It was Decemeber 2010 and a my team of anesthesia people asked me to sit in on a continuing education class in the surgery department on one my surgery days.
I realized in 1 minute this was a BigHarma circle jerk.
The primary brand name for intravenous (IV) acetaminophen in the United States is Ofirmev. The medication is used to treat mild to moderate pain, fever, and moderate to severe pain in combination with opioid analgesics. They wanted my opinion on if I was OK using this as part of the anesthesia alogrithm for post op pain management in brain and spine cases and because I did most of the neurosurgery volume in the hospital in 2010 they wanted me to make the call. They knew I knew a lot of pain, POMc, and tylenol, because I had banned the use of this drug from all my patients in 2002.
I listened to the drug reps and reviewed what they brought me. First question I asked the reps what did they think about the 1998 actions of the UK on this drug.
Dead silence in the conference room filled with free BigHarma merch and food. 5 reps to cover the entire anestheisa and surgery dept. At the time, the anesthesia and general surgery depts were filled with employed MDs who worked for the hospital system. No one in the neurosurgery or orthopod dept were employed. At this time I noted the COO of the hospital was sitting in the back of the room.
I told the room filled with MDs and CRNAs that I banned the use of this drug after the 1998 UK black box warning. The published stories of the UK action was that typical UK pack size became restricted. In 1998, the UK limited the pack sizes of paracetamol available over-the-counter to reduce cases of intentional self-poisoning. If you could self poison yourself with an OTC medicine I said I need to find out why that happens.
ROOM silent as I spoke because they knew about how I fact check everything.
3. I then asked my assistant to go into my orders set. Back then there was no electronic records. I had a manilla envelop with a printed protocol that was to be placed on every case I did in this hospital. Here is below. Note the fourth line of this document.
I asked the reps what was the effect of IV route of administration on endogenous glutathione levels.
Crickets.
The reps with skirts and stocking and revlon make up all said that no preclinical studies were done on glutathione levels and the drug.
That raised my eye brows in a big way.
WHY?
4. I told the three pretty little girls working for Cadence Pharma that any PDR would show that acetaminophen clearance is critically dependent on glutathione (GSH) for detoxification, especially during an overdose.
At thos point my anesthesia team opened the PDR in the anesthesia dept library because that is the conferemnce room where the administration of the hospital set it up.
My head gaspasser announded to the room at therapeutic doses, a small, toxic byproduct is neutralized by glutathione.
He went on to point out, that large dose can deplete the liver's glutathione stores, leading to severe and potentially fatal liver damage.
I asked the room do you think the oral route and the iV route of administration are the same?
5. I told the entire room that the PDR was written exclusively about the oral route.
I then readdressed the reps trying to give us the marketing ploy.........
What is the data on the IV route?
Crickets.
BigHarma was not required to run studies because tylenol was already approved for use.
Right about then the MDs in the room became quite uncomfortable.
I asked the room how many people were given this drug this AM before I came into the room by the staff?
The answer was 11.
I asked who were the surgeons and could I speak to a few of them. I did and I asked them to get consent to get their patient blood drawm to test it for glutathione and its metabiolities and for me to have an extratube to test it optically. I got three yes answer.
6. All three patients had critical losses of glutathione and the metabolites pathways lit up like a firework display. A week later the optical testing came back and it was more devastating.
I then asked the Anesthesia Dept who booked the meeting? I was told the COO did.
I asked the reps what was the cost of the drug to the hospital and what was the codes used. They would not answer because the COO was in the room.
So then I asked the question differently. I know the charge for two tylenol is 13 dollars a tablet in this facility. Is the use of this medication more or less the cost of two oral tylenol. The pharmacy nurse chimed in and told me the cost was exponentially more than the oral route.
At this time the COO stormed out of the room.
I made my point to everyone.
7. As I finished my lecture to these clowns......I gave them a history lesson. Optical scanning became widely available to Big Pharma for inventory, tracking, and serialization purposes in the late 1970s, but regulatory mandates didn't compel its widespread use until the 2010s. I told the room that these reps bosses had the ability to optical scan molecules just as an NMR machine does in a chemistry lab and none of them were telling you the truth because MARKETING IS LEGALIZED LYING.
I found out later that week the hospital would have pulled in 1500 bucks for one dose of this poison, FYI
Today this drug is used by 99.9% of anesthesia depts.
JUST NOT MINE.
8. Does tylenol cause anemia since it affect gluthathione recycling in humans? Yep. A small portion is converted into a toxic byproduct called NAPQI. Normally, this is neutralized by glutathione and safely excreted.
Overdose and toxicity: In an overdose, the normal metabolic pathways become saturated, leading to a large amount of toxic NAPQI being produced. This rapidly depletes the body's glutathione stores.
Oxidative stress: Without enough glutathione to neutralize it, the excess NAPQI causes oxidative stress, which damages cells, including red blood cells. ---> patreon.com/posts/decentra…
9. What centralized MDs never tell people about tylenol. The drug causes anemia. This means it alters the UPE profile of RBCs.
Implications?
Reduced heme availability in the RBCs of the eye/CNS, gut, and skin sets off a systemic cascade, signaling bone marrow dysfunction and initiating ACD.
These all directly affect UPE transformations. This is a key communication breakdown in quantum biology.
Blood is 93% water, and generates UPE via ROS from hemoglobin/heme interactions (e.g., 380-450 nm from Fenton reactions).
Now add in the neurosurgery risks: With 20% of cardiac output perfusing the brain, this UPE flux is UBER significant to millions being sold a poison, supporting mitoception and neural energy changes = brown out mechanism in many organs.
10. There is a reason Susie Wiles wants me no where near MAHA and RFK Jr.
I am a great white shark for the truth.
No one can handle the truth.
At every level they are doing harm and most of you keep allowing them to do it.
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You see what Dr. Grimm sees in this paper, but what do I see in this paper?
This answers, definitively the question I posed to Huberman on the Tetragrammaton podcast, that the KT event drove internalization of melanin in eutherian mammals but not so much in birds. Perioxisomes burn fat and release UPEs. See the slide below in #7 and 18. That is the real story here. Light sculpted many changes with a rejection of chromophores in eutherians mammals and push for endothermy that lead to optimaization of the leptin melanocortin pathways.
Expanded Biophoton Sources: Explosion Post K-T
My list of 20 intracellular biophoton sources (e.g., NADH/NADPH, ROS, mitochondrial chain, melanin) shows an "explosion" post K-T, driven by adaptations like mitochondrial/peroxisomal amplification and melanocortin internalization.
This Fits ideally into my photobiolelectric thesis. Post K-T event we had a surge of changes that lead to more UPE creation: Reduced external UV forced internal UPE reliance, with sources like peroxisomal oxidation adding to mitochondrial ROS.
This ties to leptin-melanocortin (e.g., melanin in pigment cells emitting UPEs), myelin (membrane potential changes triggering UPEs), and quantum endothermy (IR as biophotons structuring water). The list expands our UPE narrative: post K-T, mammals/birds amplified endogenous light for signaling, reducing entropy via Shannon's theorem, enabling complex behaviors and longevity (e.g., human fur loss for more UV-to-UPE conversion). I see targets that others do not even know are there.
2. What were the only two animals that made is past the 5th extinction? Therapod dinosaurs became birds and eutherian mammals became humans.
The unappreciated metric, quantum-tuned endothermy, directly affected endogenous water chemistry in cells, as IR from both mitochondria/peroxisomes structures cytoplasmic water, enhancing coherence for UPE signaling. This was a critical step in evolutionary history of the mammals post KT.
3. What was the key in eutherian mammals? Innovating a placenta from HERV retrotransposons to build a placenta that had nuclear weapon capability to build complex life because the placenta are the major way eutherians make UPEs. That should raise the question in your mind, what drove placenta; growth in eutherians? My Brain Gut series covered that 15 years ago.
Photoreceptors are useless without retinal, which is produced in the eye. When retinal is liberated oxygen becomes a toxin and Fe is a wrecking ball. phys.org/news/2018-08-c…
nnEMF activates VGCCs, flooding cells with Ca²⁺ and ROS/RNS, damaging mtDNA and heme proteins (cytochromes, CYP11A1, CYP19A1). Blue light liberates retinal, impairing melanopsin and dehydrating melanin, lowering éR and DDW production. This stalls StAR (STARD1)-mediated cholesterol import via TOM/TIMM/VDAC2, blocking pregnenolone synthesis.
Dehydrated melanin disrupts microtubule dynamics and protein synthesis, exacerbating "pregnenolone steal" toward cortisol, depleting sex steroids. The retina, as a "window to the brain," thins under suboptimal light causung blindness, degenerating brain tissue (e.g., frontotemporal dementia precursors). nnEMF/lack of sun alters AMO in skin/eye, changing central retinal pathways. Oxidative stress increases peroxide (ROS) levels, altering UPE signatures and heme construction, and is linked to hormone-related disorders by disordered UPE transformation in the CYP enzyme system.
In humans, iron is a double-edged sword, especially in the brain. It’s essential for energy production in mitochondria and for synthesizing neurotransmitters like dopamine, which governs movement and reward. Iron accumulates naturally in the brain as we age, particularly in regions like the basal ganglia, globus pallidus, and substantia nigra. These areas, rich in gray matter, hold two to four times more iron than white matter, where myelin insulates nerve fibers.
But when iron accumulates excessively, trouble brews. In neurodegenerative diseases such as Parkinson’s, Alzheimer’s, and Friedreich’s ataxia, iron overload in neurons triggers oxidative stress, resulting in the production of reactive oxygen species (ROS) that damage lipids, proteins, and DNA. This process, known as ferroptosis, is particularly devastating in the retina, where photoreceptors and intrinsically photosensitive retinal ganglion cells (ipRGCs) are particularly vulnerable.
These cells, which detect light to regulate our circadian rhythms, rely on iron-containing proteins and melanin, a pigment that chelates iron to protect against oxidative damage. When this balance falters, ferroptosis destroys neurons, disrupting circadian signaling and contributing to diseases such as Parkinson’s, where the loss of dopamine-producing neurons in the substantia nigra is linked to iron overload and reactive oxygen species (ROS).
Why does iron accumulate in sick or dying neurons? The answer echoes the stars. Just as a star amasses iron in its core as it runs out of energy, neurons hoard iron when their energy production falters, often due to mitochondrial dysfunction. In both cases, iron signals a system on the brink, teetering between stability and collapse.
2. 95% of melatonin is made from mitochondria. So what happens when mitochondria are damaged from blu elight toxicity? You get high blood glucose and insulin and flatlined cortisol.
What happens when you knock out melatonin receptors via melanopsin dysfunction from the liberation of Vitamin A? You get insulin resistance and set the stage for many mitochondrial diseases like diabetes and cancer.
Do you know what I'm talking about? Light shapes life. How is it shaping yours? The link below should open your mind. onlinelibrary.wiley.com/doi/full/10.10…
3. Here are more links of blue light and photoreceptor damage.
Deuterium's Quantum Dual Nature: Bosons vs. Fermions
At the core is deuterium (D or ²H), an isotope of hydrogen with an extra neutron. My blog explains its particle statistics: Nucleus: A boson (spin 1, even parity), following Bose-Einstein statistics. Bosons can occupy the same quantum state, enabling phenomena like superfluidity or Bose-Einstein condensates at low temperatures.
Atom: A fermion (half-integer spin, like 1/2 or 3/2 ħ when combined with an electron), obeying Fermi-Dirac statistics and the Pauli exclusion principle. This makes deuterium atoms behave like "individualists" that can't pile up in the same state. This is why biology is racist against their use in mitochondria. The raise energy resistance.
Molecule (D₂): A boson again, due to symmetric nuclear spins in the ground state. It forms antisymmetric (para-deuterium, spin 0 or 2 ħ, even L) and symmetric (ortho-deuterium, spin 1 ħ, odd L) states.
This contrasts with ordinary hydrogen (H₂), a fermion in its para form (spin 0) and boson in ortho (spin 1), leading to different behaviors at low temperatures. Cooling deuterium near absolute zero produces pure ortho-deuterium with residual spin-2 fractions that can't be fully removed, unlike hydrogen's para form with zero angular momentum.
The takeaway: Deuterium's bosonic tendencies make cold D₂ act like a collective fluid (Bose-Einstein-like), while H₂ follows fermionic exclusion. This affects heat capacities, neutron interactions, and low-energy systems—relevant for fusion, cryogenics, and, as we'll see, biology------> All covered here. optimalklubs.com/kruse-for-dumm…
2. Biochemical Implications: Hydrogen Isotopes in Melanin and Metabolic Pathways
The diagram links this to biology, showing a pathway from acetyl-CoA (a ketone precursor) through melanin dissociation, involving clock genes, sunlight, and electromagnetic spectra. Key points:Oxygen (O₂) from NADP⁺/NADPH cycles feeds into tryptophan hydroxylation, producing intermediates like 5-hydroxytryptophan (5-HTP) and 5-hydroxytryptamine (5-HT, serotonin).
Hydrogen ions (H⁺) are central, explicitly noted as "THIS HYDROGEN CAN BE H+ or D." Protons or deuterons from the pentose phosphate pathway (PPP) influence steps like aromatic L-amino acid decarboxylase, leading to glucogenic amino acids (e.g., alanine) or neurotransmitters.
Deuterium's heavier mass (twice hydrogen's) slows kinetic reactions (kinetic isotope effect), disrupting enzyme kinetics, and the dielectric constant of the metabolic pathways altering UPE function, mitochondrial function, and water structuring in cells. The diagram implies sunlight-driven melanin creates a "plasma" for harvesting electromagnetic energy, with H/D isotopes affecting unique codes in water and biomolecules.
3. Connection to deuterium's physics: In biological "condensates" (e.g., exclusion zone water around proteins), bosonic deuterium has to enable collective behaviors, like enhanced proton tunneling or spin-dependent reactions.
This fully explains why deuterium depletion (e.g., via diet) is UNDERexplored in health contexts—high deuterium foods must hinder fermionic electron flows in mitochondria, while low levels promote bosonic fluidity. This is the basis of low energy resistance and high energy resistance.
Here's how this idea flows:
Low éR = Efficiency and Flow: In healthy states, like during deep sleep or a good workout done in sunlight with proper recovery, éR is dialed down. Energy transforms smoothly, think laminar flow in a river, minimal turbulence. Your cells rebuild, adapt, and thrive. Physics analogy: It's like a superconductor with near-zero resistance, letting current (or bioenergy) zip through without loss.
High éR = Stress and Stagnation: Push too hard in a blue lit gym with nnEMF in your ears, via light stress or chronic stress of any type, poor diet, use of supplements, or disease states, and éR builds up like traffic jams in a circuit. Energy dissipates as heat, damage, or inflammation, accelerating entropy at the molecular level. This links to aging (those "hallmarks" like genomic instability) and diseases (e.g., mitochondrial disorders causing brain fog and exhaustion).
Biology tie-in: It's why exercise feels good in sunlight in moderation but wrecks you if overdone under blue light in agym it is because éR rises, signaling "back off and recover." Blue light allows deuterium to flow into the mitochondria and the KIE takes over.
The retina thins from the effect of man-made light and a lack of sunlight, and then your risk of Frontotemporal dementia rises. The OCT test is the best screening test for FTD. We have familial and mtDNA FTD.
The retina acts as a ‘window to the brain," and that window changes the photolithography of the retinal cells. When the light is not optimal, the retina thins and the brain degenerates. Retinal degeneration has been detectable in mutation carriers prior to the onset of cognitive symptoms, establishing retinal thinning as one of the earliest observable signs of familial (frontotemporal dementia).
nnEMF and a lack of sun lead to neural degeneration, which is primarily driven by the abnormal accumulation of misfolded proteins within neurons. Light controls the confirmation bending of proteins. The DNA code controls the AA sequence and secondary bending, but quantum processing determines tertiary and quaternary bending by UPE transformation in cells. The most common protein abnormality in FTD is the tau protein, also known as TDP-43. These protein aggregates damage and kill nerve cells, leading to brain atrophy (shrinkage) and the resulting behavioral, personality, language, and movement problems characteristic of FTD. I believe this protein also thins the retina. Light is the offender.
Blue light increases RBC turnover in the retina and changes the oxidation state of iron, and this affects the synthesis of new heme proteins in the retina and brain. Oxidative stress is a key trigger in this disease because it increases peroxide production (ROS), which alters the UPE signature of cells in the construction of the heme proteins, which changes the photolithography inside the retina and brain. Changing the photolithography = altered protein folding via the Golgi apparatus and RER. TDP-43 is a biomarker of redox imbalance in FTD-related UPEs.
The path of energy in life, based on the evidence we have as a species now, is that Optical photonics began 13.8 billion years ago. The photoelectric effect was born from the rudimentary physics present in the early universe. Photonics precedes all chemistry of all types. Functional medicine does not realize this or teach it. Molecules were and are innovated by redox chemistry, and each one has an electromagnetic barcode to program its possible states around the star it evolved in.
The TDP-43 molecule is codified by light in its absorption and emission spectra. This links it to aberrant UPE production in the central retinal pathways, as blue light increases heme turnover to alter its biophotonic signal. Look at all the places a UPE can be made from in a cell to cause this disease on the slide. You'll also see that light carries spin information that can create this disease.
Where there is a change in matter (TDP-43), there must also be a change in atomic molecular geometry in that tissue. Where normal cellular geometry ceases to exist, we will find light as the key agent of change. When both exist in simultaneity, you'd better understand Fermat's law and the photoelectric effect to understand what a disease really is. Right now, in centralized ophthalmology, none of them do. See Bruce Willis.
THE BIOPHYSICAL CODA of FTD: When Turing realized morphology in all living things had a photonic timeline in Nature, he wrote a key paper on morphogenesis. Light signaling predates biochemistry and molecular creation from redox chemistry. This paper suggested that a system of chemical substances, called morphogens, could react together as a symphony does and subsequently diffuse their electromagnetic, electrochemical, and photobiolelectric information through a tissue to sculpt it, changing its morphology without using the nuclear genome.
Turing stated in 1951 that this set of circumstances is adequate to account for the main phenomena of morphogenesis. In such a dissipative system, although the cells may originally be quite homogeneous at the embryo stage, this information upload may later develop a pattern or structure in the embryo due to the instability of the homogeneous equilibrium caused by light pollution in the parents' germ line, which is triggered by random disturbances in the tissue. Those random disturbances are UPEs. The random disturbance he hypothesized about turned out not to be random at all. UPEs are created in cells by light AMO interactions via redox chemistry that directs their own sculpting from the nuclear genome. The UPE energy transformation is driven by the mitochondrial genome, which is subject to light in the environment to create UPEs and eventually by reactive chemicals like ROS/RNS inside all cells. Any disease linked to aberrant UPEs will always present as having a spectrum of maladies. FTD has that optical signature. ncbi.nlm.nih.gov/books/NBK55928…
2. The GLP-1 Drug Connection: Weight Loss at a Cost to Your Eyes and Ears
GLP-1 drugs like semaglutide (Ozempic, Wegovy) and liraglutide (Victoza) are prescribed for type 2 diabetes and weight loss, helping millions shed pounds by curbing hunger and stabilizing blood sugar. However, literature suggests that they can affect the eyes and even the inner ear (cochlea), which ties into the light biology disruptions we just discussed.
Effects on the Eyes
These drugs cause rapid weight loss, which triggers fluid shifts and reduced blood volume in the body.📷This can stress the delicate blood vessels in your retina, leading to:
Worsening diabetic retinopathy: In people with diabetes, GLP-1s can make existing eye damage worse, causing blurred vision or macular issues.
Increased risk of vision loss diseases: Studies link them to a doubled risk of neovascular age-related macular degeneration (nAMD), a leading cause of blindness.
There's also a higher chance of non-arteritic anterior ischemic optic neuropathy (NAION), where blood flow to the optic nerve drops, potentially causing sudden vision loss.
Blurred vision and other issues: Common side effects include visual impairment, which can start as early as 10 days after use. While not everyone experiences this (risks are low but real), regular eye exams are recommended for users.
How does this relate to light biology? The fluid shifts and oxidative stress from GLP-1s can amplify ROS production, disrupting UPEs and protein folding in the retina, much like exposure to bad light. This thins the retina, mimicking the early FTD signs, and could raise dementia risk indirectly through disrupted circadian rhythms.
Interestingly, while some research suggests GLP-1s might protect against general dementia by reducing inflammation, their eye effects could counteract that, especially in FTD-prone folks. My TED talk was banned because BigHarma was afraid I was going to obliterate their GLP 1 train by showing the world why they banned stopped the leptin trials early on weight loss.
3. Since the ear also processes sensory info tied to your body's clock, this could feed into broader brain degeneration.
Effects on the Ears (Cochlea)The cochlea, your inner ear's hearing hub, isn't immune. GLP-1s are linked to hearing problems like hearing loss, vertigo, tinnitus (ringing), and eustachian tube dysfunction (feeling of ear fullness).
Rapid weight loss can disrupt fluid balance in the ear, similar to the eyes. Diabetes itself raises hearing loss risk via blood vessel damage, and some GLP-1s (like exendin-4 types) heighten it further. The GLP target in the ear is the stria vascularis.
I tried to pull the veil back on the layers of the Deep State and where they are linked and why they are linked. It is a nasty story of deceit and ideological fascism where science was stolen to control modern humans with Light, drugs, and jabs.
The historical links you must know. Why is Israel so misunderstood? Propaganda is its shield, so you can never know who is really behind it.
It is British Imperialism dressed in drag to protect its ideology of fascism, which is what a Fabian really is.
The billionaires of today are not the architects of Zionism
They’re the actors. Elon. Thiel. Gates.
They run infrastructure, but they don’t own the world.
They were groomed by systems older than corporations.
The real owners?
• BlackRock, Vanguard, BIS — own the assets
• Rockefeller, Rothschild, DuPont — own the timeline
• WEF, CFR, Chatham House, Fabians — write the script
• Think tanks + foundations — enforce ideology
Occult orders + Straussian elites — justify it all as “destiny”
This is not capitalism.
This is a technocratic theocracy—where power is hidden in algorithms, law, debt, and narrative.
They don’t fear elections.
They fear recognition.
They fear you finding out what their plan really is.
Why must we decentralize medicine?
Because it eliminates centralized Rockefeller Medicine from the World.
That is a world where drugs and jabs are used as weapons of control.
Time to wake up and do your diagnosing better today than you did in the past.
2. True Evil with assorted atrocities most often occurs when the most respectable and intelligent of people fall for it. The wise never do. They sniff out and diagnose the problem of centralization to avoid collateral damage. Be careful who packs your parachutes.
3. What is modern gaslighting of the jab injured really? It is cloaked in pardons and Nobel Prizes given to the architects of the crimes.
I started a huge Barista FIRE on the boat it appears with my Bitcoin talks with him every AM. He apparently was quite influential with the young staff and told them all they were working communist hours for communist pay, and when his manager heard it spill over to our morning conversations and how many of the krewe I am Orange pilling, they axed him. He was escorted off the book quickly in Peru, and I never knew it until this AM. Some of his barista folks confirmed it got hot quickly.
What Is the FIRE Movement, and Where Does Barista FIRE Fit In?
FIRE stands for “financial independence, retire early.” The FIRE movement puts forth the idea that becoming work-optional isn’t about reaching a certain retirement age; it’s about having enough money invested that the compound interest gains can sufficiently cover your annual expenses. Bitcoin really changes the mix for young people locked into communist like employee environments.
This is achieved by reaching what is called your FIRE number. A (very) rough calculation of FIRE number is to multiply expected annual expenses when no longer working by 25. This is the amount of retirement savings you’ll want to have ready to tap, but know that performance on investment accounts can vary widely from year to year. A traditional FIRE number is typically well north of $1 million.
There are many people who don’t actually want to stop working and enter full retirement. Instead, they want to downshift to doing more fulfilling work, or they want to be able to work part-time so that they can spend more time pursuing hobbies or passions. In jobs like medicine and cruiseship workers the math works rapidly but for different reasons. So when I explained this to Christopher he seemed to catch fire like I had poured diesel fuel on him. Never thought he'd get canned for it that fast. I guess capitalism is a bad antidote for the communist boat life.
2. The Origins of the FIRE Movement
In 1998, three researchers at Trinity University published the results of a study on retirement savings.
Their projections found that, if an investor had a certain multiple of their income saved up and withdrew 4% or less of their nest egg each year, their chances of depleting their savings in a 30-year period were zero. I re-did this calculation in 2013 and added Bitcoin CAGR to the mix, and the results were more stunning. That is when I realized I could bail on centralized medicine and began teaching this method to my MD clients. Sadly, most of them crumbled because they could not fathom walking away from their jobs because of their programming. The Trinity research group was based on rates of return since the invention of the 401(k) and other tax-advantaged retirement accounts, and later became known as the "Trinity study."
3. The results of the Trinity study were first published in the American Association of Individual Investors Journal in 1998.
This research led to my reframe: If you could grow your nest egg large enough that the interest alone covered annual expenses and other medical expenses, most or even all of your principal would be protecting, preserving your wealth. I tweaked this big time. I realized that the decentralized mitochondrial life could bring medical expenses to zero and then I could power up my savings with the Bitcoin CAGR i could make money grow on trees for decades. IT was how I figured out that the one thing killing me, my job, could be eliminated rapidly. I got a huge settlement from a cruise incident related to a paleo meathead, and I yolo'd it into the program, and within a year, I found out this was going to be life-changing.
The Centralized Fiat Retarded Say Money Doesn’t Grow on Trees......but decentralized geniuses know it happens.
If your tree is a large enough nest egg due to the Bitcoin CAGR, it actually does. I began to realize that the traditional retirement age wasn’t dictated by age, but by whether you reach financial independence. Thus, the ORANGE FIRED MD lifestyle was born.
FIRE stands for Financial Independence, Retire Early. Over the years, however, many ORANGE FIRED MDs Savages began to break from core FIRE principles and define FIRE variations that better suit their lifestyle goals. I helped many of my tribe do just that. Membership matters in this tribe.