. [24, 25]

The strongest positive female-fertility signal, though, comes from the poultry data already introduced above. In Wanxi white geese, the 114 mg/kg boron group showed measurable improvements in egg qualification rate, hatchability, egg yolk ratio, and egg shape index compared to controls, alongside enhanced follicular development — a genuine reproductive enhancement, not merely a safety threshold, on the female side of the ledger. [14]

Frogs: Essentiality, not enhancement

Xenopus laevis frogs deprived of boron showed reduced testis weight and sperm count compared to boron-sufficient frogs, while high-dose boric acid (15 mg B/L) caused sperm reduction and dysmorphology, establishing a NOAEC around 10 mg B/L. This is a U-shaped essentiality curve — harm at both deficiency and excess — not evidence of enhancement, and it should be read as proof that boron is a required nutrient, not proof of danger.[26, 27, 28]

Dose Comparison Across Species Table

Human Data: No Reproductive Harm, Even at High Occupational Exposure

It’s worth noting that virtually all human research on boron and reproduction has been designed to detect toxicity or harm, not to identify or measure potential fertility benefits. In spite of this, at least one such study reviewed below still picked up an improved fertility trend at moderate exposure levels.

Occupational borax miners are exposed to boron at roughly a tenth to a thirtieth of the dose that causes reproductive harm in animal studies, and even at these real-world exposure levels, they show no reproductive damage. [29]

A study of Turkish subpopulations exposed to elevated environmental boron, much of it from borax-mineral-rich soil and water, found childlessness rates of about 3.17% among the exposed group versus 4.48% in unexposed controls, statistically indistinguishable and, if anything, lower in the exposed group. A separate Turkish village study comparing drinking water at 8.5–29 mg B/L against water at only 0.03–0.40 mg B/L found no fertility or sex-ratio differences, with 96% of marriages in both groups producing children. A sibling-based “borate families” study similarly found childlessness rates of only 2.3–4.0%, showing no infertility clustering in families with generational borate exposure. [30, 31, 32]

Evidence also comes from Chinese borax and boron mineral workers in Liaoning province, who consumed an average of 31.3 mg boron per day, with heavily exposed individuals reaching up to 125 mg elemental boron per day, doses that dwarf typical dietary intake. These workers showed no significant differences in semen or reproductive parameters compared to controls aside from an unexplained shift in sperm sex-ratio that did not correlate with actual measured boron levels. A comprehensive toxicology review by Bolt (2020) concluded that even the highest occupationally exposed human blood boron levels remain far below the levels shown to cause harm in rats. Another study specifically examining chronic boron exposure and human semen parameters likewise found no evidence of reproductive harm. [1, 33, 34]

Most of this human data focused on toxicity and toxicity parameters rather than fertility benefit but, there is one important exception worth detailing: Cortés et al. (2017) studied young Chilean men exposed to varying boron levels through drinking water and found a genuine U-shaped, hormetic dose-response curve. Sperm parameters were best in the medium-exposure group, while men in the high-exposure group showed a slight decline in sperm morphology, concentration, motility, and vitality, the same four fertility-relevant parameters that improved at moderate boron levels in the animal studies discussed earlier in this article. The researchers concluded this pattern is consistent with boron’s classification as an essential micronutrient rather than a simple toxicant, since harm appeared only outside the beneficial middle range, not as a straight-line dose-response. [33]

Why a EU Ban on Borax Misrepresents the Science

The EU’s Category 1B classification, which triggered the removal of borax from household sale and forced generic concentration limits down to just 0.3% in consumer products including toys, rests almost entirely on high-dose rat studies where testicular atrophy appeared only far above the doses relevant to human dietary or occupational exposure. This regulatory posture creates a public impression that any boron exposure, from a laundry booster, a cosmetic preservative, or a trace mineral supplement, carries serious risk. That impression collapses under scrutiny. Three separate comprehensive reviews of the human and animal literature, spanning more than a decade of independent analysis, have each concluded that real-world human exposure never approaches the doses shown to cause harm in animals. [35]

The animal literature actually demonstrates the opposite pattern at the doses people realistically encounter: goats, rams, rabbits, swine, cattle, and poultry all show measurable fertility benefits from boron, often supplied specifically as borax-derived boric acid or sodium borate, at doses well below any adverse effect level. Even in rats, the species driving EU policy, a wide dose range from roughly 6 to 17.5 mg B/kg bw/day showed completely normal reproduction across three generations, on both the male and female side. Human epidemiological data, including from workers consuming up to 125 mg of boron daily, show no reproductive toxicity at all. Treating borax as a blanket reproductive hazard ignores that boron’s toxicity is dose- and species-dependent, not an intrinsic property of the molecule itself.

Curious note: 125 mg of elemental boron would be the equivalent of 1,106 mg of borax.

A more defensible regulatory approach would mirror what the science actually shows: set exposure limits based on realistic human intake scenarios, distinguish trace dietary or cosmetic exposure from industrial-scale ingestion, acknowledge that the same compound the EU restricts as a reproductive hazard has, in the animal kingdom, consistently shown to be a fertility-supporting trace mineral, and drop the borax ban.

If any single fact exposes the incoherence of the EU’s position, it is this: the same regulatory body that classifies borax as a Category 1B reproductive toxin — too dangerous for household cleaners, laundry boosters, or toy putty — carves out a specific exception allowing borax to be added directly to sturgeon caviar for human consumption. A substance supposedly capable of causing reproductive and developmental harm at trace exposure is, apparently, safe enough to eat on a cracker, provided it’s eaten by someone wealthy enough to afford sturgeon caviar. [4, 36, 37, 38] No toxicological principle explains why a compound too hazardous for a bar of soap is acceptable in a luxury food product with no realistic exposure ceiling for ambitious consumers. The only consistent explanation is that this classification was never really about dose, species, or realistic human exposure; it was about which industries or persons had the leverage to implement an unjustified reproductive toxicity ban on a trace mineral that supports fertility. That double standard is the clearest evidence yet that the EU’s borax policy does not reflect the science, and makes one question the true motive of the regulatory body or those that control it.

References

1. Bolt HM, Başaran N, Duydu Y. Effects of boron compounds on human reproduction. Arch Toxicol. 2020 Mar;94(3):717-724. doi: 10.1007/s00204-020-02700-x. Epub 2020 Mar 13. PMID: 32170343. Full Article

2. Abdelnour SA, et al. The vital roles of boron in animal health and production: A comprehensive review. J Trace Elem Med Biol. 2018 Dec;50:296-304. Full Article

3 . Calabrese E, et al. Boron enhances adaptive responses and biological performance via hormetic mechanisms. Chem Biol Interact. 2023 May 1;376:110432. https://www.sciencedirect.com/science/article/abs/pii/S0009279723000996

4 . EFSA Panel on Food Additives and Nutrient Sources Added to Food (ANS). (2013). Scientific opinion on the re-evaluation of boric acid (E 284) and sodium tetraborate (borax) (E 285) as food additives. EFSA Journal, 11(10), Article 3407. https://efsa.onlinelibrary.wiley.com/doi/pdf/10.2903/j.efsa.2013.3407

5 . Krishnan, B. B., et al. (2019). Dietary boron supplementation enhances sperm quality and immunity through influencing the associated biochemical parameters and modulating the genes expression at testicular tissue. Domestic Animal Endocrinology. https://www.sciencedirect.com/science/article/abs/pii/S0946672X19301877

6 . Ibrahim, T. B., et al. (2019). Dietary boron supplementation and its impact on testicular function, thyroid activity and serum calcium in male goats. Journal of Animal and Feed Sciences. Full Article

7 . Sani, A., et al. (2024). The use of boron as semen extender in sperm cryopreservation: A systematic review. Biomedical Research Bulletin, 2(3), 108–117. Full Article

8. Ibrahim, et al. (2019). Dietary boron supplementation and its impact on testicular function, thyroid activity and serum calcium in rams. Small Ruminant Research. 174. https://www.sciencedirect.com/science/article/abs/pii/S0921448818302293

9. Bucak, M. N., et al. (2022). Combination of trehalose and low boron in presence of decreased glycerol improves post-thawed ram sperm parameters. Cryobiology. https://pubmed.ncbi.nlm.nih.gov/34779585/

10. Elkomy, Alaa & Abd El-Hady, Ahmed & Elghalid, Osama. (2015). Dietary Boron Supplementation and its Impact on Semen Characteristics and Physiological Status of Adult Male Rabbits. Asian Journal of Poultry Science. Full Article

11. Armstrong, T. A., Spears, J. W., Crenshaw, T. D., & Nielsen, F. H. (2000). Long-term effects of boron supplementation on reproductive characteristics and bone mechanical properties in gilts. Journal of Animal Science, 79(12), 3120–3127. PubMed: https://pubmed.ncbi.nlm.nih.gov/11831513/

12. Basoglu, A., et al. (2017). Effects of boron supplementation on peripartum dairy cattle. Biological Trace Element Research. https://pubmed.ncbi.nlm.nih.gov/28229388/

13. Selvaraju S, et al. Boron Protects Sperm Functional Attributes During Cryopreservation of Bull Semen. Biol Trace Elem Res. 2026 Jan;204(1):268-276. https://link.springer.com/article/10.1007/s12011-025-04679-x

14. Pu M, et al. Impact of Boron on Reproductive Performance, Serum Biochemical Indices, and Egg Quality in Laying Wanxi White Geese. Biol Trace Elem Res. 2026 Mar;204(3):1889-1900. https://link.springer.com/article/10.1007/s12011-025-04791-y

15. Ali Kara M. The impact of different boron levels in diet on performance and eggshell quality of Japanese quails (Coturnix japonica). Saudi J Biol Sci. 2022 Mar;29(3):1796-1800. https://pmc.ncbi.nlm.nih.gov/articles/PMC8913425/

16. Koçbeker, Vildan & Bahtiyarca, Yılmaz & Demirörs, Gökhan. (2017). Effect of Diets with Various Calcium and Boron Levels in Prelaying Period on Growth, Bone Ash and Subsequent Performance and Shell Quality of Laying Hens. International Journal of Medical Science and Clinical Invention. 4. 3335-3340. Full Article

17. Bozkurt, Mehmet & Peşmen, Günnur. (2023). The effects of in ovo injected with sodium borate on hatching performance and small intestine morphology in broiler chicks. Open Chemistry. 21. 20220283. Full Article

18. Bozkurt Y , et al. Effect of Extender Supplemented with Boron on Post-Thaw Motility, Viability, DNA Damage and Fertilization Ability of Cryopreserved Brown Trout (Salmo trutta macrostigma) Spermatozoa. Cryo Letters. 2019 Sep-Oct;40(5):275-283. Cryobiology. https://pubmed.ncbi.nlm.nih.gov/33966065/

19. Karaşör ÖF, et al. The Effects of Different Doses of ROCK Inhibitor, Antifreeze Protein III, and Boron Added to Semen Extender on Semen Freezeability of Ankara Bucks. Molecules. 2022 Nov 21;27(22):8070. https://pmc.ncbi.nlm.nih.gov/articles/PMC9698151/

20. Avdatek, Fatih. (2023). The effects of boron on oxidative stress, reproductive parameters, and DNA damage in testicular tissue in wistar rats on a fatty diet. Full Article

21. Sani, Amin & Sani, et al. (2025). The Effects of Boron on Sperm Qualities and Testicular Histopathology in Animal Studies: A Systematic Review. Journal of Urological Surgery. Full Article

22. Duydu Y, Başaran N, Bolt HM. What can we learn from epidemiological studies on chronic boron exposure? Crit Rev Toxicol. 2023 Dec;53(3):168-180. https://www.tandfonline.com/doi/full/10.1080/10408444.2023.2222151

23. Agency for Toxic Substances and Disease Registry. Toxicological profile for boron. https://www.atsdr.cdc.gov/toxprofiles/tp26-c2.pdf

24. Lanoue, et al. (1998). Assessing the effects of low Boron diets on embryonic and fetal development in rodents using in vitro and in vivo model systems. Biological trace element research. 66. 271-98. Full Article

25. Fort, et al. (1999). Chronic Feeding of a Low Boron Diet Adversely Affects Reproduction and Development in Xenopus laevis. The Journal of nutrition. 129. Full Article

26. Fort DJ, et al. Adverse reproductive and developmental effects in Xenopus from insufficient boron. Biol Trace Elem Res. 1998 Winter;66(1-3):237-59. https://link.springer.com/article/10.1007/BF02783141

27. Fort DJ, et al. Impact of boron deficiency on Xenopus laevis: a summary of biological effects and potential biochemical roles. Biol Trace Elem Res. 2002 Winter;90(1-3):117-42. https://link.springer.com/article/10.1385/BTER:90:1-3:117

28. Fort, D. J., Fort, T. D., Fort, T. L., & Rogers, R. L. (2016). Boric acid is reproductively toxic to adult Xenopus laevis, but immature frogs are more sensitive. Toxicological Sciences, 154(1), 16–27. https://academic.oup.com/toxsci/article-abstract/154/1/16/2422051?redirectedFrom=fulltext

29. Duydu Y, et al. Reproductive toxicity parameters and biological monitoring in occupationally and environmentally boron-exposed persons in Bandirma, Turkey. Arch Toxicol. 2011 Jun;85(6):589-600. Full Article

30. Sayli, B. S. (1998). An assessment of fertility in boron-exposed Turkish subpopulations: 2. Evidence that boron has no effect on human reproduction. *Biological Trace Element Research, 66*(1–3), 409–422. https://pubmed.ncbi.nlm.nih.gov/10050934/

31. Sayli, B. S. (1998). An assessment of fertility in boron-exposed Turkish subpopulations. *Reproductive Toxicology, 12*(3), 297–304. https://pubmed.ncbi.nlm.nih.gov/9628553/

32. Şaylı, B. S. (2003). Relevant data from all centers [sibling-based borate families study]. https://dspace.ankara.edu.tr/bitstreams/dd165c12-e1ac-4f6e-bff3-4b718bc28c17/download

33. Cortés, Sandra & Espinoza-Navarro, Omar & Ferreccio, Catterina. (2017). High Exposure to Boron in Drinking Water and Sperm Parameters in Chilean Young People. International Journal of Morphology. 35. 99-104. Full Article

34. Scialli, A. R., et al. (2010). An overview of male reproductive studies of boron with an emphasis on studies of highly exposed Chinese workers. Reproductive Toxicology, 29(1), 10–24. https://www.scialliconsulting.com/publications/14%20Boron_RTX__2010.pdf

35 . Duydu, Yalçın & Basaran, Nursen. (2023). Effects of boron exposure on human reproduction and development. Current Opinion in Toxicology. 34. 100403. https://www.sciencedirect.com/science/article/abs/pii/S2468202023000189

36 . Scientific Committee on Consumer Safety. (2010). Opinion on boron compounds (SCCS/1249/09). European Commission. https://ec.europa.eu/health/scientific_committees/consumer_safety/docs/sccs_o_027.pdf

37 . European Commission. (2011, November 11). Commission Regulation (EU) No 1129/2011 of 11 November 2011 amending Annex II to Regulation (EC) No 1333/2008 of the European Parliament and of the Council by establishing a Union list of food additives (Text with EEA relevance). Official Journal of the European Union, L 295, 1–177. https://eur-lex.europa.eu/eli/reg/2011/1129/oj

38. Lopez A, et al. Evolution of Food Safety Features and Volatile Profile in White Sturgeon Caviar Treated with Different Formulations of Salt and Preservatives during a Long-Term Storage Time. Foods. 2021 Apr 14;10(4):850. https://pmc.ncbi.nlm.nih.gov/articles/PMC8070692/

My friend, the retired Dr. Robert Yoho coined Yoho's law. It states:

Never attribute to incompetence what might be due to malice.

I do try to give people the benefit of the doubt, and I’m quite patient with regard to incompetence if it is simply education or that is needed to correct the incompetence.

However, there comes a time when dealing with organizations such as bureaucratic governments that there’s no room for patience.

It has become quite clear that the governments of the world and the elite that run them want a large majority of people dead or infertile. As I have continued to review the literature and just how safe borax truly is, I must attribute malice to the European Union’s reclassification and essential banning of borax. I must also attribute malice to other regulatory bodies that continue to refuse to address the essentiality of boron for nutrition and health.

Here is a dosing chart that is based upon all of my research on this subject.

Part I: The Pharmaceutical Chlorite Drugs

Part II: Chlorine Dioxide and Mitochondrial Hormesis

Part III: Ozone Therapy as a Mechanistic Analog

Part IV: The Integrated Hypothesis

Part V: Anecdotal Evidence and Protocols

Part VI: Remaining Questions and the Need for Clinical Research

Conclusion

Over the last seven years since the release of my documentary about The Universal Antidote, Chlorine Dioxide, I have compiled thousands of testimonials from people safely using chlorine dioxide to help recover their health. From infections to cancer to mitochondrial dysfunction and beyond, chlorine dioxide has had a significant beneficial impact when used appropriately.

One of my primary objectives in studying and researching chlorine dioxide is to understand and explain how it produces such remarkable results across such a broad range of conditions. I have written a number of articles exploring the mechanisms of action of chlorine dioxide, and this article adds another to that series. Here is the archive link to the articles that I’ve written on The Mechanisms of Action of Chlorine Dioxide.

My objective here is to provide a foundational understanding of the mechanisms by which chlorine dioxide and its pharmaceutical-grade precursor sodium chlorite may contribute to the reversal of Type 2 diabetes and the significant improvements sometimes observed in Type 1 diabetics. The evidence presented ranges from direct clinical trial data to well-established cellular biology, and the picture that emerges is one of a compound that addresses diabetes not at a single point, but across multiple converging disease pathways simultaneously.

Diabetes mellitus is far more than a blood sugar problem. It is, at its root, a disease of chronic inflammation, mitochondrial dysfunction, impaired cellular quality control, and in the case of Type 1, autoimmune destruction of the insulin-producing beta cells of the pancreas. Conventional treatments do an admirable job of managing blood glucose levels, but they largely leave these underlying pathological processes unaddressed. This is why, despite decades of pharmaceutical advancement, diabetes remains progressive for the majority of patients.

Throughout this article, I will examine the known direct effects of chlorine dioxide and sodium chlorite, drawing on published clinical research where it exists. In areas where direct chlorine dioxide research is limited, we can gain a well-grounded understanding of what is likely occurring by examining the extensively documented mechanisms of action of ozone therapy, another oxidative therapy with a closely related biochemical profile. Both chlorine dioxide and ozone are selective oxidants that operate through mild, transient oxidative signaling; both activate the same core adaptive pathways in human cells, including NRF2 antioxidant defense, mitochondrial biogenesis, and immune modulation. The key distinction is that ozone carries a higher oxidation potential (2.07 V) compared to chlorine dioxide (1.5 V), making chlorine dioxide a somewhat milder and more selective oxidative stimulus, a distinction that may confer practical safety advantages in therapeutic use.

The scientific literature, anecdotal testimonial evidence, and pharmaceutical trial data reviewed in this article collectively build a compelling case that these compounds deserve serious clinical investigation for diabetes. What follows is an evidence-based exploration of why so many people report dramatic improvements in their blood sugar after using chlorine dioxide protocols and why those improvements make complete biochemical sense.

Part I: The Pharmaceutical Chlorite Drugs -- WF10 and NP001

WF10 (Immunokine): Direct Evidence in Diabetic Patients

WF10 is a chlorite-based drug solution originally developed by Friedrich-Wilhelm Kuehne and manufactured by OXO Chemie. Chemically designated as tetrachlorodecaoxide (TCDO), WF10 is an aqueous solution of chlorite designed for intravenous infusion. Its molecular composition is effectively equivalent to aqueous sodium chlorite. WF10 is approved in Thailand as an adjunct therapy for diabetic foot ulcers under the trade name Immunokine.[1]

The clinical evidence for WF10’s effects on diabetes is compelling and comes from multiple published studies.

Study 1: Maraprygsavan et al. (2016) -- Journal of Clinical and Translational Endocrinology

In a retrospective study of twelve diabetic patients with severe diabetic foot syndrome, five consecutive daily infusions of WF10 produced remarkable results: [2]

• HbA1c dropped from a high-risk mean of 9.1 +/- 1.6% to a low-risk 6.2 +/- 1.1% by week 8 (p < 0.001)

• HbA1c values remained low for at least 8-12 weeks after WF10 administration

• Eleven of twelve patients showed considerable wound healing improvement

• Below-knee amputation was prevented in all patients in the study group

• Fasting blood glucose levels improved, with the amount of oral hypoglycemic drugs and insulin required being gradually reduced

The investigators proposed that chlorite, the active principle of WF10, inactivates cytotoxic free hemoglobin forms (methemoglobin and hemin) that accumulate in peripheral blood after hemolysis. This process eliminates sources of hemolytic events, improves the bioavailability of nitric oxide, and enhances blood circulation, thereby increasing glucose consumption in tissues and reducing hyperglycemia. [2]

Study 2: Yingsakmongkol et al. (2021) -- Journal of Diabetes Treatment

This larger prospective, interventional clinical trial treated 40 diabetic foot ulcer patients (38 per-protocol) with HbA1c > 8.5% using standard therapy plus five weekly infusions of WF10. Results confirmed and extended the earlier findings: [3]

• HbA1c decreased from 10.48 +/- 1.46% at baseline to 8.06 +/- 1.55% at week 8 (p < 0.0001)

• Wound Severity Score dropped from 8.0 to 1.4 (p < 0.0001) by week 12

• Red blood cell distribution width (RDW-CV) decreased significantly (13.5% to 12.8%, p = 0.0021)

• In patients with elevated inflammatory markers (NLR > 3.5), the neutrophil-lymphocyte ratio decreased from 6.3 to 3.2

• Blood pressure decreased in hypertensive patients

• Platelet counts normalized in patients with elevated counts

• No serious side effects were observed

The investigators described a “blood rejuvenation” effect in which WF10 selectively removes highly glycated, dysfunctional red blood cells from circulation and stimulates compensatory erythropoiesis, generating new healthy red blood cells with low glycation levels. This was evidenced by a transient increase in reticulocytes (immature red blood cells) and increases in mean corpuscular volume (MCV). [3]

Study 3: Yingsakmongkol et al. (2011) -- Journal of Foot and Ankle Surgery

This double-blind, randomized, placebo-controlled trial of 40 participants confirmed that WF10 as an adjunct to standard diabetic foot ulcer treatment significantly improved wound severity scores compared to placebo over 9 weeks. [4]

Study 4: Yingsakmongkol (2013) -- Journal of Wound Care

A prospective, open-label study of 129 patients demonstrated good clinical outcomes in the neuropathic ulcer group and the severely infected ulcer group when WF10 was used as adjunct therapy. [5]

The WF10 Mechanism in Diabetes: Targeting the Red Blood Cell

The mechanism by which WF10 reduces HbA1c is distinct from conventional diabetes medications and directly addresses a pathological cycle unique to diabetes: [2]

1. Hyperglycemia damages red blood cells: Enhanced, insulin-independent glucose uptake by erythrocytes promotes glycation of proteins, impairs cell deformability, and creates osmotic stress through sorbitol accumulation via aldose reductase.

2. Damaged red blood cells hemolyze: There is a clear relationship between hemolysis degree and fasting plasma glucose, as well as HbA1c values, in Type 2 diabetes patients.

3. Hemolysis products are toxic: Released methemoglobin and hemin diminish nitric oxide bioavailability, impair blood circulation, and promote thrombosis and further tissue damage.

4. WF10 breaks this cycle: Chlorite inactivates toxic hemoglobin metabolites, induces splenic clearance of the most damaged erythrocytes, improves NO bioavailability and microcirculation, and depresses aldose reductase activity, which restores healthy glucose utilization in peripheral tissues.

This cycle-breaking mechanism explains why the HbA1c reduction persists for weeks to months after a brief treatment course. [2, 3]

NP001: Targeting Macrophage-Driven Inflammation

NP001 is a pH-adjusted, purified sodium chlorite formulation developed by Neuvivo, Inc. for intravenous administration. Although developed primarily for ALS, its mechanism of action as an innate immune modulator has profound implications for diabetes. [6]

Clinical Trial Evidence

NP001 has been tested in two Phase 2 placebo-controlled trials in ALS patients. In a 2024 retrospective survival analysis published in Biomedicines: [7]

• Patients receiving 2 mg/kg NP001 for 6 months showed a 4.8-month median increase in overall survival compared to placebo (HR: 0.77)

• In patients aged 65 years or younger, the survival advantage was 10.8 months (HR: 0.69, 95% CI: 0.50-0.95)

• The effect was dose-dependent; 1 mg/kg showed no benefit, suggesting a clear dose-response relationship

NP001’s Mechanism: The Macrophage Connection to Diabetes

NP001 functions as a macrophage-targeted immune regulator. Its mechanism, detailed in a 2022 Biomedicines publication by McGrath et al., involves: [8]

• Shifting macrophage polarization from pro-inflammatory (M1) to wound-healing/anti-inflammatory (M2) phenotype

• Reducing microbial translocation-- bacteria leaking from the gut into the bloodstream, setting up self-perpetuating inflammatory cycles

• Normalizing inflammatory biomarkers including C-reactive protein (CRP), interleukin-18, and lipopolysaccharide (LPS)

This mechanism is directly relevant to diabetes because macrophage-driven inflammation is now understood as a central driver of insulin resistance and beta cell destruction: [9, 10]

• In Type 2 diabetes, adipose tissue macrophages adopt a pro-inflammatory M1 phenotype and secrete TNF-alpha, IL-6, and IL-1beta, which directly impair insulin signaling and promote insulin resistance.

• IL-1beta from activated macrophages promotes beta cell dysfunction, impairs insulin secretion, and induces apoptosis of pancreatic beta cells.

• The shift from anti-inflammatory M2 to pro-inflammatory M1 macrophage dominance creates a self-reinforcing cycle of chronic inflammation and insulin resistance.

• Microbial translocation activates toll-like receptors (TLRs) on macrophages, initiating NF-kappaB inflammatory pathways that further impair insulin signaling.

As McGrath et al. stated regarding NP001: this approach is “potentially applicable to other neuroinflammatory diseases.” Given that Type 2 diabetes is fundamentally an inflammatory disease driven by macrophage dysregulation, the therapeutic logic of sodium chlorite extends naturally from ALS to diabetes. [8]

Part II: Chlorine Dioxide and Mitochondrial Hormesis -- A Theoretical Framework for Diabetes Reversal

Beyond the direct pharmaceutical evidence from WF10 and NP001, there is a compelling theoretical basis for how chlorine dioxide itself, as a mild, paramagnetic oxidant, could mitigate diabetes through the well-established biological phenomenon of mitochondrial hormesis (mitohormesis).

Mitochondrial Dysfunction: The Root of Diabetes

Mitochondrial dysfunction has emerged as a central axis in the pathophysiology of diabetes and its complications. A 2025 review in Nature Cell Death and Disease synthesized the evidence: [11]

• Pancreatic beta cells are exquisitely dependent on mitochondrial function for glucose-stimulated insulin secretion. Mitochondrial dysfunction impairs ATP synthesis, disrupts calcium signaling, and leads to beta cell failure and death.

• Skeletal muscle in Type 2 diabetes patients shows reduced mitochondrial biogenesis, with decreased expression of PGC-1alpha and downstream oxidative phosphorylation genes.

• Adipose tissue with dysfunctional mitochondria contributes to insulin resistance and chronic inflammation.

• The core features of mitochondrial quality control impairment in diabetes include suppressed biogenesis and fusion, excessive fission, and deficient mitophagy.

A 2025 review confirmed: “Mitochondria are essential organelles that are crucial for energy production and integral to cellular metabolic processes. Recent investigations have underscored the role of mitochondrial dysfunction in the advancement of diabetes.” [12]

The Mitohormesis Hypothesis

When cells experience mild, transient increases in reactive oxygen species (ROS), whether from exercise, intermittent fasting, or exogenous mild oxidants, they activate adaptive cellular responses that enhance stress resistance and improve metabolic health. This phenomenon, known as mitohormesis, contrasts with the damaging effects of chronic, excessive oxidative stress.

Chlorine dioxide, with its intermediate oxidative state (+4 to +3), functions as a mild oxidant. At low, therapeutic concentrations, it is hypothesized to induce mitohormesis through the same signaling pathways activated by exercise and caloric restriction. The three primary adaptive responses, each directly relevant to diabetes, are detailed below.

Mechanism 1: Mitochondrial Biogenesis via PGC-1alpha Activation

Moderate ROS levels activate the master regulators of mitochondrial biogenesis, PGC-1alpha and PGC-1beta. These transcriptional coactivators turn on the genes necessary for building new mitochondria and optimizing their function.

Relevance to diabetes:

• PGC-1alpha expression is reduced in skeletal muscle of Type 2 diabetes patients. This reduction correlates with decreased oxidative phosphorylation capacity and impaired fatty acid oxidation. [13]

• Physiological overexpression of PGC-1alpha in skeletal muscle has been shown to improve insulin sensitivity, increase GLUT4 expression, and enhance glucose homeostasis. [14]

• Exercise, which increases ROS production, upregulates PGC-1alpha and ameliorates cardiac inflammation while improving mitochondrial function in diabetic mouse models, as demonstrated by Botta et al. (2013) in PLOS ONE. [15]

• PGC-1alpha stimulation leads to increased metabolic flexibility, allowing cells to more efficiently oxidize both fatty acids and glucose, the exact metabolic inflexibility that characterizes Type 2 diabetes. [13]

If chlorine dioxide at therapeutic doses stimulates even modest PGC-1alpha upregulation through ROS-mediated signaling, it could theoretically enhance mitochondrial biogenesis in the tissues most affected by diabetes, including skeletal muscle, adipose tissue, and pancreatic beta cells, improving insulin sensitivity and glucose utilization.

Mechanism 2: NRF2 Activation and Antioxidant Defense

Mild oxidative stress activates NRF2 (Nuclear factor erythroid 2-related factor 2), the master transcription factor that upregulates antioxidant defense genes including superoxide dismutase (SOD), catalase, glutathione peroxidase, and NAD(P)H quinone oxidoreductase 1 (NQO1).

Relevance to diabetes:

NRF2 has emerged as a critical mediator of diabetes progression:

• NRF2 is decreased in Type 2 diabetes patients. A study in Scientific Reports (2018) found that NRF2 and its downstream targets were decreased in peripheral blood mononuclear cells of diabetic subjects, while oxidative stress markers were elevated. Restoring NRF2 signaling restored impaired insulin secretion in pancreatic beta cells. [16]

• NRF2 activation protects beta cells. Research published in Oxidative Medicine and Cellular Longevity (2019) demonstrated that NRF2-activating compounds restored mitochondrial activity, glucose-dependent ROS turnover, and antagonized glucolipotoxicity-induced inhibition of insulin release and apoptosis in beta cells. Importantly, these beneficial effects only occurred when beta cells were under metabolic stress. [17]

• NRF2 is necessary for beta cell mass expansion. A 2022 study demonstrated that NRF2 is necessary for glucose-stimulated beta cell proliferation and for adaptive expansion of beta cell mass in response to metabolic stress. Genetic or pharmacological activation of NRF2 increased beta cell proliferation in both mouse and human beta cells. NRF2 loss-of-function decreased insulin content and impaired glucose tolerance. [18]

• NRF2 activation prevents insulin resistance. Research published in JCI Insight (2018) demonstrated that activation of the NRF2 pathway profoundly ameliorated insulin resistance. [19]

Because chlorine dioxide and sodium chlorite generate transient oxidative stress, they would theoretically activate NRF2 signaling, potentially restoring the antioxidant defenses that are depleted in diabetes and protecting beta cells from the oxidative damage that drives their dysfunction and death. [20]

Mechanism 3: Autophagy and Mitophagy Stimulation

ROS serve as essential triggers for autophagy, the cellular process of breaking down and recycling damaged proteins and organelles. ROS accomplish this through:

• Direct oxidation of Atg4, promoting autophagosome formation

• Activation of AMPK, which inhibits mTOR (a major suppressor of autophagy)

• Activation of transcription factors for autophagy genes (BNIP3, LC3, p62)

• Stimulation of PINK1-Parkin and BNIP3/NIX-FUNDC1 pathways for mitophagy (selective removal of damaged mitochondria)

Relevance to diabetes:

Autophagy is critically important in diabetes:

• Beta cell function depends on autophagy. Research published in Autophagy (2011) demonstrated that autophagy is necessary to maintain the architecture and function of pancreatic beta cells. Altered autophagy is involved in both Type 1 and Type 2 diabetes. [21]

• Autophagy clears toxic protein aggregates. In beta cells, autophagy clears human islet amyloid polypeptide (hIAPP) oligomers. Mice expressing hIAPP in autophagy-deficient beta cells developed diabetes, whereas neither hIAPP nor loss of autophagy alone was sufficient to induce disease. This demonstrates that autophagy acts as a critical gatekeeper against diabetes development. [22]

• AMPK-mTOR autophagy pathway is protective. Compounds that activate AMPK to induce autophagy through mTOR inhibition have demonstrated protective effects against pancreatic beta cell damage in Type 1 diabetes models. [23]

• Balanced autophagy is essential. Both excessive activation and inhibition of autophagy through mTORC1 manipulation lead to increased beta cell apoptosis and decline in beta cell mass. This underscores that physiological, moderate stimulation, as might be achieved through low-dose ROS from chlorine dioxide, is the optimal approach. [22]

Part III: Ozone Therapy as a Mechanistic Analog -- What the Evidence Tells Us About Oxidative Therapy and Diabetes

Because direct, large-scale clinical research on oral chlorine dioxide in diabetic populations does not yet exist, examining the well-documented clinical and mechanistic evidence from ozone therapy is both scientifically justified and practically instructive. Ozone (O3) and chlorine dioxide (ClO2) share a fundamental biochemical identity: both are selective oxidants that do not act through direct toxicity at therapeutic doses, but rather through the controlled induction of mild oxidative stress that triggers adaptive cellular responses. The key difference between them is quantitative rather than qualitative -- ozone carries an oxidation potential of 2.07 V, while chlorine dioxide operates at approximately 1.5 V. This means chlorine dioxide induces a somewhat gentler oxidative signal, which may be advantageous from a safety standpoint while still engaging the same core adaptive pathways. What ozone achieves in published clinical trials, chlorine dioxide plausibly achieves through the same cellular machinery, at a more moderate intensity. [24, 25]

The Shared Oxidative Signaling Pathway

Both ozone and chlorine dioxide, upon contact with biological fluids, rapidly react with polyunsaturated fatty acids (PUFAs) and other biomolecules to generate transient quantities of hydrogen peroxide (H2O2) and lipid oxidation products (LOPs). These secondary messengers -- not the original oxidant molecules themselves -- are the actual biological signals that trigger the body’s adaptive responses. This is a critically important concept: neither ozone nor chlorine dioxide functions as a blunt chemical weapon at therapeutic concentrations. Rather, they function as pro-drugs, disappearing within seconds of biological contact and leaving behind a precisely calibrated set of molecular signals that stimulate the body’s own healing machinery. The therapeutic window for ozone has been established at 10-80 micrograms per milliliter of blood; below this threshold the oxidative signal is neutralized by plasma antioxidants before it can be biologically useful, and above this threshold oxidative damage can occur. A comparable dose-dependent therapeutic window is likely operative for chlorine dioxide, though it remains to be formally characterized. [26]

Ozone Therapy and Direct Glycemic Control

Published clinical studies have demonstrated that ozone therapy can improve glycemic control in diabetic patients through multiple direct mechanisms.

A landmark study by Martínez-Sánchez et al., published in the European Journal of Pharmacology (2005), evaluated ozone therapy in patients with Type 2 diabetes and neuroinfectious diabetic foot. Ozone treatment improved glycemic control, prevented further oxidative stress, normalized levels of organic peroxides, and activated superoxide dismutase activity. Wound healing improved significantly, and the rate of amputations in the ozone-treated group was lower than in controls. The investigators attributed the pharmacodynamic effect of ozone in part to its capacity to act as a superoxide scavenger and concluded that “medical ozone treatment could be an alternative therapy in the treatment of diabetes and its complications.” [27, 28, 29]

A 2021 clinical study evaluated ozone therapy’s effect on HbA1c levels in a Type 2 diabetic patient with obesity, demonstrating a measurable reduction in HbA1c following a course of ozone treatment. This finding is consistent with the broader pattern seen across multiple smaller studies and case reports.[29]

A systematic review and meta-analysis published in Frontiers in Endocrinology (2024), examining ozone therapy as a treatment for diabetic foot ulcers, found that patients receiving ozone therapy displayed higher rates of ulcer healing, shorter hospital stays, increased catalase activity, and reduced blood glucose levels across multiple included studies. A parallel review published in PMC (2023) concluded that “the evidence has been able to determine that ozone therapy is adequate for the treatment of diabetic foot ulcers,” with wound healing improvement being a consistent finding across studies. [30, 31]

Mechanism A: Ozone Enhances Oxygen Delivery via 2,3-DPG -- and What This Means for Diabetes

One of the most well-characterized mechanisms of ozone therapy is its ability to improve oxygen delivery to tissues through the upregulation of 2,3-diphosphoglycerate (2,3-DPG) within red blood cells.

2,3-DPG is a molecule produced inside erythrocytes that binds to hemoglobin and reduces its affinity for oxygen, shifting the oxygen-hemoglobin dissociation curve to the right. This rightward shift means that hemoglobin releases its oxygen more readily at the tissue level, ensuring that peripheral tissues receive adequate oxygen supply even under conditions of impaired circulation. Ozone treatment has been demonstrated to significantly increase 2,3-DPG synthesis in red blood cells, a finding confirmed experimentally by studies on ozonated red blood cell concentrates. [32, 33]

This mechanism is particularly relevant to diabetes for several reasons. Diabetics frequently suffer from impaired microcirculation and reduced tissue oxygenation, which contributes to poor wound healing, neuropathy, and the cycle of ischemic tissue damage that characterizes late-stage diabetic complications. Furthermore, a 2025 review in PMC confirmed that decreased 2,3-DPG levels are associated with impaired oxygen delivery, particularly during conditions of metabolic stress, and that restoring 2,3-DPG levels is clinically meaningful for tissue oxygenation and recovery. Additionally, enhanced oxygen delivery to pancreatic beta cells -- which are among the most oxygen-sensitive cells in the body -- could theoretically improve their ATP production and glucose-stimulated insulin secretion. [32, 33]

At therapeutic doses, ozone also activates erythrocyte glycolysis via the glucose-6-phosphate dehydrogenase (G6PD) pathway, increasing ATP production within red blood cells, improving their deformability, and enhancing their ability to navigate the microcapillaries where oxygen exchange occurs. This is the same pathway that WF10 engages through a different molecular mechanism, suggesting that chlorine dioxide, ozone, and WF10 all converge on improved erythrocyte function and tissue oxygenation as a shared therapeutic axis in diabetes. [26]

Mechanism B: Ozone Activates NRF2 and Suppresses NF-kappaB

The dual regulation of NRF2 and NF-kappaB by ozone is among the most extensively documented mechanisms in the ozone therapy literature and provides a direct mechanistic parallel to the theoretical effects of chlorine dioxide discussed in Part II.

Sagai and Bocci (2011), in a landmark review published in Medical Gas Research, described in detail how therapeutic doses of ozone induce mild, precisely calibrated oxidative stress that activates NRF2 (through dissociation from its inhibitor Keap-1) while simultaneously suppressing NF-kappaB, the master transcription factor of pro-inflammatory signaling. NRF2 activation drives transcription of the antioxidant response element (ARE), upregulating a comprehensive battery of protective enzymes including SOD, catalase, glutathione peroxidase, heme oxygenase-1 (HO-1), NQO1, and heat shock protein 70 (HSP70). [26]

Critically, NRF2 activation simultaneously antagonizes NF-kappaB, which is the primary transcription factor driving the chronic low-grade inflammation that underlies insulin resistance in Type 2 diabetes. A 2025 review on ozone as an immunomodulator, published in Current Issues in Molecular Biology, confirmed that low-dose ozone (10-40 micrograms per milliliter) activates the Nrf2/ARE antioxidant pathway, increases enzymatic defense via SOD, catalase, and GPx, and reduces levels of proinflammatory cytokines such as TNF-alpha, IL-1beta, and IL-6 -- the exact cytokines that drive insulin resistance and beta cell destruction in diabetes. [34]

NRF2 also interacts synergistically with PGC-1alpha. Research published in 2019 demonstrated that the NRF2 and PGC-1alpha signaling pathways are co-regulated, with NRF2 activation supporting and amplifying PGC-1alpha-driven mitochondrial biogenesis. This means that ozone-mediated (and by analogy, chlorine dioxide-mediated) NRF2 activation does not occur in isolation -- it simultaneously promotes the mitochondrial biogenesis discussed in Part II, creating a compounding beneficial effect in diabetic tissues. [35]

Mechanism C: Ozone Modulates Macrophage Polarization

In the same manner as NP001 (sodium chlorite), ozone therapy has been shown to modulate macrophage function -- shifting macrophages from a pro-inflammatory M1 phenotype toward a wound-healing, anti-inflammatory M2 phenotype and enhancing phagocytic efficiency.

The 2025 review by Napiorkowska-Baran et al. in Current Issues in Molecular Biology reported that ozone therapy significantly modulates macrophage functions through activation of the NRF2/ARE pathway, resulting in increased antioxidant enzyme activity and a shift in cytokine secretion toward anti-inflammatory profiles. Specifically, ozone treatment increases production of IL-10 and TGF-beta (anti-inflammatory) while reducing TNF-alpha, IL-1beta, and IL-6 (pro-inflammatory). This is precisely the cytokine profile shift needed to interrupt the macrophage-driven inflammatory cascade that perpetuates insulin resistance in Type 2 diabetes and contributes to beta cell destruction in Type 1 diabetes. [34]

Furthermore, ozone was shown to suppress the NLRP3 inflammasome, reducing caspase-1 activity and lowering IL-1beta production. This is particularly significant for diabetes, as NLRP3 inflammasome activation in islet macrophages is now recognized as a key driver of beta cell dysfunction and death in both Type 1 and Type 2 diabetes. [34, 36, 37, 38]

Mechanism D: Ozone Reduces Chronic Oxidative Stress in Diabetic Tissues

Paradoxically, the controlled, transient increase in oxidative signaling produced by ozone therapy actually reduces chronic oxidative stress in diabetic tissues over time. This is the hallmark of hormesis: the short-term stressor triggers an adaptive response that leaves the system more resilient than it was before exposure.

A study evaluating ozone therapy in diabetic patients confirmed that ozone treatment normalized levels of organic peroxides, activated superoxide dismutase, and prevented further oxidative stress progression -- demonstrating net antioxidant benefit despite the pro-oxidant nature of the intervention. Clinical studies on ozone autohemotherapy in the context of other inflammatory diseases have similarly found significant reductions in CRP, IL-6, and markers of lipid peroxidation following treatment courses.[27, 34]

In the context of diabetes, where chronic oxidative stress is both a cause and a consequence of disease progression -- driving beta cell death, impairing insulin signaling, damaging vascular endothelium, and accelerating neuropathy -- the ability of a mild oxidative therapy to interrupt and reverse this cycle represents a fundamentally different therapeutic approach from conventional antioxidant supplementation, which has largely failed in clinical trials. The key distinction is that exogenous antioxidants attempt to neutralize ROS directly, while oxidative hormesis teaches the body to produce its own, far more powerful and precisely regulated antioxidant response.

Mechanism E: Ozone Improves Diabetic Wound Healing and Peripheral Vascular Disease

One of the most clinically established applications of ozone therapy in diabetes is the treatment of diabetic foot ulcers and peripheral vascular disease. This is directly analogous to the diabetic foot ulcer applications of WF10 described in Part I.

Ozone therapy stimulates antioxidant enzyme expression and activity, regulates growth factor production, increases local blood flow, and provides direct antibacterial protection against the polymicrobial infections that complicate diabetic wounds. A systematic review found that ozone therapy significantly improved effective wound healing rates in diabetic foot ulcer patients, with increased collagen content in healing tissues and upregulation of endogenous growth factors at wound sites. Ozone also promotes peripheral vascular integrity via induction of vascular endothelial growth factor (VEGF), improving blood flow to ischemic tissues in diabetic patients. [39, 40]

A review of oxygen-ozone therapy in peripheral arterial disease, published in *PMC* (2020), confirmed improvement in tissue oxygenation, reduction in ischemic pain, and promotion of collateral circulation formation in diabetic patients with vascular complications.[41]

The Comparative Picture: Ozone vs. Chlorine Dioxide in Diabetes

The convergence of mechanisms is striking. In every domain where ozone therapy has demonstrated clinical benefit in diabetes and its complications, there exists either direct clinical evidence (from WF10 and NP001) or a well-grounded theoretical basis for expecting similar or analogous effects from chlorine dioxide. Given that chlorine dioxide operates through milder oxidative signaling, it may prove to be a more practical and more easily tolerated oxidative therapy for daily, long-term use in diabetic patients than ozone, which typically requires clinical administration.

Part IV: The Integrated Hypothesis

Bringing together the pharmaceutical evidence, the mitohormesis framework, and the ozone therapy parallel, we can construct a comprehensive, multi-mechanistic hypothesis for how chlorite-based compounds including chlorine dioxide could address diabetes.

Direct Mechanisms (Supported by Clinical Evidence from WF10)

Theoretical Mechanisms (Supported by Scientific Literature on ROS Signaling)

The Convergence Effect

What makes the chlorine dioxide and sodium chlorite hypothesis particularly compelling for diabetes is that these compounds appear to simultaneously address multiple pathological processes through converging mechanisms:

1. The inflammatory axis: Macrophage regulation (M1 to M2 shift) reduces the chronic inflammation that drives insulin resistance and beta cell destruction. [9, 10]

2. The mitochondrial axis: Mitohormesis restores mitochondrial function in tissues where dysfunction underlies the disease. [11, 12, 35]

3. The hematological axis: “Blood rejuvenation” breaks the hemolytic cycle that perpetuates hyperglycemia and vascular complications. [32, 33, 38]

4. The cellular quality control axis: Stimulated autophagy and NRF2 activation protect beta cells and clear the cellular debris that accumulates in diabetic tissues. [17, 18, 19, 20, 21, 22, 23]

5. The ozone-parallel oxidative signaling axis: NRF2/NF-kappaB regulation, 2,3-DPG upregulation, macrophage modulation, and NLRP3 inflammasome suppression, all documented in ozone therapy, are theoretically operative for chlorine dioxide via shared hormetic mechanisms. [24, 25, 26, 32, 33, 34, 36, 37, 41]

This multi-target approach contrasts sharply with conventional diabetes drugs, which typically address only one pathway.

Part V: Anecdotal Evidence and The Protocols

While anecdotal testimonials cannot substitute for controlled clinical trials, the pattern of reports from individuals using chlorine dioxide for various conditions consistently includes dramatic improvements in blood glucose control. Over the past six years I have compiled numerous anecdotal reports of apparent reversal of Type II diabetes, and also a significant improvement in Type I diabetes blood sugar control. Below are a compilation of anecdotal reports that provide a good overview of the improvements that can be achieved when people use chlorine dioxide and sodium chlorite protocols.

Anecdotal Testimonials

Testimonial 1: UNCONTROLLED DIABETES NOW WELL CONTROLLED

“Started MMS about a month ago. I have had uncontrollable diabetes for years. I have now reduced my insulin to just a small amount as my sugar levels were dropping too low. After decades of fighting this I am now staying in the normal to upper 100 range where before I was in a greater than 250 average. I am astounded.”

‼️➡️Source Link

Testimonial 2: BLINDNESS REVERSED, DIABETES IMPROVED, AND BACK PAIN CURED

I received this email below from a ophthalmologist in (country of origin deleted)

“Dear nurse

It is almost a year since I began on the CDS road, since I read your book.

One of my diabetic patients came for consultation yesterday

Diabetic, using insulin, Metformin, yet uncontrolled diabetes

She came for the first time , 03 months ago, seeing just 1%, she was really blind because of dense vitreous hemorrhage.

I recommended eye surgery, vitrectomy, but

She has no resources.

What do I do???

I told her she could try using CDS , Chlorine Dioxide (Only used protocol C). Now 3 months later, she has has incredible benefits, incredible !!!!

1 . She is seeing again, 70% of vision

2. Diabetes is now controlled , she had to reduce her insulin , a lot.

3. I didn’t know, but she had a herniated disc, a lot of pain, used Pregabalin, Duloxetine.

Now Pain gone, no pain, no medication

I almost did not believe!

She has her live back again!

Thanks a lot for your book

Thanks to you I can help patients without resources

(name removed) MD

Ophthalmologist

(Country name deleted)

Testimonial 3: HYPERGLYCEMIA AND PRE-DIABETES REVERSED

“My testimonial about using CDS:

A few years ago, I was diagnosed as hyperglycaemic and pre-diabetic. I’ve been working on my nutrition to keep full-blown Diabetes at bay for quite some time, without seeing any positive changes to my fasting glucose levels for my efforts. Soooo, I recently had blood work done for another matter and my doctor was shocked to see my glucose levels were the lowest they’ve been in years. They asked what I had suddenly done differently to alter the results. The only thing I can contribute it to is my, now regular use, of CDS—about 6-8mths’ effort. I’m so stoked! CDS really is the Universal Antidote.”

‼️▶️Source Link

Testimonial 4: TYPE 2 DIABETES IMPROVING

“I’m overweight, developed type 2 diabetes. Was on 2000 mg of metformin a day, tired of the side effects. On the suggestion of my cardiologist, switched to Jardiance. But with Jardiance my A1c claimed to 7.8. Been on MMS 1000 protocol for a month and a half now and my blood test results shows my A1c dropped to 6.5, it was 6.8 with metformin.”

‼️▶️Source Message

Testimonial 5: DIABETES AND ARTHRITIS IMPROVING

“We got the results of my dad’s A1C. I definitely think the DMSO helped him. April it was 11.7 and now it’s 7.7. After the first couple of weeks he started taking 1ml of DMSO twice a day. Now he’s taking it 3-4 times per day. He’s still drinking CDS in between meals. His aches and pains are completely gone. His knees don’t hurt anymore and neither does his lower back.”

Protocol C

‼️➡️Source Link

Testimonial 6: TYPE 2 DIABETES REVERSED

“a family member who has diabetes type 2 has been taking mms drops for 3 months and no longer takes insulin,he has successfully brought his blood sugars down between 7-9 mml daily from high 20ies for yrs. Now he’s worried that his blood sugars are too low and have been dropping to between 3.5 to 2.5 , dangerous levels. Hes only been taking 1 activated drop a day .He in turn eats what he can quickly to bring his sugars up. Does anyone have any experience in this area. Some suggest it’s pancreatic enzymes issue, any suggestions appreciated”

‼️➡️Source Link

Testimonial 7: TYPE 2 DIABETES REVERSED (A1C FROM 15 TO 6.2) IN 5 MONTHS

“I have helped my sister get rid of type 2 diabetes with a combination of MMS1 and healthy eating. We have to eat correctly with healthy foods to stop the rush of insulin everytime we eat the western diet. My sister was taking 60 units of insulin every night ... now her blood sugar is normal and her A1C went from 15 to 6.2. A healthy keto diet is what I had her on along with MMS1 once a day.”

“she called me from hospital bed Sept 2021 scared... I asked her if she was finally ready to listen to me... she said I will eat dog shit if you tell me too... Feb 2022 her A1c was 6.2, lost 8 lbs, no more insulin”

‼️▶️ Source Message 1

‼️▶️ Source Message 2

Testimonial 8: TYPE 2 DIABETES REVERSED

“Maria Evita Moreno Cornejo, diabetic mellitus type 2, since May 2015. She was on insulin. Her nephew gave her CDS. She took 1 ml 8 times per day. She felt very fatigued at first because she continued with insulin. Her previous levels were between 300 and 400. The doctor told her that only if she went down to 60 she could stop the insulin. After three months she was off insulin. The doctor told her he had never seen that before. He believed she did that just with her diet (she didn’t tell the doctor that she had taken CDS). Her initial reaction to CDS was diarrhea. She’s fine now. Her current maintenance dose is for activated drops of MMS.”

https://odysee.com/@cdscuramundial:4/TESTIMONIO-DIABETES-CDS-DIOXIDO-DE-CLORO:3

Testimonial 9: 17-YEAR CASE REPORTS LOWER INSULIN USE AFTER MMS

Transcript translated from Spanish:

(Full video at source link at the bottom of the testimony)

“For the same reason as she did, I want to give my testimony because I am also here now.

I was diagnosed with diabetes about 17 years ago. When they diagnosed me, my blood sugar was 350, which means the diabetes had probably been developing for years already. We started with pills, but after some time my blood sugar reached 500 and they put me on insulin. I have been on insulin for four years, but I could never accept the idea that one day my pancreas simply stopped working. I just could not get it into my head that I had to be diabetic for the rest of my life. No matter how many times they insisted, it never made sense to me.

Two months ago, through the son of a very good friend of mine, I received a video from Andrés. As soon as I heard it, I said to myself, “This is for me.” The next day I ordered the book by Jim Humble without hesitation, and within weeks I was already taking MMS.

Since I’m a bit of a daredevil and I’m tired of so much nonsense, I started quite aggressively. Yes, I had my vomiting and everything that comes with it, but I kept insisting and continuing. About two weeks later I also did a parasite cleanse, and I passed some worms that were really something to see.

After about one month of taking MMS, my blood sugar levels began dropping dramatically. Before that I had to inject 18 or 20 units of insulin in the morning, 18 at midday, and 20 at night. Today I no longer inject insulin at midday. In the mornings I take only 4 units and at night I take 6. I cannot say my illness is completely gone yet, but it has improved tremendously.

Something very important also happened. After about 6 or 7 days of taking MMS, the diabetic gingivitis in my mouth disappeared. After about 8 or 9 days, the numb padded feeling that some diabetics get in their feet also began to change. The first thing that disappeared was the pain, and little by little the numbness faded away. Now I can feel my feet touching the ground again, something I had lost before. Conventional medicine has nothing for that.

So it not only improves diabetes, but it also corrects many of the complications caused by high blood sugar.

I thought it was important to talk about this because if there is a plague in our countries today, it is diabetes. Many people are condemned to live with something that, with proper parasite cleansing and taking a few drops regularly and with discipline, could possibly be solved. We do not necessarily have to be diabetic our entire lives.

There is a huge business built around us — tests, pens, strips, insulin, pills — things meant to keep us dependent for life. And that is all I wanted to say.”

‼️▶️ Source link

Testimonial 10: TYPE 1 DIABETES CURED

Note: This is not a typical outcome that I have seen and it’s the first type one diabetes cure with Chlorine Dioxide that I have seen. I think it probably depends upon the cause of the type one diabetes whether or not it will cure it.

“Diabetes 1 Cured!

Hi Mark Praise God for his healing and miracle on Matthew. As Ron has suggested that I need to share Matthew’s miracle healing with you. I am so sorry it has taken me awhile to get back to you but it has been quite busy for me, plus I am trying to deal with my 15 year son who is starting to explore this world not as parents always expected. Matthew Fa’anunu is 10 years old from Vava’u, Tonga. He was diagnosed with Type 1 Diabetic in January 2018, a very rare disease not common with the Polynesian people. He was hospitalized for 3 weeks and he was hyperglycemia. The doctor advised my family that’s Matthew’s pancreas is totally damaged, and he would be on insulin injection for the rest of his life. I had to monitor his sugar level by measuring it at 7.a.m, 12 p.m. and 7 p.m. daily plus recording

all his food intake and regular clinic appointment. Matthew was re-admitted to the hospital as he was consuming the wrong foods at school and went through hyperglycemia again. He was in the hospital for 2 weeks. He was on insulin all right through until I met Ron Pringle in September in Vava’u. He shared with me about MMS and I immediately joined Ron in taking the MMS both for myself and also for my son Matthew. I continued to measure his blood sugar as usual and finally decided to take him off the insulin on the 1st week of

October. Matthew will be 7th week this Saturday without the insulin, which is a MIRACLE. His blood sugar has never gone above 6.2 (BSL) so far, even he had enjoyed coconut cake and chocolate brownie. Matthew is a blessing and MMS IS TRULY A MIRACLE. I am so grateful to God that Ron was sent to us. Matthew is now a very happy young boy free of insulin injection which he complained about. I am so grateful for this healing and curing of Matthew’s Type 1 Diabetic with MMS. Imagine if the world knows about this, and what MMS can do. I am a firm believer of MMS and am promoting it in Tonga. I am yet to get the sodium chlorite from USA as I have asked my sister to order for me. I want to share with you the miracle happened to my son Matthew. My family is all on MMS. As for me, I have lost weight and also my aching joints are no longer in pain. I am very active now, thanks to MMS.”

‼️▶️ Source Link

Testimonial 11: TYPE 2 DIABETES GREATLY IMPROVED

“My Dad is 84 and is thankfully listening to me and allow me to guide him with clo2 usage after he witness my personal healing of a serious colon disease using mms and CDS (unlike most people I know who think I am crazy, and discount my own personal healing as “antiodotal” and think i am blowing smoke lol. It is sad for me to see them suffer over their ignorance and stupidity! ) He had a lot of artritic pain that is now gone! and even better yet, in the last few years he has been diagnosed with type 2 diabetes and it is now close to being totally eradicated from his body. Before using The Universal Antidote he was using 2 metformin pills per day and still had his blood sugar too high. I forget his exact blood sugar numbers but I can find out. Now after about 5 months and buidling up to about 20 to 30 ML of CDS and 5 drops of stomach activated mms per day he is only using 1/4 of a pill of metformin two times per day, 25% of his previous amounts and his blood sugar levels are low and in the normal range! As I’ve heard many other total diabetic healing testimonies using mms, I expect a full recovery and my Dad to totally eradicate type 2 diabetes from his body with more time! He said he noticed the biggest improvement to his blood sugar levels when he started adding the mms drops which he added to a built up level of around 30ml of CDS per day. I plan to encourage him to lower his CDS intake to around 10 to 15 ML and raise the drops 10 to 15 next. I leaned from Scott that 1 drop of mms equals about 2 to 2.5 ML of CDS and I’ve also learned that 50 to 70 ML of CDS (or 30 drops of mms)per day is enough with 70 being on the high side. I am convinced that the drops are more effective for disorders that are deeper in the body than CDS, as I have witnessed in my own body that mms has a different effect than CDS, however; I feel both are powerful and both have their place. I don’t think anyone knows exactly why and how clo2 can eradicate the dis-ease state of the body and just about every symptoms of a dis-ease state known to man (symptoms that the medical cartel label as the “disease”) such as diabetes, like why does a pancreas that quit producing insulin start producing it again, but I don’t think that matters. What matters is that it does! Ill keep everyone posted on my Dads diabetes status.”

Source: this came from a private chat group (see image)

Testimonial 12: DIABETES IMPROVING

Short history, was healthy 5 years ago in May with an A1C of 5.0 and fasting glucose level of 104. In November of the same year, hospitialized with glucose of 850+ and A1C of 12.5. That is only 5 months, not the normal 10 – 12 years before failing to insulin. I immediately was insulin dependent, which I kept tight control of the glucose levels

I stumbled accross MMS a year ago, and just last month started on MMS due to a bad flu bug. Did the Clara 6 and 6 protocol, and poof, no flu the next day. So, I did 6 drops in the morning and 6 in the evening and after a week noticed that I had to dial the insulin usage down. Then I read the full protocol 1000, I started that 3 weeks ago, and had a doc visit today. My A1C is back to 5.0, and I was taken off all insulin. I am still taking Metformin to protect the kidneys that are stressed (blood work). I also have hyper-tension, which is not under control yet. This is a work in progress, as I am beginning to start MMS2 to speed things up.

I will update again when I am off all diabetic meds, and hopefully blood pressure meds as well. Side note, I had a gall bladder attack last month, and have several stones, largest is 12 mm. Since starting protocol 1000 I have had no acute attacks.

‼️▶️ Source Link

Testimonial 13: TYPE 1 DIABETES WELL CONTROLLED. USES UNACTIVATED SODIUM CHLORITE

This is two testimonials for the same person (JC)

“I’ve been a Type 1 Diabetic for over 30 years. Taking Chlorine Dioxide has taken my Diabetic A1C scores to the next level. A normal heathy person will typically have an A1C score of 5.5%.

A Type 1 or 2 Diabetic with a score of 7% and below is considered under good control. However, I honestly believe a score above 6% is considered poor control.

Chlorine Dioxide has not cured my Type 1 Diabetes yet, but it has greatly improved my A1C score. My last results were 5.7%. That’s only two tenths of a percent (0.2%) from a perfect score. Although I am Type 1, they classify me as a pre-diabetic. See attached lab results for the proof.

Chlorine Dioxide works.”

This is a conversation that I had back-and-forth with a admin in one of the Chlorine Dioxide groups. This person is a Type 1 Diabetic.

Me:

Hi JC,

How do you use Chlorine Dioxide to keep your A1c prediabetic? What is your regimen?

JC:

“I typically take three drops of MMS per dose, about four times per day (my maintenance protocol). The solution I use contains 22.4% Sodium Chlorite. Instead of adding an acid activator, I allow my stomach’s Hydrochloric Acid to react with the Sodium Chlorite, which in turn produces Chlorine Dioxide gas.

From my personal experience as someone with Type 1 diabetes, I’ve noticed that maintaining lower A1C levels is closely tied to understanding glycation. Glycation occurs when excess glucose attaches to hemoglobin inside the red blood cell. This process increases the percentage of glycated hemoglobin, which is what an A1C test measures.

Higher A1C levels (generally 7% or above) indicate greater glycation. When hemoglobin becomes glycated, its structure and electrical charge distribution change, which increases its affinity for oxygen. In other words, hemoglobin holds onto oxygen more tightly and releases less of it to tissues. Reduced oxygen delivery over time can contribute to long term diabetic complications involving nerves, kidneys, eyes, and the cardiovascular system.

When I use MMS consistently, my A1C levels range between 5.6 and 5.7 which classifies me as a prediabetic. This relates to how glycation affects hemoglobin’s flexibility and charge characteristics, which in turn influences oxygen release. Lower glycation means better oxygen delivery and potentially less stress on tissues that are vulnerable in diabetes.”

Me:

“That’s great! So you just take the three drops in a cup of water four times per day?

You’ve never felt like that has been too much for your body to handle? That’s quite a bit of sodium chloride on a daily basis. Do you ever take breaks? What about antioxidants or supplementing with things that make sure to replenish your glutathione?”

JC:

“Yes, three drops of MMS in two ounces of filter water per dose, four times per day. I have never felt the need to slowdown or take breaks as my body handles it well.

I take high quality supplements in the morning and evening. I reserve antioxidant supplements for the evening so they have less interaction with the chlorine dioxide I use during the day.”

Me:

I hope it’s OK to ask you a few more questions. I’m just fascinated by the effect on the A1c and diabetes in general and would like to understand it better.

Do you notice an effect on your blood sugars or more so on your A1c?

Also, does it seem to help regulate the blood or more so just affect the glycated hemoglobin.

Do you have a strict diet on top of using the sodium chlorite.

Do you always make sure to take it on an empty stomach or does that seem to matter?

I’m hoping that you can answer these questions because I get asked so many questions about type one and type two diabetes and the use of Chlorine Dioxide and it would be great to have detailed information from someone who has direct experience. 🙏🏻

JC:

“Q: Do you notice an effect on your blood sugars or more so on your A1c?

A: Ever since I started taking Sodium Chlorite (Chlorine Dioxide) I have seen great improvements with my daily blood glucose levels. Also, I have seen glucose numbers increase when I don’t follow my maintenance protocol (3 drops of MMS per dose / four times per day). My A1C is where I see the biggest improvement. It’s also the reason why I believe I have no diabetic complications as I explained above.

Q: Also, does it seem to help regulate the blood or more so just affect the glycated hemoglobin.

A: Sodium Chlorite (Chlorine Dioxide) has helped me with both as explained above.

Q: Do you have a strict diet on top of using the sodium chlorite.

A: Yes, I have had a very strict diet for the last 35 years with my Type 1 Diabetes. However, Sodium Chlorite (Chlorine Dioxide) has helped me maintain tighter blood glucose level as explained above.

Q: Do you always make sure to take it on an empty stomach or does that seem to matter?

A: No, it really doesn’t matter, but I usually wait a half hour before or after eating and taking my Sodium Chlorite (Chlorine Dioxide).

Testimonial 14: DIABETES MUCH BETTER CONTROLLED

“Just my own experience: Jim Humble’s mold/fungus protocol saved my life. I had been diagnosed with COPD. By the 2nd day my lungs completely cleared as did my sinuses. Sometimes these protocols will heal more than just a few symptoms.

During that protocol I believe I killed off candida that was systemic to my body. I was diagnosed with diabetes 2. I was having my blood A1C tested quarterly. My last test before starting MMS1 was 9.3. I started the protocol for MMS1 and then did the mold/fungus protocol.

After clearing my lungs and myriad other earth shattering healing, I went for quarterly blood work. A1C crashed from 9.3 to 6.4. That is when I knew the doctors were quacks.

They only know what they have been taught. There’s a whole world of healing in herbs and plants they have no knowledge of.

My latest find is that high doses of curcumin will heal spike protein. No kidding”

️‼️➡️Source Link

Testimonial 15: HEMOGLOBIN A1C GREATLY IMPROVED

“I never managed to do it for 8 hours in a row. Rarely did it 8 times in one day. But when I had my next 6 month lab work & check up, my A1C was in normal range for first time many years and my high PSA (indicator of possible prostate cancer) reading had lowered, back into normal range.”

‼️▶️ Source link

These reports are consistent with the mechanisms described in this article. The combination of improved mitochondrial function, reduced inflammation, enhanced tissue oxygenation, and normalized glucose metabolism could explain the rapid improvements in blood sugar control observed anecdotally.

The Protocols

From a review of anecdotal reports, there are three core protocols that appear to achieve similarly effective results: MMS1 Protocol, CDS Protocol, and Sodium Chlorite Protocol. It is up to the individual to choose their preference.

Curious Note: If I were diabetic and needed to use one of these protocols on a permanent basis, I would likely choose the Sodium Chlorite Protocol. This is because sodium chlorite, in its unactivated form, is completely tasteless. If, for some reason, I was not achieving the results I needed with the unactivated form, then I would try one of the other protocols.

The goal is to use the lowest possible dose to achieve the greatest possible effect on blood sugar and hemoglobin A1c. One way this objective can more likely be achieved is by following the three golden rules established for use with all chlorine dioxide protocols.

The Three Golden Rules Adapted for Diabetes

Rule 1:

Is your blood sugar improving at your current dose? Do not change anything. Continue with what you are doing.

Rule 2:

Feeling worse? Experiencing prolonged nausea or severe diarrhea? Reduce your intake by 50% (but continue taking it).

Rule 3:

Blood sugar not improving and not feeling worse? If there are no signs of improvement, proceed with the next dosage increase.

Once an ideal blood sugar average and hemoglobin A1c are achieved, an individualized maintenance protocol can be developed. Each person has a unique biochemical makeup, and an individualized daily plan of action will likely be necessary to ensure good outcomes for blood sugar and hemoglobin A1c.

MMS1 Protocol

The ideal starting approach is the Starting Procedure followed by Protocol 1000. After completing 14 to 21 days of Protocol 1000, there should be a significant improvement in blood sugar regulation and, within approximately one month, a significant improvement in hemoglobin A1c.

Due to wide variability in individual metabolic states, an individualized maintenance protocol should be adopted with the goal of maintaining optimized blood sugar and hemoglobin A1c. Some individuals may only need to follow the maintenance protocol 2 to 3 times per week, while others may require a daily protocol. This variation is influenced by metabolic flexibility and other factors such as diet and exercise. By the time you have completed Protocol 1000, you should have a good sense of how your body responds to CD and can transition to maintenance by tapering the dose while monitoring blood glucose and A1c.

CDS Protocol

If using CDS, the ideal starting approach is Protocol S followed by Protocol C. After completing 14 to 21 days of Protocol C, there should be a significant improvement in blood sugar regulation and, within approximately one month, a significant improvement in hemoglobin A1c.

Due to wide variability in individual metabolic states, an individualized maintenance protocol should be adopted with the goal of maintaining optimized blood sugar and hemoglobin A1c. Some individuals may only need to follow the maintenance protocol 2 to 3 times per week, while others may require a daily protocol. This variation is influenced by metabolic flexibility and other factors such as diet and exercise. By the time you have completed Protocol C, you should have a good sense of how your body responds to CDS and can transition to maintenance by tapering the dose while monitoring blood glucose and A1c.

Sodium Chlorite Protocol

Some individuals have used what is referred to as Protocol 1. This protocol utilizes sodium chlorite in its unactivated form. Initially, this protocol is carried out identically to the Starting Procedure followed by Protocol 1000. The only difference is that unactivated sodium chlorite is used rather than activating it with an acid activator.

After completing 14 to 21 days of this protocol, there should be a significant improvement in blood sugar regulation and, within approximately one month, a significant improvement in hemoglobin A1c.

Due to wide variability in individual metabolic states, an individualized maintenance protocol should be adopted with the goal of maintaining optimized blood sugar and hemoglobin A1c. Some individuals may only need to follow the maintenance protocol 2 to 3 times per week, while others may require a daily protocol. This variation is influenced by metabolic flexibility and other factors such as diet and exercise. By the time you have completed the protocol, you should have a good sense of how your body responds to unactivated sodium chlorite and can transition to maintenance by tapering the dose while monitoring blood glucose and A1c.

A detailed description of the maintenance protocol for unactivated sodium chlorite can be found in Testimonial 13 by JC, a Type 1 diabetic.

Part VI: Remaining Questions and the Need for Clinical Research

Despite the compelling convergence of clinical evidence from WF10, mechanistic evidence from NP001, theoretical support from the mitohormesis literature, and the ozone therapy parallel, several critical questions remain:

1. Dose optimization: What is the optimal concentration and frequency of chlorine dioxide or sodium chlorite administration for diabetes-specific outcomes? The WF10 studies used intravenous infusion at 0.3-0.5 mL/kg, while oral chlorine dioxide use involves different pharmacokinetics.

2. Type 1 vs. Type 2 specificity: Do the mechanisms differ between Type 1 (autoimmune beta cell destruction) and Type 2 (insulin resistance with eventual beta cell exhaustion)? The macrophage modulation and NLRP3 suppression mechanisms may be particularly relevant to Type 1 diabetes, while the mitochondrial and hematological mechanisms may be more relevant to Type 2.

3. Long-term effects: The WF10 studies show HbA1c improvements lasting 8-16 weeks. What are the effects of chronic, low-dose oral chlorine dioxide use on diabetes over months to years?

4. Interaction with existing medications: How does chlorine dioxide or sodium chlorite interact with insulin, metformin, sulfonylureas, and other diabetes medications? The anecdotal reports of improving blood sugar results suggest that medication adjustments may be necessary.

5. Safety in diabetic populations: While WF10 has shown a favorable safety profile in clinical studies, comprehensive safety data specifically for diabetic patients using various formulations and routes of administration are needed.

Conclusion

The scientific evidence, when considered in aggregate, supports a plausible multi-mechanistic hypothesis for how chlorine dioxide and its precursor sodium chlorite could mitigate diabetes:

• WF10 clinical trials provide direct evidence that intravenous sodium chlorite significantly reduces HbA1c, improves wound healing, and modulates inflammatory markers in diabetic patients.

• NP001 clinical trials demonstrate that sodium chlorite modulates macrophage-driven inflammation, a central driver of insulin resistance and beta cell destruction in diabetes.

• The mitohormesis framework provides a coherent theoretical basis for how chlorine dioxide as a mild oxidant could stimulate mitochondrial biogenesis, activate NRF2 antioxidant defenses, and promote autophagy, three cellular processes whose impairment is directly implicated in diabetes pathogenesis.

• Ozone therapy evidence provides a clinically validated parallel, demonstrating that oxidative hormesis improves glycemic control, reduces HbA1c, heals diabetic foot ulcers, modulates macrophage polarization, suppresses NLRP3-mediated inflammation, and upregulates antioxidant enzymes in diabetic patients. Given the shared biochemical mechanisms, these effects are theoretically applicable to chlorine dioxide.

• Anecdotal reports are consistent with these mechanisms and suggest that the effects may be robust enough to reduce or eliminate the need for insulin in some individuals.

The convergence of clinical evidence, established biochemistry, ozone therapy parallels, and consistent anecdotal reports makes a compelling case for prioritizing rigorous, controlled clinical trials of chlorine dioxide and sodium chlorite formulations in diabetic populations. Given that WF10 is already approved and used clinically in Thailand for diabetic foot ulcers, the pathway to expanded investigation in diabetes is not without precedent.

As the scientific community continues to recognize that diabetes is fundamentally a disease of mitochondrial dysfunction, chronic inflammation, and impaired cellular quality control, therapeutic approaches that simultaneously address all of these pillars deserve serious investigation.

References

1. Tetrachlorodecaoxide. Wikipedia. https://en.wikipedia.org/wiki/Tetrachlorodecaoxide

2. Maraprygsavan P, Mongkolsuk J, Arnhold J, Kuehne FW. The chlorite-based drug WF10 constantly reduces hemoglobin A1c values and improves glucose control in diabetes patients with severe foot syndrome. J Clin Transl Endocrinol. 2016;4:53-58. https://pmc.ncbi.nlm.nih.gov/articles/PMC5680448/

3. Yingsakmongkol N, Tanunyutthawongse C, Flemmig J, Kuehne FW. Effect of the Chlorite-Based Drug WF10 on Hemoglobin A1c, Hematological Biomarkers in Uncontrolled Diabetic Patients with Foot Ulcer. J Diabetes Treat. 2021;6:1086. Full article.

4. Yingsakmongkol N, Maraprygsavan P, Sukosit P. Effect of WF10 (Immunokine) on diabetic foot ulcer therapy: a double-blind, randomized, placebo-controlled trial. J Foot Ankle Surg. 2011;50(6):635-640. PMID: 21723750. https://www.jfas.org/article/S1067-2516(11)00256-0/abstract

5. Yingsakmongkol N. Clinical outcomes of WF10 adjunct to standard treatment of diabetic foot ulcers. J Wound Care. 2013;22(3):130-136. https://www.magonlinelibrary.com/doi/abs/10.12968/jowc.2013.22.3.130

6. Miller RG, Block G, Katz JS, Barohn RJ, Gopalakrishnan V, Cudkowicz M, Zhang JR, McGrath MS, Ludington E, Appel SH, Azhir A; Phase 2 Trial NP001 Investigators. Randomized phase 2 trial of NP001-a novel immune regulator: Safety and early efficacy in ALS. Neurol Neuroimmunol Neuroinflamm. 2015 Apr 9;2(3):e100. https://pmc.ncbi.nlm.nih.gov/articles/PMC4396529/

7. Forrest BD, Goyal NA, Fleming TR, et al. he Effectiveness of NP001 on the Long-Term Survival of Patients with Amyotrophic Lateral Sclerosis. Biomedicines. 2024 Oct 16;12(10):2367. https://pmc.ncbi.nlm.nih.gov/articles/PMC11504292/

8. Zhang R, et al. Macrophage-Targeted Sodium Chlorite (NP001) Slows Progression of Amyotrophic Lateral Sclerosis (ALS) through Regulation of Microbial Translocation. Biomedicines. 2022 Nov 12;10(11):2907. https://pmc.ncbi.nlm.nih.gov/articles/PMC9687998/

9. Berbudi A, Khairani S, Tjahjadi AI. Interplay Between Insulin Resistance and Immune Dysregulation in Type 2 Diabetes Mellitus: Implications for Therapeutic Interventions. Immunotargets Ther. 2025 Apr 3;14:359-382. https://pmc.ncbi.nlm.nih.gov/articles/PMC11974557/

10. Li H, Meng Y, He S, Tan X, Zhang Y, Zhang X, Wang L, Zheng W. Macrophages, Chronic Inflammation, and Insulin Resistance. Cells. 2022 Sep 26;11(19):3001. https://pmc.ncbi.nlm.nih.gov/articles/PMC9562180/

11. Chen Y, et al Mitochondrial quality control in diabetes mellitus and complications: molecular mechanisms and therapeutic strategies. Cell Death Dis. 2025 Aug 27;16(1):652. https://pmc.ncbi.nlm.nih.gov/articles/PMC12391366/

12. Qin B, Wang Y, Ding J. The role of mitochondrial function in the pathogenesis of diabetes. Front Endocrinol (Lausanne). 2025 Aug 8;16:1607641. https://pmc.ncbi.nlm.nih.gov/articles/PMC12370513/

13. Lira VA, Benton CR, Yan Z, Bonen A. PGC-1alpha regulation by exercise training and its influences on muscle function and insulin sensitivity. Am J Physiol Endocrinol Metab. 2010 Aug;299(2):E145-61. https://pmc.ncbi.nlm.nih.gov/articles/PMC2928513/

14. Summermatter S, Shui G, Maag D, Santos G, Wenk MR, Handschin C. PGC-1α improves glucose homeostasis in skeletal muscle in an activity-dependent manner. Diabetes. 2013 Jan;62(1):85-95. https://pmc.ncbi.nlm.nih.gov/articles/PMC3526021/

15. Botta A, et al. Short term exercise induces PGC-1α, ameliorates inflammation and increases mitochondrial membrane proteins but fails to increase respiratory enzymes in aging diabetic hearts. PLoS One. 2013 Aug 1;8(8):e70248. https://pmc.ncbi.nlm.nih.gov/articles/PMC3731348/

16. Sireesh D, et al. Association of NF-E2 Related Factor 2 (Nrf2) and inflammatory cytokines in recent onset Type 2 Diabetes Mellitus. Sci Rep. 2018 Mar 23;8(1):5126. https://pmc.ncbi.nlm.nih.gov/articles/PMC5865120/

17. Schultheis J, et al. Nrf2 Activation Protects Mouse Beta Cells from Glucolipotoxicity by Restoring Mitochondrial Function and Physiological Redox Balance. Oxid Med Cell Longev. 2019 Nov 11;2019:7518510. https://pmc.ncbi.nlm.nih.gov/articles/PMC6885177/

18. Baumel-Alterzon S, et al. Nrf2 Regulates β-Cell Mass by Suppressing β-Cell Death and Promoting β-Cell Proliferation. Diabetes. 2022 May 1;71(5):989-1011. https://pmc.ncbi.nlm.nih.gov/articles/PMC9044139/

19. Chartoumpekis DV, et al. Nrf2 prevents Notch-induced insulin resistance and tumorigenesis in mice. JCI Insight. 2018 Mar 8;3(5):e97735. https://pmc.ncbi.nlm.nih.gov/articles/PMC5922294/

20. Dodson M, et al. NRF2 and Diabetes: The Good, the Bad, and the Complex. Diabetes. 2022 Dec 1;71(12):2463-2476. https://pmc.ncbi.nlm.nih.gov/articles/PMC9750950/

21. Chen ZF, et al. The double-edged effect of autophagy in pancreatic beta cells and diabetes. Autophagy. 2011 Jan;7(1):12-6. https://pmc.ncbi.nlm.nih.gov/articles/PMC3039729/

22. Marasco MR, Linnemann AK. β-Cell Autophagy in Diabetes Pathogenesis. Endocrinology. 2018 May 1;159(5):2127-2141. https://pmc.ncbi.nlm.nih.gov/articles/PMC5913620/

23. Chen H, et al. The protective roles of allicin on type 1 diabetes mellitus through AMPK/mTOR mediated autophagy pathway. Front Pharmacol. 2023 Feb 3;14:1108730. https://pmc.ncbi.nlm.nih.gov/articles/PMC9937553/

24. Reversible Chlorite Anion/Chlorine Dioxide Redox Couple for Aqueous Redox Flow Batteries. (2023). The Journal of Physical Chemistry C, 127(7), 3531–3541. https://doi.org/10.1021/acs.jpcc.2c08136

25. Xue W, Macleod J, Blaxland J. The Use of Ozone Technology to Control Microorganism Growth, Enhance Food Safety and Extend Shelf Life: A Promising Food Decontamination Technology. Foods. 2023 Feb 14;12(4):814. https://pmc.ncbi.nlm.nih.gov/articles/PMC9957223/

26. Sagai M, Bocci V. Mechanisms of Action Involved in Ozone Therapy: Is healing induced via a mild oxidative stress? Med Gas Res. 2011 Dec 20;1:29. https://pmc.ncbi.nlm.nih.gov/articles/PMC3298518/

27. Martínez-Sánchez G, Al-Dalain SM, Menéndez S, Re L, Giuliani A, Candelario-Jalil E, Alvarez H, Fernández-Montequín JI, León OS. Therapeutic efficacy of ozone in patients with diabetic foot. Eur J Pharmacol. 2005 Oct 31;523(1-3):151-61. Full PDF Reference

28. Al-Dalain SM, Martínez G, Candelario-Jalil E, Menéndez S, Re L, Giuliani A, León OS. Ozone treatment reduces markers of oxidative and endothelial damage in an experimental diabetes model in rats. Pharmacol Res. 2001 Nov;44(5):391-6. Full PDF Reference

29. Alp, H. B. (2021). The effective of ozone therapy on HBA1C levels and microcirculation in a diabetic patient [Conference paper]. Medicine and Environmental Science. Reference

30. Sun H, et al. Evaluation of the healing potential of short-term ozone therapy for the treatment of diabetic foot ulcers. Front Endocrinol (Lausanne). 2024 Jan 15;14:1304034. https://pmc.ncbi.nlm.nih.gov/articles/PMC10825947/

31. Astasio-Picado Á, et al. Use of Ozone Therapy in Diabetic Foot Ulcers. J Pers Med. 2023 Sep 27;13(10):1439. https://pmc.ncbi.nlm.nih.gov/articles/PMC10608575/

32. Hoffmann, G., & Viebahn, R. (2015). The influence of ozone on 2,3-diphosphoglycerate synthesis in red blood cell concentrates. Reference.

33. Jaafar LS, Kourie CMR, El-Mallah CA, Obeid O. 2,3-Diphosphoglycerate: the forgotten metabolic regulator of oxygen affinity. Br J Nutr. 2025 Nov 28;134(10):803-815. https://pmc.ncbi.nlm.nih.gov/articles/PMC12795640/

34. Napiórkowska-Baran K, et al. Ozone as an Immunomodulator-New Therapeutic Possibilities in the Treatment of Immunodeficiencies-A Narrative Review. Curr Issues Mol Biol. 2025 Dec 5;47(12):1016. https://pmc.ncbi.nlm.nih.gov/articles/PMC12731440/

35. Gureev AP, Shaforostova EA, Popov VN. Regulation of Mitochondrial Biogenesis as a Way for Active Longevity: Interaction Between the Nrf2 and PGC-1α Signaling Pathways. Front Genet. 2019 May 14;10:435. https://pmc.ncbi.nlm.nih.gov/articles/PMC6527603/

36. Yu G, et al. The NLRP3 inflammasome is a potential target of ozone therapy aiming to ease chronic renal inflammation in chronic kidney disease. Int Immunopharmacol. 2017 Feb;43:203-209. https://www.sciencedirect.com/science/article/abs/pii/S1567576916305239

37. Cenci A, et al. Mechanisms of Action of Ozone Therapy in Emerging Viral Diseases: Immunomodulatory Effects and Therapeutic Advantages With Reference to SARS-CoV-2. Front Microbiol. 2022 Apr 21;13:871645. https://pmc.ncbi.nlm.nih.gov/articles/PMC9069003/

38. Jourdan T, et al. Activation of the Nlrp3 inflammasome in infiltrating macrophages by endocannabinoids mediates beta cell loss in type 2 diabetes. Nat Med. 2013 Sep;19(9):1132-40. https://pmc.ncbi.nlm.nih.gov/articles/PMC4050982/

39. Filho MLES, et al. Ozone therapy as a treatment for diabetic foot ulcers: a systematic review and meta-analysis. J Wound Care. 2024 Dec 2;33(12):958-967. Full PDF Reference

40. Wen Q, Liu D, Wang X, et al. A systematic review of ozone therapy for treating chronically refractory wounds and ulcers. Int Wound J. 2022;19(4):853-870. doi:10.1111/iwj.13687. https://onlinelibrary.wiley.com/doi/10.1111/iwj.13687

41. Juchniewicz H, Lubkowska A. Oxygen-Ozone (O2-O3) Therapy in Peripheral Arterial Disease (PAD): A Review Study. Ther Clin Risk Manag. 2020 Jun 29;16:579-594. https://pmc.ncbi.nlm.nih.gov/articles/PMC7334138/

Note: This article is for educational and research purposes only. It is not medical advice. The hypotheses and observational evidence presented here are based on published scientific literature, established biochemical principles, and anecdotal reports. Rigorous clinical trials are needed to validate these theoretical mechanisms in diabetic populations.

Curious Note: Since producing The Universal Antidote Documentary just over six years ago, I have continued to compiled thousands of testimonials (here and more here) from people safely using chlorine dioxide to help recover their health. From infections to cancer to mitochondrial dysfunction and beyond, chlorine dioxide has had a significant beneficial impact when used appropriately. One of my primary objectives in studying and researching chlorine dioxide is to understand and explain how it produces such remarkable results across such a broad range of conditions. I have written a number of articles exploring the mechanisms of action of chlorine dioxide, and this article adds another to that series. Here is the archive link to the articles that I’ve written on The Mechanisms of Action of Chlorine Dioxide.

Diabetes affects millions of people, and most treatments only manage blood sugar without fixing what is actually broken inside the body. A growing body of research suggests that chlorine dioxide, and its precursor sodium chlorite, might address several root causes of diabetes at once. This article breaks down that research in plain language provides, anecdotal testimonials, general protocols, and points curious readers who need more toward the full technical paper on this subject which is to be released Saturday July 24, 2026.

What Is Really Wrong in Diabetes

Diabetes is often described simply as “too much sugar in the blood.” But scientists now understand it as something deeper. It involves chronic inflammation, poor mitochondrial function (the tiny engines inside cells that make energy), and in Type 1 diabetes, an immune attack on the pancreas cells that make insulin. Standard diabetes drugs control blood sugar numbers, but they do not fix these underlying problems, which is part of why diabetes tends to get worse over time even with treatment.

This article looks at chlorine dioxide and sodium chlorite, two closely related compounds, and asks a bold question: could they help reverse the disease and mitigate the actual damage behind diabetes, not just mask the symptoms? To answer this, we will look at real clinical drug trials, the biology of cells under mild stress, and a related therapy called ozone that has already been tested in diabetic patients. After this we will review some the testimonials that I have received over the last 6+ years and then review protocol basics.

Two Real Drugs Built From Chlorine Dioxide Precursor, Sodium Chlorite

Before diving into theory, it helps to know that chlorite-based drugs already exist and have been tested in patients.

WF10: Tested Directly in Diabetic Patients

WF10, also sold as Immunokine, is a chlorite solution given through an IV drip. It is approved in Thailand to help treat diabetic foot ulcers, a serious complication of diabetes. [1] Several published studies have tested WF10 directly in people with diabetes, and the results are striking.

In one study of twelve patients with severe diabetic foot problems, five days of WF10 infusions dropped average HbA1c (a key long-term blood sugar marker) from a risky 9.1 percent down to a much safer 6.2 percent within eight weeks. [2] That improvement lasted for two to three months after treatment stopped. Wounds healed in eleven of the twelve patients, and doctors were able to avoid amputating the leg in every case in the study group. [2]

A larger follow-up study of 40 patients confirmed these findings. HbA1c fell from 10.48 percent to 8.06 percent, wound scores improved dramatically, and markers of inflammation dropped as well. [3] Two more clinical trials, including a placebo-controlled study, backed up these wound-healing results. [4, 5]

So how does WF10 pull off this trick? Researchers believe high blood sugar damages red blood cells over time, making them stiff and prone to bursting open, a process called hemolysis [2]. When these cells burst, they release toxic byproducts that block a helpful molecule called nitric oxide, which normally keeps blood vessels open and healthy [2]. WF10 seems to neutralize these toxic byproducts, clear out the damaged cells, and encourage the body to build fresh, healthy red blood cells instead. Researchers have called this a “blood rejuvenation” effect [3]. With better blood flow and healthier red cells, tissues can use glucose more effectively, and blood sugar readings improve.

NP001: A Second Angle on Inflammation

NP001 is another purified chlorite drug, originally developed for a very different disease, ALS (a nerve disease). [6] In long-term follow-up research, patients on the right dose of NP001 lived nearly five months longer on average, and younger patients saw an even bigger benefit. [7]

Why mention an ALS drug in an article about diabetes? Because NP001 works by calming down overactive immune cells called macrophages, shifting them from an aggressive, inflammation-causing mode into a calmer, healing mode. [8] This matters enormously for diabetes. Scientists now know that angry, inflamed macrophages inside body fat are a major reason cells become resistant to insulin, and that inflammatory signals from these same cells can damage the insulin-producing cells in the pancreas. [9, 10] If a chlorite-based drug can calm these cells down in ALS patients, the same mechanism could plausibly help calm the inflammation driving diabetes.

The Bigger Idea: Mild Stress Can Make Cells Stronger

Beyond these two drugs, there is a broader theory worth understanding, and it starts with the mitochondria, the energy factories inside every cell.

Broken Energy Factories

In diabetes, mitochondria often stop working properly. This is especially damaging in the pancreas, where insulin-producing beta cells rely heavily on healthy mitochondria to sense sugar and release insulin correctly. [11] Muscle cells in diabetic patients also show weaker mitochondrial activity, which makes it harder for the body to burn sugar and fat for fuel. [12] When the natural process of clearing out and rebuilding worn-out mitochondria breaks down, energy problems pile up throughout the body. [11]

A Little Stress, In the Right Dose, Helps

Here is a concept that might sound backwards at first: a small, brief dose of oxidative stress, the same kind of stress you get from exercise or short-term fasting, actually makes cells healthier and more resilient over time. Scientists call this mitohormesis. It differs completely from the damage caused by constant, high levels of stress.

Chlorine dioxide acts as a mild oxidant, gentler than many other treatments in this category. The theory is that, in small therapeutic amounts, it triggers the same healthy stress response that exercise triggers. This happens through three main pathways.

Building new mitochondria. Mild stress switches on a protein called PGC-1alpha, which tells cells to build fresh, more efficient mitochondria. People with Type 2 diabetes tend to have low levels of this protein in their muscles. [13] Studies show that boosting PGC-1alpha improves how well the body responds to insulin and helps muscle cells pull in more sugar. [14] Exercise studies in diabetic animals back this up, showing improved heart mitochondria and reduced inflammation when PGC-1alpha rises. [15]

Turning on the body’s antioxidant shield. Mild stress also activates a master switch called NRF2, which turns on a whole set of protective antioxidant genes. NRF2 activity is measurably lower in people with Type 2 diabetes. [16] When researchers activated NRF2 in lab studies, it protected insulin-producing beta cells from damage and restored their ability to release insulin properly. [17] NRF2 is also required for the pancreas to grow new beta cells when needed [18], and activating it has been shown to significantly reduce insulin resistance. [19, 20]

Cleaning out cellular junk. The third pathway is autophagy, the process cells use to break down and recycle damaged parts, including worn-out mitochondria. Mild oxidative signals are one of the main triggers that switch autophagy on. This process is essential for keeping beta cells healthy, and problems with autophagy show up in both Type 1 and Type 2 diabetes. [21] Autophagy also clears out a toxic, clumping protein that can build up in the pancreas and contribute to diabetes if left unchecked. [22] Other studies show that boosting this cleanup process protects insulin-producing cells from damage in Type 1 diabetes models. [23]

What Ozone Therapy Teaches Us

Because large clinical trials of chlorine dioxide for diabetes do not exist yet, researchers can look at a very similar therapy that has already been tested extensively: medical ozone. Ozone and chlorine dioxide are chemical cousins. Both are mild oxidants that work by sending small, controlled stress signals into the body rather than causing direct damage. [24, 25] Ozone is a slightly stronger oxidant, while chlorine dioxide is gentler, which may make it easier to tolerate for everyday use in therapeutic doses. [26]

Ozone Already Improves Blood Sugar in Real Patients

A well known study published in the European Journal of Pharmacology treated diabetic patients who had foot infections with ozone therapy. Their blood sugar control improved, oxidative stress markers normalized, and fewer patients needed amputations compared to those who did not receive ozone. [27, 28, 29] Other studies found that ozone lowered HbA1c in an obese diabetic patient [29], and a larger review of multiple studies found that ozone therapy consistently improved diabetic foot ulcer healing, shortened hospital stays, and lowered blood glucose. [30, 31]

How Ozone Pulls This Off

One key mechanism involves a molecule called 2,3-DPG, found inside red blood cells. This molecule helps blood release oxygen more easily into tissues that need it. Ozone therapy increases 2,3-DPG levels, helping starved tissues like the feet and even the pancreas get more oxygen. [32, 33] This matters because diabetics often suffer from poor circulation, and better oxygen delivery to the pancreas could support healthier insulin release.

Ozone also flips the same NRF2 antioxidant switch discussed earlier, while simultaneously turning down a separate switch called NF-kappaB, which drives chronic inflammation. [26] A detailed 2025 review confirmed that low-dose ozone reduces the same inflammatory chemicals, TNF-alpha, IL-1beta, and IL-6, that are known to cause insulin resistance and damage beta cells. [34] NRF2 and PGC-1alpha also work together as a team, meaning that turning on one supports the other, doubling the benefit for mitochondria. [35]

Ozone additionally nudges immune macrophages toward their calmer, healing mode, the same shift seen with NP001, and suppresses a dangerous inflammatory alarm system called the NLRP3 inflammasome, which is now recognized as a direct cause of beta cell damage in both types of diabetes. [34, 36, 37, 38] On top of all this, ozone therapy has repeatedly been shown to speed up healing of diabetic foot wounds by boosting blood flow and collagen growth [39, 40, 41].

Putting the Pieces Together

When you line up all of this evidence, a clear pattern emerges. Chlorite-based compounds work on diabetes from several angles at the same time, rather than targeting just one broken piece.

• Calming inflammation: shifting immune cells away from the aggressive mode that drives insulin resistance and beta cell destruction [9, 10]

• Repairing energy production: triggering the cell’s natural rebuilding process for damaged mitochondria [11, 12, 35]

• Refreshing the blood: clearing out damaged red blood cells and encouraging healthier ones, which improves circulation [32, 33, 38]

• Protecting cells from the inside: switching on natural cleanup and antioxidant systems that guard beta cells from stress [17, 18, 19, 20, 21, 22, 23]

• Mirroring a proven therapy: matching many of the same biological effects already documented for ozone, a related and well-studied oxidative treatment [24, 25, 26, 32, 33, 34, 36, 37, 41]

This is very different from most diabetes medications, which usually work on just one target. A drug that lowers blood sugar in one way rarely also fixes inflammation, mitochondria, and blood cell health at the same time.

What People Are Reporting Through Anectdotal Testimonials

While anecdotal testimonials cannot substitute for controlled clinical trials, the pattern of reports from individuals using chlorine dioxide for various conditions consistently includes dramatic improvements in blood glucose control. Over the past six years I have compiled numerous anecdotal reports of apparent reversal of Type II diabetes, and also a significant improvement in Type I diabetes blood sugar control and Hemoglobin-a1C values. Below are a compilation of anecdotal reports that provide a good overview of the improvements that can be achieved when people use chlorine dioxide and sodium chlorite protocols.

Anecdotal Testimonials

Testimonial 1: UNCONTROLLED DIABETES NOW WELL CONTROLLED

“Started MMS about a month ago. I have had uncontrollable diabetes for years. I have now reduced my insulin to just a small amount as my sugar levels were dropping too low. After decades of fighting this I am now staying in the normal to upper 100 range where before I was in a greater than 250 average. I am astounded.”

‼️➡️Source Link

Testimonial 2: BLINDNESS REVERSED, DIABETES IMPROVED, AND BACK PAIN CURED

I received this email below from a ophthalmologist in (country of origin deleted)

“Dear nurse

It is almost a year since I began on the CDS road, since I read your book.

One of my diabetic patients came for consultation yesterday

Diabetic, using insulin, Metformin, yet uncontrolled diabetes

She came for the first time , 03 months ago, seeing just 1%, she was really blind because of dense vitreous hemorrhage.

I recommended eye surgery, vitrectomy, but

She has no resources.

What do I do???

I told her she could try using CDS , Chlorine Dioxide (Only used protocol C). Now 3 months later, she has has incredible benefits, incredible !!!!

1 . She is seeing again, 70% of vision

2. Diabetes is now controlled , she had to reduce her insulin , a lot.

3. I didn’t know, but she had a herniated disc, a lot of pain, used Pregabalin, Duloxetine.

Now Pain gone, no pain, no medication

I almost did not believe!

She has her live back again!

Thanks a lot for your book

Thanks to you I can help patients without resources

(name removed) MD

Ophthalmologist

(Country name deleted)

Testimonial 3: HYPERGLYCEMIA AND PRE-DIABETES REVERSED

“My testimonial about using CDS:

A few years ago, I was diagnosed as hyperglycaemic and pre-diabetic. I’ve been working on my nutrition to keep full-blown Diabetes at bay for quite some time, without seeing any positive changes to my fasting glucose levels for my efforts. Soooo, I recently had blood work done for another matter and my doctor was shocked to see my glucose levels were the lowest they’ve been in years. They asked what I had suddenly done differently to alter the results. The only thing I can contribute it to is my, now regular use, of CDS—about 6-8mths’ effort. I’m so stoked! CDS really is the Universal Antidote.”

‼️▶️Source Link

Testimonial 4: TYPE 2 DIABETES IMPROVING

“I’m overweight, developed type 2 diabetes. Was on 2000 mg of metformin a day, tired of the side effects. On the suggestion of my cardiologist, switched to Jardiance. But with Jardiance my A1c claimed to 7.8. Been on MMS 1000 protocol for a month and a half now and my blood test results shows my A1c dropped to 6.5, it was 6.8 with metformin.”

‼️▶️Source Message

Testimonial 5: DIABETES AND ARTHRITIS IMPROVING

“We got the results of my dad’s A1C. I definitely think the DMSO helped him. April it was 11.7 and now it’s 7.7. After the first couple of weeks he started taking 1ml of DMSO twice a day. Now he’s taking it 3-4 times per day. He’s still drinking CDS in between meals. His aches and pains are completely gone. His knees don’t hurt anymore and neither does his lower back.”

Protocol C

‼️➡️Source Link

Testimonial 6: TYPE 2 DIABETES REVERSED

“a family member who has diabetes type 2 has been taking mms drops for 3 months and no longer takes insulin,he has successfully brought his blood sugars down between 7-9 mml daily from high 20ies for yrs. Now he’s worried that his blood sugars are too low and have been dropping to between 3.5 to 2.5 , dangerous levels. Hes only been taking 1 activated drop a day .He in turn eats what he can quickly to bring his sugars up. Does anyone have any experience in this area. Some suggest it’s pancreatic enzymes issue, any suggestions appreciated”

‼️➡️Source Link

Testimonial 7: TYPE 2 DIABETES REVERSED (A1C FROM 15 TO 6.2) IN 5 MONTHS

“I have helped my sister get rid of type 2 diabetes with a combination of MMS1 and healthy eating. We have to eat correctly with healthy foods to stop the rush of insulin everytime we eat the western diet. My sister was taking 60 units of insulin every night ... now her blood sugar is normal and her A1C went from 15 to 6.2. A healthy keto diet is what I had her on along with MMS1 once a day.”

“she called me from hospital bed Sept 2021 scared... I asked her if she was finally ready to listen to me... she said I will eat dog shit if you tell me too... Feb 2022 her A1c was 6.2, lost 8 lbs, no more insulin”

‼️▶️ Source Message 1

‼️▶️ Source Message 2

Testimonial 8: TYPE 2 DIABETES REVERSED

“Maria Evita Moreno Cornejo, diabetic mellitus type 2, since May 2015. She was on insulin. Her nephew gave her CDS. She took 1 ml 8 times per day. She felt very fatigued at first because she continued with insulin. Her previous levels were between 300 and 400. The doctor told her that only if she went down to 60 she could stop the insulin. After three months she was off insulin. The doctor told her he had never seen that before. He believed she did that just with her diet (she didn’t tell the doctor that she had taken CDS). Her initial reaction to CDS was diarrhea. She’s fine now. Her current maintenance dose is for activated drops of MMS.”

https://odysee.com/@cdscuramundial:4/TESTIMONIO-DIABETES-CDS-DIOXIDO-DE-CLORO:3

Testimonial 9: 17-YEAR CASE REPORTS LOWER INSULIN USE AFTER MMS

Transcript translated from Spanish:

(Full video at source link at the bottom of the testimony)

“For the same reason as she did, I want to give my testimony because I am also here now.

I was diagnosed with diabetes about 17 years ago. When they diagnosed me, my blood sugar was 350, which means the diabetes had probably been developing for years already. We started with pills, but after some time my blood sugar reached 500 and they put me on insulin. I have been on insulin for four years, but I could never accept the idea that one day my pancreas simply stopped working. I just could not get it into my head that I had to be diabetic for the rest of my life. No matter how many times they insisted, it never made sense to me.

Two months ago, through the son of a very good friend of mine, I received a video from Andrés. As soon as I heard it, I said to myself, “This is for me.” The next day I ordered the book by Jim Humble without hesitation, and within weeks I was already taking MMS.

Since I’m a bit of a daredevil and I’m tired of so much nonsense, I started quite aggressively. Yes, I had my vomiting and everything that comes with it, but I kept insisting and continuing. About two weeks later I also did a parasite cleanse, and I passed some worms that were really something to see.

After about one month of taking MMS, my blood sugar levels began dropping dramatically. Before that I had to inject 18 or 20 units of insulin in the morning, 18 at midday, and 20 at night. Today I no longer inject insulin at midday. In the mornings I take only 4 units and at night I take 6. I cannot say my illness is completely gone yet, but it has improved tremendously.

Something very important also happened. After about 6 or 7 days of taking MMS, the diabetic gingivitis in my mouth disappeared. After about 8 or 9 days, the numb padded feeling that some diabetics get in their feet also began to change. The first thing that disappeared was the pain, and little by little the numbness faded away. Now I can feel my feet touching the ground again, something I had lost before. Conventional medicine has nothing for that.

So it not only improves diabetes, but it also corrects many of the complications caused by high blood sugar.

I thought it was important to talk about this because if there is a plague in our countries today, it is diabetes. Many people are condemned to live with something that, with proper parasite cleansing and taking a few drops regularly and with discipline, could possibly be solved. We do not necessarily have to be diabetic our entire lives.

There is a huge business built around us — tests, pens, strips, insulin, pills — things meant to keep us dependent for life. And that is all I wanted to say.”

‼️▶️ Source link

Testimonial 10: TYPE 1 DIABETES CURED

Note: This is not a typical outcome that I have seen and it’s the first type one diabetes cure with Chlorine Dioxide that I have seen. I think it probably depends upon the cause of the type one diabetes whether or not it will cure it.

“Diabetes 1 Cured!

Hi Mark Praise God for his healing and miracle on Matthew. As Ron has suggested that I need to share Matthew’s miracle healing with you. I am so sorry it has taken me awhile to get back to you but it has been quite busy for me, plus I am trying to deal with my 15 year son who is starting to explore this world not as parents always expected. Matthew Fa’anunu is 10 years old from Vava’u, Tonga. He was diagnosed with Type 1 Diabetic in January 2018, a very rare disease not common with the Polynesian people. He was hospitalized for 3 weeks and he was hyperglycemia. The doctor advised my family that’s Matthew’s pancreas is totally damaged, and he would be on insulin injection for the rest of his life. I had to monitor his sugar level by measuring it at 7.a.m, 12 p.m. and 7 p.m. daily plus recording

all his food intake and regular clinic appointment. Matthew was re-admitted to the hospital as he was consuming the wrong foods at school and went through hyperglycemia again. He was in the hospital for 2 weeks. He was on insulin all right through until I met Ron Pringle in September in Vava’u. He shared with me about MMS and I immediately joined Ron in taking the MMS both for myself and also for my son Matthew. I continued to measure his blood sugar as usual and finally decided to take him off the insulin on the 1st week of

October. Matthew will be 7th week this Saturday without the insulin, which is a MIRACLE. His blood sugar has never gone above 6.2 (BSL) so far, even he had enjoyed coconut cake and chocolate brownie. Matthew is a blessing and MMS IS TRULY A MIRACLE. I am so grateful to God that Ron was sent to us. Matthew is now a very happy young boy free of insulin injection which he complained about. I am so grateful for this healing and curing of Matthew’s Type 1 Diabetic with MMS. Imagine if the world knows about this, and what MMS can do. I am a firm believer of MMS and am promoting it in Tonga. I am yet to get the sodium chlorite from USA as I have asked my sister to order for me. I want to share with you the miracle happened to my son Matthew. My family is all on MMS. As for me, I have lost weight and also my aching joints are no longer in pain. I am very active now, thanks to MMS.”

‼️▶️ Source Link

Testimonial 11: TYPE 2 DIABETES GREATLY IMPROVED

“My Dad is 84 and is thankfully listening to me and allow me to guide him with clo2 usage after he witness my personal healing of a serious colon disease using mms and CDS (unlike most people I know who think I am crazy, and discount my own personal healing as “antiodotal” and think i am blowing smoke lol. It is sad for me to see them suffer over their ignorance and stupidity! ) He had a lot of artritic pain that is now gone! and even better yet, in the last few years he has been diagnosed with type 2 diabetes and it is now close to being totally eradicated from his body. Before using The Universal Antidote he was using 2 metformin pills per day and still had his blood sugar too high. I forget his exact blood sugar numbers but I can find out. Now after about 5 months and buidling up to about 20 to 30 ML of CDS and 5 drops of stomach activated mms per day he is only using 1/4 of a pill of metformin two times per day, 25% of his previous amounts and his blood sugar levels are low and in the normal range! As I’ve heard many other total diabetic healing testimonies using mms, I expect a full recovery and my Dad to totally eradicate type 2 diabetes from his body with more time! He said he noticed the biggest improvement to his blood sugar levels when he started adding the mms drops which he added to a built up level of around 30ml of CDS per day. I plan to encourage him to lower his CDS intake to around 10 to 15 ML and raise the drops 10 to 15 next. I leaned from Scott that 1 drop of mms equals about 2 to 2.5 ML of CDS and I’ve also learned that 50 to 70 ML of CDS (or 30 drops of mms)per day is enough with 70 being on the high side. I am convinced that the drops are more effective for disorders that are deeper in the body than CDS, as I have witnessed in my own body that mms has a different effect than CDS, however; I feel both are powerful and both have their place. I don’t think anyone knows exactly why and how clo2 can eradicate the dis-ease state of the body and just about every symptoms of a dis-ease state known to man (symptoms that the medical cartel label as the “disease”) such as diabetes, like why does a pancreas that quit producing insulin start producing it again, but I don’t think that matters. What matters is that it does! Ill keep everyone posted on my Dads diabetes status.”

Source: this came from a private chat group (see image)

Testimonial 12: DIABETES IMPROVING

Short history, was healthy 5 years ago in May with an A1C of 5.0 and fasting glucose level of 104. In November of the same year, hospitialized with glucose of 850+ and A1C of 12.5. That is only 5 months, not the normal 10 – 12 years before failing to insulin. I immediately was insulin dependent, which I kept tight control of the glucose levels

I stumbled accross MMS a year ago, and just last month started on MMS due to a bad flu bug. Did the Clara 6 and 6 protocol, and poof, no flu the next day. So, I did 6 drops in the morning and 6 in the evening and after a week noticed that I had to dial the insulin usage down. Then I read the full protocol 1000, I started that 3 weeks ago, and had a doc visit today. My A1C is back to 5.0, and I was taken off all insulin. I am still taking Metformin to protect the kidneys that are stressed (blood work). I also have hyper-tension, which is not under control yet. This is a work in progress, as I am beginning to start MMS2 to speed things up.

I will update again when I am off all diabetic meds, and hopefully blood pressure meds as well. Side note, I had a gall bladder attack last month, and have several stones, largest is 12 mm. Since starting protocol 1000 I have had no acute attacks.

‼️▶️ Source Link

Testimonial 13: TYPE 1 DIABETES WELL CONTROLLED. USES UNACTIVATED SODIUM CHLORITE

This is two testimonials for the same person (JC)

“I’ve been a Type 1 Diabetic for over 30 years. Taking Chlorine Dioxide has taken my Diabetic A1C scores to the next level. A normal heathy person will typically have an A1C score of 5.5%.

A Type 1 or 2 Diabetic with a score of 7% and below is considered under good control. However, I honestly believe a score above 6% is considered poor control.

Chlorine Dioxide has not cured my Type 1 Diabetes yet, but it has greatly improved my A1C score. My last results were 5.7%. That’s only two tenths of a percent (0.2%) from a perfect score. Although I am Type 1, they classify me as a pre-diabetic. See attached lab results for the proof.

Chlorine Dioxide works.”

The conversation below, I had back-and-forth with a admin in one of the Chlorine Dioxide groups. This person is a Type 1 Diabetic.

Me:

Hi JC,

How do you use Chlorine Dioxide to keep your A1c prediabetic? What is your regimen?

JC:

“I typically take three drops of MMS per dose, about four times per day (my maintenance protocol). The solution I use contains 22.4% Sodium Chlorite. Instead of adding an acid activator, I allow my stomach’s Hydrochloric Acid to react with the Sodium Chlorite, which in turn produces Chlorine Dioxide gas.

From my personal experience as someone with Type 1 diabetes, I’ve noticed that maintaining lower A1C levels is closely tied to understanding glycation. Glycation occurs when excess glucose attaches to hemoglobin inside the red blood cell. This process increases the percentage of glycated hemoglobin, which is what an A1C test measures.

Higher A1C levels (generally 7% or above) indicate greater glycation. When hemoglobin becomes glycated, its structure and electrical charge distribution change, which increases its affinity for oxygen. In other words, hemoglobin holds onto oxygen more tightly and releases less of it to tissues. Reduced oxygen delivery over time can contribute to long term diabetic complications involving nerves, kidneys, eyes, and the cardiovascular system.

When I use MMS consistently, my A1C levels range between 5.6 and 5.7 which classifies me as a prediabetic. This relates to how glycation affects hemoglobin’s flexibility and charge characteristics, which in turn influences oxygen release. Lower glycation means better oxygen delivery and potentially less stress on tissues that are vulnerable in diabetes.”

Me:

“That’s great! So you just take the three drops in a cup of water four times per day?

You’ve never felt like that has been too much for your body to handle? That’s quite a bit of sodium chloride on a daily basis. Do you ever take breaks? What about antioxidants or supplementing with things that make sure to replenish your glutathione?”

JC:

“Yes, three drops of MMS in two ounces of filter water per dose, four times per day. I have never felt the need to slowdown or take breaks as my body handles it well.

I take high quality supplements in the morning and evening. I reserve antioxidant supplements for the evening so they have less interaction with the chlorine dioxide I use during the day.”

Me:

I hope it’s OK to ask you a few more questions. I’m just fascinated by the effect on the A1c and diabetes in general and would like to understand it better.

Do you notice an effect on your blood sugars or more so on your A1c?

Also, does it seem to help regulate the blood or more so just affect the glycated hemoglobin.

Do you have a strict diet on top of using the sodium chlorite.

Do you always make sure to take it on an empty stomach or does that seem to matter?

I’m hoping that you can answer these questions because I get asked so many questions about type one and type two diabetes and the use of Chlorine Dioxide and it would be great to have detailed information from someone who has direct experience. 🙏🏻

JC:

“Q: Do you notice an effect on your blood sugars or more so on your A1c?

A: Ever since I started taking Sodium Chlorite (Chlorine Dioxide) I have seen great improvements with my daily blood glucose levels. Also, I have seen glucose numbers increase when I don’t follow my maintenance protocol (3 drops of MMS per dose / four times per day). My A1C is where I see the biggest improvement. It’s also the reason why I believe I have no diabetic complications as I explained above.

Q: Also, does it seem to help regulate the blood or more so just affect the glycated hemoglobin.

A: Sodium Chlorite (Chlorine Dioxide) has helped me with both as explained above.

Q: Do you have a strict diet on top of using the sodium chlorite.

A: Yes, I have had a very strict diet for the last 35 years with my Type 1 Diabetes. However, Sodium Chlorite (Chlorine Dioxide) has helped me maintain tighter blood glucose level as explained above.

Q: Do you always make sure to take it on an empty stomach or does that seem to matter?

A: No, it really doesn’t matter, but I usually wait a half hour before or after eating and taking my Sodium Chlorite (Chlorine Dioxide).“

Testimonial 14: DIABETES MUCH BETTER CONTROLLED

“Just my own experience: Jim Humble’s mold/fungus protocol saved my life. I had been diagnosed with COPD. By the 2nd day my lungs completely cleared as did my sinuses. Sometimes these protocols will heal more than just a few symptoms.

During that protocol I believe I killed off candida that was systemic to my body. I was diagnosed with diabetes 2. I was having my blood A1C tested quarterly. My last test before starting MMS1 was 9.3. I started the protocol for MMS1 and then did the mold/fungus protocol.

After clearing my lungs and myriad other earth shattering healing, I went for quarterly blood work. A1C crashed from 9.3 to 6.4. That is when I knew the doctors were quacks.

They only know what they have been taught. There’s a whole world of healing in herbs and plants they have no knowledge of.

My latest find is that high doses of curcumin will heal spike protein. No kidding”

‼️️➡️Source Link

Testimonial 15: HEMOGLOBIN A1C GREATLY IMPROVED

“I never managed to do it for 8 hours in a row. Rarely did it 8 times in one day. But when I had my next 6 month lab work & check up, my A1C was in normal range for first time many years and my high PSA (indicator of possible prostate cancer) reading had lowered, back into normal range.”

‼️▶️ Source link

These reports are consistent with the mechanisms described in this article. The combination of improved mitochondrial function, reduced inflammation, enhanced tissue oxygenation, and normalized glucose metabolism could explain the rapid improvements in blood sugar control observed anecdotally.

The Protocols

From a review of anecdotal reports, there are three core protocols that appear to achieve similarly effective results: MMS1 Protocol, CDS Protocol, and Sodium Chlorite Protocol. It is up to the individual to choose their preference.

Curious Note: If I were diabetic and needed to use one of these protocols on a permanent basis, I would likely choose the Sodium Chlorite Protocol. This is because sodium chlorite, in its unactivated form, is completely tasteless. If, for some reason, I was not achieving the results I needed with the unactivated form, then I would try one of the other protocols.

The goal is to use the lowest possible dose to achieve the greatest possible effect on blood sugar and hemoglobin A1c. One way this objective can more likely be achieved is by following the three golden rules established for use with all chlorine dioxide protocols.

The Three Golden Rules Adapted for Diabetes

Rule 1:

Is your blood sugar improving at your current dose? Do not change anything. Continue with what you are doing.

Rule 2:

Feeling worse? Experiencing prolonged nausea or severe diarrhea? Reduce your intake by 50% (but continue taking it).

Rule 3:

Blood sugar not improving and not feeling worse? If there are no signs of improvement, proceed with the next dosage increase.

Once an ideal blood sugar average and hemoglobin A1c are achieved, an individualized maintenance protocol can be developed. Each person has a unique biochemical makeup, and an individualized daily plan of action will likely be necessary to ensure good outcomes for blood sugar and hemoglobin A1c.

MMS1 Protocol

The ideal starting approach is the Starting Procedure followed by Protocol 1000. After completing 14 to 21 days of Protocol 1000, there should be a significant improvement in blood sugar regulation and, within approximately one month, a significant improvement in hemoglobin A1c.

Due to wide variability in individual metabolic states, an individualized maintenance protocol should be adopted with the goal of maintaining optimized blood sugar and hemoglobin A1c. Some individuals may only need to follow the maintenance protocol 2 to 3 times per week, while others may require a daily protocol. This variation is influenced by metabolic flexibility and other factors such as diet and exercise. By the time you have completed Protocol 1000, you should have a good sense of how your body responds to CD and can transition to maintenance by tapering the dose while monitoring blood glucose and A1c.

CDS Protocol

If using CDS, the ideal starting approach is Protocol S followed by Protocol C. After completing 14 to 21 days of Protocol C, there should be a significant improvement in blood sugar regulation and, within approximately one month, a significant improvement in hemoglobin A1c.

Due to wide variability in individual metabolic states, an individualized maintenance protocol should be adopted with the goal of maintaining optimized blood sugar and hemoglobin A1c. Some individuals may only need to follow the maintenance protocol 2 to 3 times per week, while others may require a daily protocol. This variation is influenced by metabolic flexibility and other factors such as diet and exercise. By the time you have completed Protocol C, you should have a good sense of how your body responds to CDS and can transition to maintenance by tapering the dose while monitoring blood glucose and A1c.

Sodium Chlorite Protocol

Some individuals have used what is referred to as Protocol 1. This protocol utilizes sodium chlorite in its unactivated form. Initially, this protocol is carried out identically to the Starting Procedure followed by Protocol 1000. The only difference is that unactivated sodium chlorite is used rather than activating it with an acid activator.

After completing 14 to 21 days of this protocol, there should be a significant improvement in blood sugar regulation and, within approximately one month, a significant improvement in hemoglobin A1c.

Due to wide variability in individual metabolic states, an individualized maintenance protocol should be adopted with the goal of maintaining optimized blood sugar and hemoglobin A1c. Some individuals may only need to follow the maintenance protocol 2 to 3 times per week, while others may require a daily protocol. This variation is influenced by metabolic flexibility and other factors such as diet and exercise. By the time you have completed the protocol, you should have a good sense of how your body responds to unactivated sodium chlorite and can transition to maintenance by tapering the dose while monitoring blood glucose and A1c.

A detailed description of the maintenance protocol for unactivated sodium chlorite can be found in Testimonial 13 by JC, a Type 1 diabetic.

Why This Deserves a Closer Look

Diabetes is not just a blood sugar problem. It is a disease built from inflammation, damaged energy factories inside cells, and a body struggling to repair itself. The evidence gathered here, from real clinical trials of WF10 and NP001, from the science of mitohormesis, and from decades of ozone therapy research, points toward chlorine dioxide and sodium chlorite as compounds that appear work on several of these root causes simultaneously.

Given that chlorite-based medications are already approved and used clinically for diabetic foot ulcers in Thailand, the idea of studying these compounds further for diabetes is not far fetched. It fits squarely within mainstream biology and deserves a fair scientific hearing.

Readers who want the full technical detail, including every study cited here along with additional mechanisms, dosing protocols, and a deeper discussion of the remaining research questions, can find the complete long form article, “How Chlorine Dioxide Reverses Diabetes: The Science, Theory, Evidence, and Protocols,” for a full expert-level breakdown which will be released on Saturday, July 25, 2026.

References

1. Tetrachlorodecaoxide. Wikipedia. https://en.wikipedia.org/wiki/Tetrachlorodecaoxide

2. Maraprygsavan P, Mongkolsuk J, Arnhold J, Kuehne FW. The chlorite-based drug WF10 constantly reduces hemoglobin A1c values and improves glucose control in diabetes patients with severe foot syndrome. J Clin Transl Endocrinol. 2016;4:53-58. https://pmc.ncbi.nlm.nih.gov/articles/PMC5680448/

3. Yingsakmongkol N, Tanunyutthawongse C, Flemmig J, Kuehne FW. Effect of the Chlorite-Based Drug WF10 on Hemoglobin A1c, Hematological Biomarkers in Uncontrolled Diabetic Patients with Foot Ulcer. J Diabetes Treat. 2021;6:1086. Full article.

4. Yingsakmongkol N, Maraprygsavan P, Sukosit P. Effect of WF10 (Immunokine) on diabetic foot ulcer therapy: a double-blind, randomized, placebo-controlled trial. J Foot Ankle Surg. 2011;50(6):635-640. PMID: 21723750. https://www.jfas.org/article/S1067-2516(11)00256-0/abstract

5 . Yingsakmongkol N. Clinical outcomes of WF10 adjunct to standard treatment of diabetic foot ulcers. J Wound Care. 2013;22(3):130-136. https://www.magonlinelibrary.com/doi/abs/10.12968/jowc.2013.22.3.130

6. Miller RG, Block G, Katz JS, Barohn RJ, Gopalakrishnan V, Cudkowicz M, Zhang JR, McGrath MS, Ludington E, Appel SH, Azhir A; Phase 2 Trial NP001 Investigators. Randomized phase 2 trial of NP001-a novel immune regulator: Safety and early efficacy in ALS. Neurol Neuroimmunol Neuroinflamm. 2015 Apr 9;2(3):e100. https://pmc.ncbi.nlm.nih.gov/articles/PMC4396529/

7. Forrest BD, Goyal NA, Fleming TR, et al. he Effectiveness of NP001 on the Long-Term Survival of Patients with Amyotrophic Lateral Sclerosis. Biomedicines. 2024 Oct 16;12(10):2367. https://pmc.ncbi.nlm.nih.gov/articles/PMC11504292/

8. Zhang R, et al. Macrophage-Targeted Sodium Chlorite (NP001) Slows Progression of Amyotrophic Lateral Sclerosis (ALS) through Regulation of Microbial Translocation. Biomedicines. 2022 Nov 12;10(11):2907. https://pmc.ncbi.nlm.nih.gov/articles/PMC9687998/

9. Berbudi A, Khairani S, Tjahjadi AI. Interplay Between Insulin Resistance and Immune Dysregulation in Type 2 Diabetes Mellitus: Implications for Therapeutic Interventions. Immunotargets Ther. 2025 Apr 3;14:359-382. https://pmc.ncbi.nlm.nih.gov/articles/PMC11974557/

10. Li H, Meng Y, He S, Tan X, Zhang Y, Zhang X, Wang L, Zheng W. Macrophages, Chronic Inflammation, and Insulin Resistance. Cells. 2022 Sep 26;11(19):3001. https://pmc.ncbi.nlm.nih.gov/articles/PMC9562180/

11. Chen Y, et al Mitochondrial quality control in diabetes mellitus and complications: molecular mechanisms and therapeutic strategies. Cell Death Dis. 2025 Aug 27;16(1):652. https://pmc.ncbi.nlm.nih.gov/articles/PMC12391366/

12. Qin B, Wang Y, Ding J. The role of mitochondrial function in the pathogenesis of diabetes. Front Endocrinol (Lausanne). 2025 Aug 8;16:1607641. https://pmc.ncbi.nlm.nih.gov/articles/PMC12370513/

13. Lira VA, Benton CR, Yan Z, Bonen A. PGC-1alpha regulation by exercise training and its influences on muscle function and insulin sensitivity. Am J Physiol Endocrinol Metab. 2010 Aug;299(2):E145-61. https://pmc.ncbi.nlm.nih.gov/articles/PMC2928513/

14. Summermatter S, Shui G, Maag D, Santos G, Wenk MR, Handschin C. PGC-1α improves glucose homeostasis in skeletal muscle in an activity-dependent manner. Diabetes. 2013 Jan;62(1):85-95. https://pmc.ncbi.nlm.nih.gov/articles/PMC3526021/

15. Botta A, et al. Short term exercise induces PGC-1α, ameliorates inflammation and increases mitochondrial membrane proteins but fails to increase respiratory enzymes in aging diabetic hearts. PLoS One. 2013 Aug 1;8(8):e70248. https://pmc.ncbi.nlm.nih.gov/articles/PMC3731348/

16. Sireesh D, et al. Association of NF-E2 Related Factor 2 (Nrf2) and inflammatory cytokines in recent onset Type 2 Diabetes Mellitus. Sci Rep. 2018 Mar 23;8(1):5126. https://pmc.ncbi.nlm.nih.gov/articles/PMC5865120/

17. Schultheis J, et al. Nrf2 Activation Protects Mouse Beta Cells from Glucolipotoxicity by Restoring Mitochondrial Function and Physiological Redox Balance. Oxid Med Cell Longev. 2019 Nov 11;2019:7518510. https://pmc.ncbi.nlm.nih.gov/articles/PMC6885177/

18. Baumel-Alterzon S, et al. Nrf2 Regulates β-Cell Mass by Suppressing β-Cell Death and Promoting β-Cell Proliferation. Diabetes. 2022 May 1;71(5):989-1011. https://pmc.ncbi.nlm.nih.gov/articles/PMC9044139/

19 . Chartoumpekis DV, et al. Nrf2 prevents Notch-induced insulin resistance and tumorigenesis in mice. JCI Insight. 2018 Mar 8;3(5):e97735. https://pmc.ncbi.nlm.nih.gov/articles/PMC5922294/

20. Dodson M, et al. NRF2 and Diabetes: The Good, the Bad, and the Complex. Diabetes. 2022 Dec 1;71(12):2463-2476. https://pmc.ncbi.nlm.nih.gov/articles/PMC9750950/

21. Chen ZF, et al. The double-edged effect of autophagy in pancreatic beta cells and diabetes. Autophagy. 2011 Jan;7(1):12-6. https://pmc.ncbi.nlm.nih.gov/articles/PMC3039729/

22. Marasco MR, Linnemann AK. β-Cell Autophagy in Diabetes Pathogenesis. Endocrinology. 2018 May 1;159(5):2127-2141. https://pmc.ncbi.nlm.nih.gov/articles/PMC5913620/

23. Chen H, et al. The protective roles of allicin on type 1 diabetes mellitus through AMPK/mTOR mediated autophagy pathway. Front Pharmacol. 2023 Feb 3;14:1108730. https://pmc.ncbi.nlm.nih.gov/articles/PMC9937553/

24. Reversible Chlorite Anion/Chlorine Dioxide Redox Couple for Aqueous Redox Flow Batteries. (2023). The Journal of Physical Chemistry C, 127(7), 3531–3541. https://doi.org/10.1021/acs.jpcc.2c08136

25 . Xue W, Macleod J, Blaxland J. The Use of Ozone Technology to Control Microorganism Growth, Enhance Food Safety and Extend Shelf Life: A Promising Food Decontamination Technology. Foods. 2023 Feb 14;12(4):814. https://pmc.ncbi.nlm.nih.gov/articles/PMC9957223/

26. Sagai M, Bocci V. Mechanisms of Action Involved in Ozone Therapy: Is healing induced via a mild oxidative stress? Med Gas Res. 2011 Dec 20;1:29. https://pmc.ncbi.nlm.nih.gov/articles/PMC3298518/

27. Martínez-Sánchez G, Al-Dalain SM, Menéndez S, Re L, Giuliani A, Candelario-Jalil E, Alvarez H, Fernández-Montequín JI, León OS. Therapeutic efficacy of ozone in patients with diabetic foot. Eur J Pharmacol. 2005 Oct 31;523(1-3):151-61. Full PDF Reference

28. Al-Dalain SM, Martínez G, Candelario-Jalil E, Menéndez S, Re L, Giuliani A, León OS. Ozone treatment reduces markers of oxidative and endothelial damage in an experimental diabetes model in rats. Pharmacol Res. 2001 Nov;44(5):391-6. Full PDF Reference

29. Alp, H. B. (2021). The effective of ozone therapy on HBA1C levels and microcirculation in a diabetic patient [Conference paper]. Medicine and Environmental Science. Reference

30. Sun H, et al. Evaluation of the healing potential of short-term ozone therapy for the treatment of diabetic foot ulcers. Front Endocrinol (Lausanne). 2024 Jan 15;14:1304034. https://pmc.ncbi.nlm.nih.gov/articles/PMC10825947/

31. Astasio-Picado Á, et al. Use of Ozone Therapy in Diabetic Foot Ulcers. J Pers Med. 2023 Sep 27;13(10):1439. https://pmc.ncbi.nlm.nih.gov/articles/PMC10608575/

32. Hoffmann, G., & Viebahn, R. (2015). The influence of ozone on 2,3-diphosphoglycerate synthesis in red blood cell concentrates. Reference.

33. Jaafar LS, Kourie CMR, El-Mallah CA, Obeid O. 2,3-Diphosphoglycerate: the forgotten metabolic regulator of oxygen affinity. Br J Nutr. 2025 Nov 28;134(10):803-815. https://pmc.ncbi.nlm.nih.gov/articles/PMC12795640/

34. Napiórkowska-Baran K, et al. Ozone as an Immunomodulator-New Therapeutic Possibilities in the Treatment of Immunodeficiencies-A Narrative Review. Curr Issues Mol Biol. 2025 Dec 5;47(12):1016. https://pmc.ncbi.nlm.nih.gov/articles/PMC12731440/

35. Gureev AP, Shaforostova EA, Popov VN. Regulation of Mitochondrial Biogenesis as a Way for Active Longevity: Interaction Between the Nrf2 and PGC-1α Signaling Pathways. Front Genet. 2019 May 14;10:435. https://pmc.ncbi.nlm.nih.gov/articles/PMC6527603/

36. Yu G, et al. The NLRP3 inflammasome is a potential target of ozone therapy aiming to ease chronic renal inflammation in chronic kidney disease. Int Immunopharmacol. 2017 Feb;43:203-209. https://www.sciencedirect.com/science/article/abs/pii/S1567576916305239

37. Cenci A, et al. Mechanisms of Action of Ozone Therapy in Emerging Viral Diseases: Immunomodulatory Effects and Therapeutic Advantages With Reference to SARS-CoV-2. Front Microbiol. 2022 Apr 21;13:871645. https://pmc.ncbi.nlm.nih.gov/articles/PMC9069003/

38. Jourdan T, et al. Activation of the Nlrp3 inflammasome in infiltrating macrophages by endocannabinoids mediates beta cell loss in type 2 diabetes. Nat Med. 2013 Sep;19(9):1132-40. https://pmc.ncbi.nlm.nih.gov/articles/PMC4050982/

39. Filho MLES, et al. Ozone therapy as a treatment for diabetic foot ulcers: a systematic review and meta-analysis. J Wound Care. 2024 Dec 2;33(12):958-967. Full PDF Reference

40. Wen Q, Liu D, Wang X, et al. A systematic review of ozone therapy for treating chronically refractory wounds and ulcers. Int Wound J. 2022;19(4):853-870. doi:10.1111/iwj.13687. https://onlinelibrary.wiley.com/doi/10.1111/iwj.13687

41. Juchniewicz H, Lubkowska A. Oxygen-Ozone (O2-O3) Therapy in Peripheral Arterial Disease (PAD): A Review Study. Ther Clin Risk Manag. 2020 Jun 29;16:579-594. https://pmc.ncbi.nlm.nih.gov/articles/PMC7334138/

A trace mineral, a regulatory straitjacket, and the calculation nobody was willing to publish — until now.

Note: This is for educational purposes. This is not medical advice, and I am not telling you what you should do. Every person is or should be in control of their own health in spite of what the current medical establishment would like you to believe.

Curious Note: Most vitamin and mineral recommended intakes are set to prevent deficiency, not to optimize health, performance, or longevity. This article addresses boron specifically, and what the research suggests about dosing for optimized human health, rather than for the mere absence of deficiency.

Over the past year, I have spent at least 100 hours trying to build a comprehensive understanding of boron and its effects on human health and disease. The focus of that work has been on elemental boron as provided by borax, and the process has involved reading across a large and scattered literature that spans over 100 years of food science, nutrition, toxicology, endocrinology, bone biology, neurology, immunology, and cancer research.

That research gradually came to feel less like reading isolated papers and more like assembling a complex puzzle. Piece by piece, the literature began to reveal a subtle but remarkable picture of boron’s far-reaching role in disease prevention, disease reversal, and the optimization of human physiology across multiple systems.

As the data accumulated, a pattern became difficult to ignore. Again and again, papers described significant benefits in animal models at doses expressed in milligrams per kilogram, and again and again the human implication was left unstated. The final empty piece of the puzzle was now in front of me: the arithmetic. To my knowledge, the specific application of standard animal‑to‑human dose conversion to the beneficial boron doses reported in animal studies has not been laid out explicitly in the published nutrition and trace mineral literature. Using the standard animal‑to‑human conversion method on these beneficial boron doses, rather than only on toxicological thresholds, revealed something striking. Once that arithmetic was applied, it became hard to avoid the conclusion that nutrition scientists have been pointing toward something important for a very long time, but have been effectively straitjacketed and unable to say it directly because of the (UL) upper limit dose threshold placed on boron of 20 mg/day.

The Sentence That Finally Opened My Eyes

Buried in a peer-reviewed paper on boron’s important roles in biochemistry is a passage most readers would scroll past:

“Administration of boron 5, 10, and 20 mg/kg/d reversed malathion-induced oxidative stress, lipid peroxidation, and suppression of antioxidant enzyme activity. Boron decreased malathion-induced oxidative stress, enhanced antioxidant defense mechanisms, and regenerated damaged liver, kidney, and brain tissues in rats.” [1, 2] Curious Note: malathion is a pesticide.

If you read that quote and moved on, you missed something important. It is important because oxidative stress is one of the root mechanisms implicated in aging, neurodegeneration, kidney disease, and liver damage, and antioxidant enzyme activity — superoxide dismutase, catalase, glutathione peroxidase — is a foundational marker of how well the body defends its own tissue. Yet when readers encounter “5, 10, and 20 mg/kg/d” in boron papers, the dose is usually left as an animal number rather than translated into a human-equivalent intake. This type of language is prolific in the literature.

That omission is not accidental. And understanding why it exists takes you into one of the more fascinating and consequential gaps in modern nutritional science.

What Boron Actually Does

Boron is not classified as an essential nutrient in humans. There is no Recommended Daily Allowance. There is no established deficiency disease with a name. Yet the research literature, accumulated over four decades, led largely by USDA researcher Dr. Forrest Nielsen and colleagues, paints a picture of a mineral with extraordinarily wide metabolic reach. Boron has been shown in animal and human studies to affect: [2]

• Brain electrical activity and cognitive performance, including manual dexterity, attention, short-term memory, and long-term memory [2]

• Bone formation, mineralization, and fracture healing [2]

• The methylation cycle, specifically SAM-e (S-adenosylmethionine) production and homocysteine regulation [2]

• Steroid hormone metabolism including testosterone, estradiol, and vitamin D activation [2, 3]

• Immune function, T-cell populations, immunoglobulin production, and cytokine balance [2, 3]

• Prostate cancer risk and PSA levels [2]

• Lipid metabolism and cardiovascular risk markers [2]

• Blood glucose regulation [2]

• Wound healing and tissue repair [2]

• Mitochondrial function, specifically uncoupling proteins that regulate thermogenesis and oxidative stress [2]

This is not a short list. It spans virtually every major domain of human physiological optimization. And in every single case, the literature carefully reports the effective animal dose in milligrams per kilogram and then stops.

Why The Scientists Can’t State What Is Obvious

How is it that we’ve found over 5,000+ planets outside our solar system and we’ve sequenced the entire human genome in the last 25 years, yet we still can’t give boron the essential mineral status it likely deserves?

To understand the significance of the weight-based dosages, you need to understand what prevents researchers from simply stating their implications outright.

First, the regulatory status problem. Establishing essentiality requires proving that one specific enzyme or biochemical reaction depends entirely on a substance which is the equivalent of proving a single missing musician silences an entire orchestra. Orchestra’s do not work that way and neither does boron. It behaves more like a conductor subtly adjusting the tempo across every section of the orchestra at once. No instrument stops playing. No section goes silent. But take the conductor away, and the whole performance noticeably loses its precision. Boron’s actions are broad and pleiotropic. It modulates multiple pathways rather than serving a single defined function. Without essentiality status, no regulatory body will issue a formal recommended intake above minimal amounts. [2]

Second, the GRAS (Generally Regarded As Safe) and UL problem. The established Tolerable Upper Intake Level (UL) for boron in adults is 20 mg/day, derived from reproductive toxicity studies in rats and rabbits. This regulatory ceiling prevents researchers from recommending or stating higher doses than 20 mg of elemental boron per day could be beneficial. Any researcher who formally recommends human doses near or above it, without controlled human clinical trial data, faces institutional and legal exposure. [4]

Third, the funding problem. Boron cannot be patented. There is no pharmaceutical or commercial engine to fund the large-scale, dose-escalation human trials that would be required to formally establish higher optimal intakes. The research that does exist is largely government-funded and deliberately conservative in its clinical recommendations.

So researchers do something elegant and, once you see it, it’s hard to miss: they publish the animal mg/kg data in full detail, embed it in papers targeted at human nutrition audiences, surround it with mechanistic human-relevance context (SAM-e depletion, homocysteine elevation, brain electrical activity, PSA suppression), and leave the conversion to the attentive reader.

Dr. Nielsen spent a career doing exactly this. His repeated framing of boron as “of more practical nutritional importance than currently acknowledged” is the scientific literature’s equivalent of stating that which is obvious. Boron at higher amounts than the 20 mg per day UL could potentially optimize human health and prevent certain disease processes.[2]

What Is an “Uncertainty Factor”?

Before comparing the two ways of doing the math, it helps to understand one simple concept — the “uncertainty factor”: an uncertainty factor is basically a safety cushion. Scientists use it when they don’t know everything, so they build in extra room for error. [5]

Here’s how it works. Researchers find the highest dose that causes no harm in animal studies. This is called the NOAEL (no-observed-adverse-effect level). But animals aren’t humans, and not all humans are the same. So instead of using that number directly, regulators shrink it down twice, just to be “extra careful”: [5, 6]

• First cut: Divide by 10, because animals and humans can react differently to the same substance.

• Second cut: Divide by 10 again, because some people (like pregnant women, older adults, or those with health conditions) may be more sensitive than others.

That’s a combined shrink of 100 times smaller than the original safe animal dose. For boron specifically, researchers have used even bigger safety cushions in some studies — up to 247 times smaller than the original number, depending on which study they used. [6, 7]

This is very different from the allometric (Km) scaling. Allometric scaling tries to answer the question: “What human dose would produce the same beneficial effect as this animal dose?” The uncertainty factor approach asks a completely different question: “How far below any risk can we stay, just to be safe?” [5, 8]

The Arithmetic Nobody Published

The FDA has a standard method for converting animal study doses to human equivalent doses (HEDs). It uses Body Surface Area (BSA) allometric scaling, based on species-specific Km factors: [9, 10, 11]

The FDA Km factors are: Rat = 6, Mouse = 3, Human = 37. [9, 10, 11]

The 20 mg/day ceiling wasn’t built using the same body-surface-area math this article uses to translate the beneficial animal doses. Regulators used a simpler, more conservative body-weight method on the no-harm dose, then divided by a safety factor of roughly 100. Nobody has ever run the beneficial animal doses through the FDA body-surface-area method which is the same one used to set starting doses for new drugs. Do that, and the human benefit equivalent lands at 9.6 to 113.5 mg/day depending on body system. [4]

Here is what happens when you do the math using the FDA-scaled Human Equivalent Dose (HED) of 0.81 mg/kg/day

For the cited animal effective dose 5 mg/kg BW/day, the dose that decreased malathion-induced oxidative stress, enhanced antioxidant defense mechanisms, and regenerated damaged liver, kidney, and brain tissues — the FDA-scaled Human Equivalent Dose (HED) for a 70 kg (154 lb) adult is 56.8 mg/day.

The Full Table Across Body Systems

Now consider the reference points:

• Average American dietary boron intake: ~1.0–1.35 mg/day [2]

• Typical supplement dose recommended in most literature: 3–10 mg/day [2]

• Established UL: 20 mg/day [4]

  The human equivalent dose (HED) range — from the lowest tested dose that showed prostate benefit to the highest tested dose that showed improved wound healing and diabetes benefit — spans 9.6 to 113.5 mg/day. That is roughly 7 to 113 times what most Americans consume daily from food. It is roughly 1 to 38 times the typical supplementation dose seen in mainstream supplements and recommendations. And it ranges from about half the current UL to nearly 6 times higher than it.

Across the nine body-weight-based animal studies reviewed here, the median human-equivalent effective dose is 51.1 mg/day (0.73 mg/kg/day) which is several multiples above the current 20 mg/day UL. It’s worth noting this figure blends different body systems and disease models, so it reflects a general pattern rather than one precise optimal dose. It’s also worth noting that the higher doses seen for diabetes and wound healing may relate to boron’s known chemical affinity for sugar molecules, which could mean these particular pathologies draw on a different, less efficient interaction than the lower-dose pathways above, a distinction worth keeping in mind if considering boron for these conditions specifically.

The Structural Contradiction at the Heart of the Boron Literature

There are two things to keep in mind, and together they reveal a contradiction the literature has never addressed directly.

First, the dietary Upper Limit for boron is based on toxicity data from animal studies, in which the no-effect dose observed in rats was divided by a “uncertainty” safety factor of roughly 100. In other words, the human “uncertainty” safety limit was deliberately set at about 1/100th of the dose that caused no harm in those animal studies — not even remotely close to any level where actual harm was observed.

Second, run that same conversion on the animal doses that actually produced benefits, and the human equivalent lands at around 10 to 113 mg/day, depending on the body system. Most of these fall well above the 20 mg/day ceiling — a number set roughly 100 times lower than the dose that caused no harm at all in animals. The UL sits below the human-equivalent effective dose for 8 of the 9 body systems analyzed above.

No one has published this calculation in over five decades. It isn’t complicated. It just hasn’t been done, and it’s worth asking why. I’ll let you answer that question for yourself. My opinion is that no one had the intestinal fortitude to risk their career calling out the misuse of toxicology on an important, and possibly essential, trace nutrient.

This is not a conspiracy. It is an institutional architecture comprised of a combination of regulatory classification, funding gaps, liability concerns, and the slow inertia of nutritional science that has produced a systematic blind spot. The researchers working closest to this data know what it implies. The mg/kg figures are in every paper. The math simply hasn’t been done in public.

A novel drug entering human trials for the first time, with a genuinely unknown risk profile, typically gets a 10-fold safety margin. Boron, a mineral humans have consumed for the entire breadth of human history, was buried under a safety margin up to 25 times larger. The drug we understand less gets treated with more trust than the mineral we’ve been eating for millennia.

What Would Real Research Look Like?

To answer the questions this literature raises but cannot ask out loud, the field would need:

1. Human dose-escalation trials measuring immune markers, prostate-specific antigen, glucose regulation, wound-healing rates, and oxidative stress biomarkers at 10, 20, 30, 40, 50, and 60+ mg/day in controlled conditions

2. Body-weight-stratified analyses — no published human boron trial has ever examined whether a 120 kg individual responds differently than a 55 kg individual, despite this being the most basic pharmacological question

3. Pharmacokinetic studies comparing boron tissue distribution and metabolic rate between humans and rodents at equivalent mg/kg doses

4. Long-term safety data at 20–60 mg/day in adults without reproductive endpoints — the UL is based on reproductive toxicity, not general adult toxicity, yet it is applied universally

None of this research exists. None of it is currently funded at meaningful scale. The mineral cannot be patented. The regulatory status provides no incentive. And the researchers who understand the implications are institutionally constrained from making the recommendations the data logically supports.

The Bottom Line

The boron literature, read carefully, is making a consistent argument through the language of animal dose data. Every time a paper reports that a given number in mg/kg normalizes some critical physiological parameter in a rat, and then discusses its human relevance without performing the scaling calculation, it is extending an invitation to the reader to do the math.

When you do the math, using the FDA’s own methodology, the picture that emerges is this:

Most people in the Western world are consuming boron at just 2 to 3 percent of the typical dose associated with measurable physiological benefit across immune regulation, prostate health, glucose regulation, wound healing, and oxidative stress defense — based on the same animal literature that the field itself cites as its primary evidence base.

The current UL of 20 mg/day, which is routinely treated as a near-dangerous ceiling, sits below the human-equivalent effective dose for many of the studied body systems. The gap between the average American diet and any measurable biological effect is not a gap of a few milligrams. It is an order of magnitude.

The researchers know this. The numbers are all in the papers. The arithmetic just hasn’t been published in a single place, applied systematically, and stated plainly.

Until now.

*All dose calculations in this article use FDA-recommended Body Surface Area allometric scaling (Km factors: Rat=6, Mouse=3, Human=37). Animal study sources include Coban, F. K., et al. (2015), Pizzorno (2015), and Naghii et al. (2011). This article is for educational and does not constitute medical advice. If you need to, consult a qualified clinician you trust before altering supplementation protocols. [1, 2, 3, 9]

References

1. Coban, F. K., et al. (2015). Boron attenuates malathion-induced oxidative stress and acetylcholinesterase inhibition in rats. Drug and Chemical Toxicology, 38(4), 391–399. Full PDF Paper

2. Pizzorno, L. (2015). Nothing boring about boron. Integrative Medicine: A Clinician’s Journal, 14(4), 35–48. https://pmc.ncbi.nlm.nih.gov/articles/PMC4712861/

3. Naghii, M. R., Mofid, M., Asgari, A. R., Hedayati, M., & Daneshpour, M. S. (2011). Comparative effects of daily and weekly boron supplementation on plasma steroid hormones and proinflammatory cytokines. Journal of Trace Elements in Medicine and Biology, 25(1), 54–58. https://doi.org/10.1016/j.jtemb.2010.10.001

4. Institute of Medicine (US) Panel on Micronutrients. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington (DC): National Academies Press (US); 2001. 13, Arsenic, Boron, Nickel, Silicon, and Vanadium.Available from: https://www.ncbi.nlm.nih.gov/books/NBK222322/

5 . European Food Safety Authority. (n.d.). Safety/uncertainty factor, also known as assessment factor. EFSA Glossary. https://www.efsa.europa.eu/en/glossary/safety-uncertainty-factor-also-known-assessment-factor

6 . Johanson G, Moto TP, Schenk L. A scoping review of evaluations of and recommendations for default uncertainty factors in human health risk assessment. J Appl Toxicol. 2023 Jan;43(1):186-194. https://pmc.ncbi.nlm.nih.gov/articles/PMC10087398/

7. Hasegawa, R., Hirata-Koizumi, M., Dourson, M. L., Parker, A., Ono, A., & Hirose, A. (2013). Safety assessment of boron by application of new uncertainty factors and their subdivision. Regulatory Toxicology and Pharmacology, 65(1), 108–114. https://doi.org/10.1016/j.yrtph.2012.10.013 (see also https://pubmed.ncbi.nlm.nih.gov/23137930/)

8. Reagan-Shaw S, Nihal M, Ahmad N. Dose translation from animal to human studies revisited. FASEB J. 2008 Mar;22(3):659-61. Full PDF Paper

9. U.S. Food and Drug Administration. (2005). Guidance for industry: Estimating the maximum safe starting dose in initial clinical trials for therapeutics in adult healthy volunteers. Center for Drug Evaluation and Research. https://www.fda.gov/files/drugs/published/Estimating-the-Maximum-Safe-Starting-Dose-in-Initial-Clinical-Trials-for-Therapeutics-in-Adult-Healthy-Volunteers.pdf

10. Nair AB, Jacob S. A simple practice guide for dose conversion between animals and human. J Basic Clin Pharm. 2016 Mar;7(2):27-31. https://pmc.ncbi.nlm.nih.gov/articles/PMC4804402/

11. Reagan-Shaw S, Nihal M, Ahmad N. Dose translation from animal to human studies revisited. FASEB Journal. 2008;22(3):659–661. See Table 4 for species-specific Km conversion factors.https://pmc.ncbi.nlm.nih.gov/articles/PMC2758486/table/T4/

Introduction and Overview

This is a multi-phase CDS (chlorine dioxide solution CLO2 — 3000 ppm) that was developed by a dog rescuer that has had tremendous success with treating Parvo and a few cases of Distemper. This dog rescuer who is based out of Mexico, states that since they started using this protocol five months ago, they have not lost any cases of Pavo, but you have to be absolutely militant and disciplined with the protocol from day 1. If you need help, Phoenix has generously given her telegram username. Just reach out if needed. @Phoenix5440

Thank you Phoenix for sharing this protocol and helping me develop it so that others can benefit. 🙏🏻

This protocol is designed for puppies 4 weeks to 6 months old, inspired by a combination of the malaria and cancer protocols. The idea is a hard, fast initial hit followed by sustained lower dosing to keep the treatment active in the system.

Notes

• Make sure to isolate infected pups from other animals and contain them to a small area to prevent spread.

• Wash hands after every dose. Pups will get saliva or mucus on themselves and they can carry it around spreading to surfaces. It won’t affect us we have immunity by the age of 12. We get it as kids too but it’s not deadly for us. But for other vulnerable animals it’s important to clean after and make sure to throw out syringes and anything else. Don’t reuse. Don’t share any equipment with other animals.

• Do not fast puppies ever. That’s death for a sick puppy. DON’T stop doses and Do encourage them to eat small bits of food as often as possible to help get their hunger back. The CDS will still help. Once they recover, and are eating regular meals, take the one hour breaks with CDS after they eat but not while they are severely ill and coming out of the lethargy.

Phase 1: Crisis Dosing (First 3 Hours)

• 2.5kg or under. 0.25ml to 0.5ml of CDS mixed with 1ml water, given every 30 minutes for up to 3 hours. Depends on the severity - if caught late. Use the higher dose.

• 5kg to 7kg 0.5ml to 1ml CDS in 1.5 to 2ml of water.

• Larger pups: increase by 0.5ml increments up to 1.5ml, diluted in 5-8ml water, same 30-minute schedule

• Goal: get lethargic pups standing again — With a good outcome, this should happen by hour 3, sometimes even in last-minute cases

Phase 2: Sustained Dosing (Next 8 Hours)

• Switch to a diluted stock: 20ml CDS in 1 liter of water

• Give hourly doses from that dilution — 1ml to 10ml depending on pup size

• This continues for 8 hours after the pup is standing or Phase 1 is complete

Key Rules Throughout Treatment

• Never fast the puppy — you consider fasting dangerous for a sick pup

• Never stop or pause doses during the acute phase

• Encourage small, frequent food intake throughout to rebuild appetite

• Once eating normal meals and stabilized, resume the “1-hour gap after eating” rule you normally follow

• Crate/home hospital rest for the first 2 days post-recovery — pups will overexert and set back recovery if allowed to move freely

• By day 3, pups are typically back to normal activity but don’t let them go full free range yet. Keep them on lower activity than usual to help ensure recovery - but their energy levels will have returned by this point.

Maintenance Phase (2+ Weeks)

• Continue CDS dosing for a minimum of 2 weeks after recovery

• Reasoning: parvo-recovered pups can still shed the virus afterward, and extended CDS exposure clears it from the system and halts shedding.

Observed Recovery Markers

• Stool firms up within 6-7 hours of starting treatment

• Energy returns, but needs to be restrained via crate rest

• Full normal energy by day 3, no more need to crate rest them, but keep their activity lower than normal while they are still healing. 5 days max should be fine.

Applying This to Distemper

Same basic structure — the 3-hour crisis dose to “kick-start the fight,” but you’d increase the follow-up sustained dose to be higher and faster than the parvo maintenance phase, since distemper progresses slower but has worse long-term neurological effects and higher fatality if not addressed aggressively.

Notes From Phoenix About CLEANING and Disinfecting After Parvo and Distemper Infection

Parvo can live outside of the body for many years afterwards! It’s extremely important to clean all surfaces with CDS, carpets sofas, door knobs light switches etc.. AND spray all and any grass spots, patio spots, etc where the animal went to the bathroom with a CDS dilution. It wont kill your grass and it’ll get rid of any bacteria in the soil. Clean all surfaces by spraying with CDS dillution leaving for 10 mins and wipe away. Sofas and carpets - spray with appropriate dillution youve pre tested and either let air dry (just mist it, no need to heavily soak it) and vaccum after 10 mins. Repeat once this with parvo IF youre nervous. If the pup wasn’t ever on the couch or drooling on it and no one wiped their hands on the sofa after handling the pup, once is sufficient.

These are public health suggested cleaning protocols for ridding shelters of Parvo after they’ve had an infection- they use 5% to 10% chlorine bleach dilution but that limits what you can clean. CDS is safe for any surface, including sofas and carpets. I use usually a 10% to 15% dillution of CDS. Test first in a spot unseen and use lightly. I mist carpets and sofas, dog beds etc, hard surfaces I’m more liberal with spraying. Any grass, or dirt areas the pup went to the bathroom in, need to be sprayed down throughly.

5 days straight, at night after the sun goes down, I use fertilizer spray attachment for the hose, only I use pour in pure CDS. It mixes in the water and sprays it out directly. It’ll actually make your grass and plants grow faster and rid the soil of any parvo bacteria.

Distemper only survives outside of the body for up to 2 weeks. It’s a lot easier to clean. Only requires one night treatment of lawns, yard, patio and one treatment cleaning surfaces and floors in the house.

Signs and Symptoms of Parvo

Given how fast parvo can turn fatal, catching these earliest signs matters more than almost anything.

Earliest Signs (Often Subtle, Day 1)

• Lethargy or unusual quietness — often the very first thing noticed

• Loss of appetite or reduced interest in food

• Fever (sometimes intermittent)

• General depression or withdrawal from normal activity

As It Progresses (Days 1-3 of Symptoms)

• Vomiting, often frequent and persistent

• Diarrhea — starts watery, then often becomes bloody and foul-smelling

• Abdominal pain or a bloated, tender belly

• Dehydration from fluid loss (dry gums, skin that doesn’t spring back when gently pinched)

Severe/Critical Signs (Usually Day 1-4, Highest Risk Window)

• Hypothermia (low body temperature) replacing the earlier fever

• Weakness or collapse

• Rapid heart rate, weak pulse, pale gums (signs of shock)

• Difficulty breathing

Signs and Symptoms of Distemper

Earliest Signs (Days 10 to 14 After Exposure)

• Watery green or yellow to pus-like eye discharge

• Runny or mucousy nasal discharge (starts watery, thickens over time, yellow or green)

• Fever, though it can be intermittent and easy to miss

• Lethargy and low energy

• Loss of appetite

• Coughing

As It Progresses (Roughly Days 14 to 21)

• Vomiting and diarrhea as the virus spreads systemically

• Thickened paw pads and nose (“hard pad disease”)

• Pneumonia or labored breathing in more severe respiratory involvement

• Yellow green discharge from eyes and nose thick and constant

Warning Signs of Neurological Involvement (Can Appear 1-3 Weeks Later, Even After Apparent Recovery)

• Muscle twitching, especially rhythmic jaw movements sometimes called “chewing gum” seizures, top of the head twitches on a timed pace, not stopping, sometimes this is only seen when pups are sleeping and involuntary, constant limb or head movement, waving constantly, raising paw off the ground constantly, some will lose control of their head and bag their heads as they sleep - this is more severe and leading to seizures

• Tremors, circling, or pacing

• Seizures ranging from mild jaw tremors to full-body convulsions

• Limb weakness, incoordination (ataxia), or muscle stiffness

• Partial or complete paralysis

If you need help, Phoenix has generously given her telegram username. Just reach out on Telegram if needed. @Phoenix5440

Surprise, Surprise.....He is Dying.