DECENTRALIZED MEDICINE # 41: THE OXYGEN HOLOCAUST AND LIGHT CHOICES

So if you followed the decentralized medicine series closely so far and what I said in this podcast when I went back into the ICUs to rescue COVID patients from DARPA shots, you might be asking this question: Can knowing someone's blood gas or SpO2 help choose a light frequency for patients to pull them from the grave?

The surprising answer is that it is beneficial for the clinician to know what light to use at the bedside. For example, you might take patients out of the grave after their ICU doctors have told the family they are dying. I apologize in advance to the lay public. This blog is clinically oriented and designed for MDs to make sense of my last two blogs. If you want better MDs, you'll like them to read this information carefully.

This blog is key info to know before some idiot in the hospital tries Remdesivir as a Hail Mary.

 Pulse Oximetry and Light Absorption Basics

The package insert from any new pulse oximeter is spot-on with its description of how it works. Pulse oximeters use two wavelengths of light—red (around 660 nm) and NIR (around 905 nm) because oxygenated hemoglobin (HbO2) and deoxygenated hemoglobin (Hb) absorb these wavelengths differently:

• Oxygenated hemoglobin (HbO2) absorbs more NIR light (905 nm) and less red light (660 nm).

• Deoxygenated hemoglobin (Hb) absorbs more red light (660 nm) and less NIR light (905 nm).

• MetHb in Hypoxia and Injury: MetHb has a strong absorption peak around 405-410 nm, known as the Soret band. MetHb also shows broad absorption with distinct peaks at 540 nm and 576 nm. A characteristic peak emerges here, unique to metHb and absent in HbO₂ or Hb. This “metHb signature” is often used clinically to identify its presence, especially in co-oximetry, as it’s a marker of the Fe³⁺ state. The exact peak can shift slightly depending on pH and conditions, but 630 nm is a reliable reference.

  Decentralized MDs need to remember that MetHb accumulates in hypoxia-related injuries (e.g., ARDS, COPD exacerbations) or oxidative stress states (e.g., sepsis, toxin exposure like nitrates or anesthetics) because ROS or other oxidants convert Hb’s Fe²⁺ to Fe³⁺. Typically, metHb levels are <1% of total hemoglobin, kept low by enzymes like NADH-dependent methemoglobin reductase. But in injury:

  • Hypoxia: Low oxygen availability can exacerbate metHb’s impact, as tissues already starved for oxygen lose even more carrying capacity. Even 10% metHb can drop functional SpO₂ significantly, mimicking or worsening hypoxia.

  • Mitochondrial Context: If mtDNA damage from LIGHT STRESS impairs oxygen utilization, metHb’s rise should be expected to compound the problem, shifting metabolism further toward lactate and Warburg-like states. I found this to be the case for every patient in the ICU for 3.5 years when I went back during COVID to find the smoking gun in the vials. I found a lot more light in the ICUs.

  • I found that NADH-dependent methemoglobin reductase (cytochrome b5 reductase) activity could indeed be reduced if mitochondria aren’t functioning optimally, though it’s an indirect effect. This allowed metHb levels to rise way more than anyone knew in the ICU because none of them had the right oxygen saturation equipment. Since this enzyme relies on NADH as an electron donor to reduce methemoglobin, any condition that impairs mitochondrial function and, thus, NADH production could limit its effectiveness. In the COVID epoch, this was a tremendous insight.

  • Typically, NADH-dependent methemoglobin reductase uses NADH to transfer electrons (via its FAD cofactor) to reduce methemoglobin (Fe³⁺) back to hemoglobin (Fe²⁺). However, this enzyme accounts for only about 60-70% of methemoglobin reduction under normal conditions, and its activity can be insufficient in cases of severe methemoglobinemia or when NADH production is impaired (e.g., due to mitochondrial dysfunction, which just about everyone has today due to nnEMF).

    Methylene blue acts as an alternative electron carrier. When administered, it is reduced by NADPH (not NADH) in a reaction catalyzed by NADPH-dependent methemoglobin reductase (a minor pathway in red blood cells) or other NADPH-dependent enzymes like glutathione reductase. Reduced methylene blue (leucomethylene blue) then transfers electrons directly to methemoglobin nonenzymatically, converting it back to oxy hemoglobin. This process effectively bypasses the NADH-dependent cytochrome b5 reductase system, providing a faster and more efficient way to clear methemoglobin. 

  • We can use this in emergencies, such as acquired methemoglobinemia caused by toxins (e.g., nitrates or aniline). In ICUs, I was able to pull people from graves. Hospitalists were telling families their loved ones would die, and I would then speak to the families and tell them there was a bail out. I'd say to them this was a Hail Mary, even though I knew it was not. I could not let anyone know what I was doing in the ICU; otherwise, I would have faced what Mary Talley Bowden has in Texas. I picked the patients already speaking to Jesus, and nurses would call me in the middle of the night and tell me the patients were having miraculous changes. I told them to call their attendings. I played dumb the entire time, by design. I was using the wisdom I got from Becker, Brain Surgery Without a Scapel, which you will soon read in this series. Eventually, most of the nurses were more intelligent than the MDs, and they would ask me what I was doing.

  • This brings us to the big point: Pulse oximeters can misread metHb diagnosis because it absorbs at both 660 nm and 905 nm, often reporting a falsely stable SpO₂ (~85%) regardless of true oxygenation. I highlighted this pitfall in centralized ICU critical care medicine in this podcast. Co-oximetry, which measures metHb directly at multiple wavelengths (e.g., 630 nm), is needed for accuracy. Very few centralized medicine MDs know this information. Now you do.

• In a nontrauma or non-stressed situation, the device calculates the ratio of absorbed light by shining these lights through a pulsating capillary bed (like your fingertip) and measuring what comes out the other side. Using the Beer-Lambert Law (which relates light absorption to the concentration of a substance), it then estimates your SpO2, the percentage of hemoglobin saturated with oxygen in arterial blood. Normal SpO2 typically ranges from 95-100% in healthy individuals, though it can dip lower in certain conditions. The lower it dips, the more chances you have a Warburg shift and an undiagnosed metHb problem. Few centralized MDs know this.  

Pulse oximeters focus on arterial blood because they detect the pulsatile flow driven by your heartbeat, filtering out the steady-state venous blood and tissue noise.

SpO2 Effects in COPD and ARDS with mtDNA Dysfunction

Substantial evidence shows that SpO2 levels impact outcomes in COPD and ARDS, particularly when mitochondrial DNA (mtDNA) damage is involved. These diseases mimic what COVID presentations really were at the core. Let’s establish that first:

• COPD: In COPD, low SpO2 (hypoxemia) is a hallmark of disease progression, especially during exacerbations. Studies like those in the SPIROMICS cohort show that elevated plasma mtDNA levels correlate with disease severity, suggesting mitochondrial stress or dysfunction. Hypoxemia drives oxidative stress, which damages mtDNA, reducing mitochondrial efficiency and ATP production. This can shift metabolism toward glycolysis (Warburg-like), increasing lactate and lowering NAD+; a state of hypoxic metabolism even when oxygen is present. Not a good place to be unless you want to visit heaven

• Research also shows titrating oxygen to a SpO2 of 88-92% in acute COPD exacerbations halves mortality compared to high-flow oxygen, indicating that TOO MUCH oxygen can worsen outcomes, possibly by amplifying reactive oxygen species (ROS) in already compromised mitochondria = Oxygen Allergy = Oxygen Holocaust is a real problem in LIGHT STRESSED humans with any sickness.

• ARDS: In ARDS, SpO2/FiO2 ratios predict mortality and ventilator-free days, with lower ratios (e.g., <190) linked to worse outcomes. mtDNA damage is implicated here too—circulating mtDNA is a biomarker of severity, reflecting mitochondrial injury from hypoxia and inflammation. Patients with ARDS often exhibit a Warburg shift (aerobic glycolysis), where cells favor lactate production over oxidative phosphorylation, even when oxygen is available. This is tied to low NAD+ and impaired mitochondrial respiration, creating a pseudo-hypoxic state. Studies like those on the oxygenation saturation index (OSI) confirm SpO2-based metrics track disease progression, and hyperoxia (high SpO2) can exacerbate lung injury and organ failure, possibly via ROS overwhelming damaged mitochondria. Excess oxygen is a killer in a Warburg shifted organ. This is why ventilators killed millions.

In both conditions, mtDNA mutations or depletion impair the electron transport chain (ETC), particularly complexes I and IV, which rely on oxygen as the final electron acceptor. This inefficiency mimics an “oxygen allergy” or Oxygen Holocaust because cells can’t utilize oxygen effectively, leading to ROS spikes, more mtDNA damage, and a vicious cycle of metabolic dysfunction. This is why no one should be using exogenous oxygen treatments indiscriminately.

Linking SpO2 to Red/NIR Light Therapy to Disease

My argument made in the podcast with the Australian MD was that a patient's metabolic state will influence red/NIR light therapy choices. He looked stunned when I said it, but I am sure he did not understand my science. He tried to tell you all we are on the same page, and we are far from birds of a feather. I gave him a compelling biophysical answer, and I’ll bet he'll concede once he opens some biophysics books and realizes there’s more to explore here than he initially thought. The clinical point I am bringing out is that no studies directly test SpO2 levels as a decision point for choosing 660 nm vs. 850-905 nm in therapy protocols. However, my decentralized reasoning knows that breathing is an electromagnetic activity that employs a current (IMM), a magnetic field (Fo's head), and a paramagnetic gas with a known proton spin rate in health. My idea is rooted in mtDNA failure, NAD+ depletion, and Warburg metabolism, and it offers a mechanistic basis to hypothesize such a link. When I returned to the ICUs during COVID, I used this to save people from centralized MDs. Soon, you are going to see the raw power behind my clinical moves. They will stun you, a promise not a threat.

• Mitochondrial Mechanism: Red (660 nm) and NIR (850-905 nm) light stimulate cytochrome c oxidase (CCO) in the ETC, CREATING WATER while enhancing oxygen utilization and ATP production. Light therapy could theoretically compensate by boosting residual mitochondrial activity in COPD/ARDS with mtDNA damage, where CCO function is compromised if SpO2 is low (e.g., <90%), oxygen delivery to tissues is already limited. NIR’s deeper penetration might better target hypoxic mitochondria in muscles or lungs, improving oxygen use where it’s most needed. Conversely, if SpO2 is high but utilization is poor (hyperoxia with mtDNA failure), the superficial action of red light might suffice for skin-level detox or anti-inflammatory effects, avoiding ROS overproduction in deeper tissues. This is the targeted red light therapy I use on my patients.

• Warburg Shift and NAD+: The Warburg-like metabolism linked to nnEMF is associated with low NAD+ and high lactate and reflects a hypoxic cellular state despite adequate SpO2. Light therapy increases NAD+ availability by enhancing mitochondrial respiration (via CCO), potentially reversing this shift.

  

•  Since we know SpO2 is a proxy for oxygen availability, it hints to the decentralized clinician how much mitochondrial “help” is needed. Low SpO2 might signal a need for NIR to push oxygen deeper into hypoxic tissues, getting rid of NO. At the same time, normal/high SpO2 with metabolic dysfunction might favor red light to fine-tune surface-level mitochondrial activity without overloading ROS. This level of sophistication was absent in every ICU I worked in during COVID. Not one centralized MD knew this science until I taught it to them.

  THE DECENTRALIZED RED LIGHT LESSON GETS DEEPER

  Biophotons, Oxygen’s Paramagnetism, and F0 Spin: My Asprey 2014 Event.

  When you consider that it is well known and axiomatic that mtDNA release biophotons, oxygens have paramagnetic properties, and the F0 head spin rate for protons is known, this adds a fascinating decentralized layer to help diagnose patients who are dying. Let’s connect these to my argument:

  • Biophoton Release: Damaged mitochondria emit more biophotons (ultra-weak light) due to oxidative stress, ETC leakage. In COPD/ARDS with mtDNA failure, higher ROS correlates with increased biophoton emission, quantifiable via sensitive detectors. This could reflect the “electrical resistance” described in the DM #36 blog, disrupting the proton gradient across the mitochondrial membrane and slowing ATP synthase (F0/F1). If red/NIR light reduces ROS by optimizing CCO and displacing NO to make more ATP, biophoton release should decrease as a marker of therapeutic efficacy tied to SpO2 status. My decentralized model never allowed me to make a mistake in 3.5 years.

  • Oxygen’s Paramagnetism and F0 Spin: Oxygen’s unpaired electrons make it paramagnetic, interacting with magnetic fields in the ETC. The F0 head of ATP synthase spins at ~9000 RPM in healthy cells, driven by the proton motive force, but slows in disease (e.g., mtDNA damage), reducing ATP output and oxygen utilization. This drop increases ROS and biophotons, as I've noted. Red/NIR light should enhance F0 spin by improving ETC efficiency, particularly in low SpO2 states where oxygen is scarce or in high SpO2 states where utilization is impaired. Quantizing this via SpO2 would indeed guide therapy. Why? Anyone with a low SpO2 will need NIR to kickstart more profound mitochondrial activity, while high SpO2 might use red light to stabilize surface-level respiration. This science explains fibromyalgia patients as well.

  • SpO2 reflects oxygen availability, and in mtDNA-damaged states, it indirectly indicates how much light therapy is needed to overcome hypoxic metabolism or ROS overload. For example:

    • Low SpO2 (<90%): NIR (850-905 nm) is the optimal choice of light to penetrate deeper, boosting oxygen use in hypoxic, Warburg-shifted tissues. Most ICU patients fall into this group.

    • High SpO2 (>95%) with mtDNA failure: Red (660 nm) light might suffice for superficial benefits, avoiding ROS spikes in oxygen-rich but utilization-poor cells. Most people with fibromyalgia, ME, mold, chronic fatigue, and long covid fall into these groups.

    This isn’t a nutty idea, it is basic biophysics of breathing. I know that breathing is 100% an electromagnetic process in humans. Few others have this insight. For Centralized medicine, it’s a hypothesis worth testing. Because I know the laws of physics and have been using this for 20 years in my practice, I did just that during COVID.

  • The lack of direct studies doesn’t negate the mechanistic logic because these are all based on the laws of nature. This is especially true with biophotons and F0 spin as potential quantifiers. I’d argue that ICU trials would need experiments measuring SpO2, NAD+, lactate, ROS, and biophoton emission pre- and post-light therapy in these patients to confirm this. Until then, my decentralized thinking had bridged a clinical gap in critical medicine that this field hadn’t fully explored. This is why I admonished the MD from OZ during the podcast on his across-the-board use of HBOT on all patients.

    

  • MetHb absorbs strongly at 405 nm and 630 nm, with moderate absorption at 660 nm and 905 nm. You need to know this is enough to disrupt pulse oximetry but not necessarily light therapy’s mitochondrial effects. In hypoxia and injury, its rise reflects oxidative damage, potentially tying into my mtDNA-NAD+ photo-bioelectric hypothesis. It’s a decentralized wildcard worth considering: I have used this to pull people from the grave. In patients, when metHb levels spike, SpO₂ becomes less reliable, and light therapy’s optimal wavelength and duration might need to be shifted based on tissue oxygenation and redox state.

  • This means the Arndt-Schulz law may not be operational for this circumstance. The Arndt-Schulz rule assumes a dose-response relationship where low-intensity light (e.g., photobiomodulation, PBM) stimulates mitochondrial cytochrome c oxidase (CCO), boosts ATP, and reduces ROS. At the same time, excessive doses could overstimulate and harm cells. Usually, this works fine:

    • Low-dose red/NIR light (e.g., 1-5 J/cm²) enhances oxygen utilization and cellular repair.

    • Tissue oxygenation and redox state set the stage for how much stimulation is “low” or “optimal.”

    But with high metHb: more bad ICU lights and excessive nnEMF

    • Reduced oxygen availability: Even if SpO₂ reads decently, metHb’s inability to release oxygen starves mitochondria, alters NO levels, and affects stem cell depots needed to regenerate, lowering baseline respiration and recovery. Light therapy might still stimulate CCO, but with less oxygen to work with, the ATP boost could be muted, shifting the “low-dose” benefit curve.

    • Oxidative overload: MetHb reflects a high-ROS environment (since it forms via oxidation). Red Light, normally stimulatory, might instead tip the redox balance toward damage, especially if mitochondria are already leaking electrons (e.g., mtDNA failure). The “moderate dose” inhibition or “high dose” destruction thresholds could kick in earlier than expected. This is why dosing MB before PBM is a critically important teaching lesson for MDs.

    • Absorption interference: MetHb’s higher absorption at 660 nm (vs. HbO₂) and moderate absorption at 905 nm could alter light penetration. More energy might be absorbed superficially, reducing delivery to deeper mitochondria and skewing the effective dose.

    In short, the Arndt-Schulz rule might not hold its usual shape here. The “optimal” dose and wavelength for PBM could shift unpredictably because the tissue’s starting point, hypoxic, ROS-heavy, and metHb-laden, changes the biological response.

    Adjusting Light Therapy: Wavelength and Duration Will Be Decentralized Wisdom Few Have

    If metHb spikes render SpO₂ unreliable and disrupt the Arndt-Schulz framework, tailoring light therapy becomes a game of educated guesswork based on tissue state rather than pulse oximetry. Here’s how wavelength and duration might need to shift based on my COVID experience over the last 4 years:

    • Wavelength:

      • 660 nm (Red): MetHb absorbs more here than HbO₂, potentially limiting penetration in high-metHb states. This favors superficial effects (e.g., skin repair, local inflammation reduction), but red light might not reach deeper mitochondria effectively if tissues are hypoxic and ROS-saturated. It risks being “wasted” on a redox system that is too stressed to benefit, pushing the dose-response curve for PBM toward inhibition sooner.

      • 905 nm (NIR): MetHb’s lower absorption here (vs. 660 nm) allows deeper penetration, potentially reaching hypoxic mitochondria in muscles or organs. NIR might better support oxygen-starved cells by enhancing CCO activity where oxygen is still present, even if it is scarce. In COPD/ARDS with mtDNA damage, this could align with my earlier logic about NIR for low-SpO₂-like states. The key is to know when and who to hit with MB first. No one who does not have this understanding should be fucking around with MB.

    • Duration/Dose:

      • Lower doses: With high metHb and ROS, starting with very low doses (e.g., 0.5-2 J/cm²) might avoid overwhelming compromised mitochondria. The Arndt-Schulz stimulatory phase could be narrower, so shorter sessions (e.g., 5-10 minutes vs. 20) might stay in the “enhancement” zone.

      • Monitoring response: Without reliable SpO₂, you’d need proxies like lactate levels, NAD+/NADH ratios, or subjective energy/fatigue to gauge efficacy. If ROS spikes (e.g., via biophoton release, as you suggested), the duration might need to be reduced.

    Practical Implications

    In patients with metHb spikes, say, from sepsis, nitrite poisoning, or severe hypoxia due to light injuries, the injury contexts are:

    • NIR (e.g., 850-905 nm) might be the safer bet because of its penetration advantage. It targets deeper hypoxic tissues where mitochondria need the most help. A PBM-styled panel or NIR sauna could work, assuming low-dose protocols. Generally, a commercial sauna is not well powered, so it is usually ineffective for my patients. Decentralized wisdom:  Light’s a different beast, yes, it can, and it’s got flair. Pump enough energy into tissues and Fe²⁺ with the right wavelength (usually UV or high-energy visible light), and you can excite an electron right out of its orbit, leaving Fe³⁺ behind.  Proof that I am right about the power of biophotons is below.

      

    • Red (660 nm) light might still help superficially (e.g., wound healing), but its efficacy could drop if metHb absorbs too much light before it reaches viable mitochondria.

    • Duration adjustments: Start low and slow, as the Arndt-Schulz curve’s sweet spot likely shifts left (less tolerance for higher doses) in this redox chaos.

    You can see that my intuition is spot-on and that metHb complicates the picture. The rule’s predictability falters when oxygen delivery and utilization are decoupled, and SpO₂ can’t guide us clinically. It’s less about the law failing outright and more about its parameters needing recalibration. Clinical studies haven’t tackled this head-on for PBM in metHb-heavy states. I faced this state in 1998 when that 16-year-old girl had a massive trauma to her brain. My intuition about tissue oxygenation and the redox state of iron as the real drivers (not just SpO₂) was a solid leap, and it’s a gap that centralized researchers need to probe with data!

  SUMMARY

  Pulse oximeters are valuable tools if you know how to use them. They are also critical in understanding who should and should not get methylene blue. You must realize that pulse oximeters misread metHb levels because they absorb red light at both 660 nm and 905 nm. The machine often reports a falsely stable SpO₂ (~85%) regardless of actual oxygenation, a real pitfall in critical care medicine. Co-oximetry, which measures metHb directly at multiple wavelengths (e.g., 630 nm), is needed for accuracy.

  Relevance to Red/NIR Light Therapy

  Since I've explored light therapy (660 nm red, 850-905 nm NIR) in hypoxia, metHb’s spectra matter in people with significant mtDNA mutations, damage, and high heteroplasmy ratio in organs:

  • 660 nm: MetHb absorbs here more than HbO₂, so in high-metHb states (e.g., injury), red light LIKELY interacts differently with blood near the surface. It could theoretically stimulate cytochrome c oxidase (CCO) less efficiently to create water if metHb’s presence reflects broader oxidative stress, though direct evidence is lacking in the biophysics literature. This is where so much muscle pain comes from in FM cases.

  • 905 nm: MetHb’s moderate absorption suggests that NIR will penetrate deeper due to its physics, potentially reaching hypoxic mitochondria despite metHb buildup. Its lower absorption than Hb might mean less interference in NIR’s therapeutic effects.

  SUMMARY

  MetHb’s role in light therapy is uncharted territory for centralized medicine. Its absorption might alter light penetration or energy delivery to tissues, but no studies quantify this because they never thought to ask the questions I did 20 years ago when I began using this on my patients. If metHb signals severe hypoxia or ROS overload, it would argue for NIR’s frequencies to reach a deeper reach to target compromised mitochondria, aligning with my earlier point about low SpO₂ states. NIR also reverses the NO switch and turns the injury site from hypoxia to normoxia, so the MDs better know what they are really doing. So far, I have not met anyone who figured this out. But I have taught a lot of ICU MDs these decentralized tricks. Every one of my farm clients had peripheral blood smears and was monitored for oxygen saturation. Now they know why. I was collecting data on their biophysical status to make the correct decisions for them.

  Centralized data is thin here, but the biophysics of breathing is fully decentralized because it is 100% electromagnetic. This made me intuitively aware that I needed to take this into account for many patients with nnEMF-induced hypoxia and nasty peripheral blood smears. Its relevance isn’t off the mark!

  

• The Brutal Art of Choosing Your Life is YOURS and YOURS ALONE

  Deciding what you want your life to scream isn’t hard because it’s a primal pulse built around your light choices, a gut howl that erupts when you strip away the noise. No, the real gut-punch is staring down what you’re willing to torch, what you’ll carve out of your soul to chase what sets you ablaze. Life’s a feral tapestry, woven from decisions with sharp ones that cut deep, dumb ones that scar, all threading together into the jagged shape of your destiny. You don’t stumble onto beauty by playing it safe; you hack through the tangled weeds, lost and bleeding, until the path reveals itself. Act boldly and messily, so you’re not choking on regrets when the reaper knocks.

  I have no time for people who do not put in the time to understand how regeneration really operates. You operate on Nature's timescales, not your own.

   

  CITES

https://rumble.com/v6qrm46-graham-and-john-interview-dr-jack-kruse-with-a-panel-discussion.html