1. What do your photoreceptors have in common with your red blood cells? The outersegments of photoreceptors have no mitochondria. Neither do adult RBCs. Why? What does it mean? Shannon's theory on information transfer tells us for a message to high fidelity, the message has to be unusually. The message built into certain cells in our biology is whispering some of Nature secrets to us. Are we listening?
2. When a cell does not have mitochondria it means that the TCA metabolic efficiency is very low. It means that these tissue are starved of oxygen. It means their physiologic ability is atsavistic. It reverts to older evolutionary pathways to exist than the more modern TCA cycle that high efficiency organs require. Remember the human brain gets 20% of the cardiac output. That is a lot of oxygen. That tell us the brain like the TCA cycle.
3. Many of the biochemist food gurus like Seyfried will tell you the Warburg metabolism is pathologic. Very few of them will tell you that humans have tissues that only use it to operate in adult human life. They are impotent to tell you why it is useful in one place and cancerous in another. The teleological explanation for the presence of the Warburg effect in the mammalian retina is simple to understand once you have a basic idea of what Krebs bicycle really is. This is where the TCA cycle and urea cycle overlap.
When proteins synthesis is massively upregulated by ubiquitin, the cell cannot rely on the steady removal of anions from the TCA or urea cycle to fuel biosynthesis because of slowed down metabolic kinetics of either cycle. These cycles slow down because OXYGEN is absent. These cycle mimic what life ws like during the GOE.
4. This situation creates a logjam for the cell with respect to the cell cycle. The collateral effects are felt in the mito matrix, with respect to hydrogen movements, because of the need for of H+ to run the ATPase to power both cycles. So what does a cell do when redox drops and the kinetics of the TCA and urea cycle have lowered cycle rates? What happens when they are lowered for any reason?
Cells who use a Warburg shift must rely on the older evolutionary pathways, glycolysis with the help of H+ to transfer information over energy to get the job done. Each C-N bond in proteins costs 5 ATP. This is very costly on an energy basis. Information costs are even greater when this happens. This has huge implications for Shannon theory on information entropy. This means biosynthesis becomes like the interest rate on our debt; it becomes an energy hog for the cell.
Does the retina use the TCA or urea cycle exclusively for biosynthesis? No, they do not. This should surprise people considering the metabolic rate of the retina. So how does this process occur in the retina? The retina is a tissue with a high oxygen demand in the back of the eye but a poor supply in the front of the eye.
5. The anterior chamber of the eye has to rely on getting oxygen from diffusion through the cornea from the air because the cornea and lens must remain transparent for vision and no blood vessels can impede the passage of light.
If the cells of the eye used TCA intermediates exclusively for biosynthesis, considering this oxygen issue, it would create a chronic proliferative state in areas of the eye and this would impede its function.
This defeats the purpose and the physiologic requirements of the central retinal pathways, pituitary, and hypothalamus. All of these places in the brain that are light relay stations are quite small in size. The reason these parts of the brain are small in stature is that they deal almost exclusively in information quanta processing over a growth and proliferation state. They are using UV and IR light to transfer information from cell to cell.
6. This implies that the retina must run two different metabolisms to get the job done in vision. Is this true? Yes, it is. It turns out the adult mammalian retina is non-proliferative because of how it is built to interact with light, it shares similar biosynthesis requirements to neoplastic tissue because of the prodigious turnover of the opsin proteins in the disc membranes of the photoreceptor outer segments.
This explains why certain cells of the retina use the Pasteur effect. I gave you a blog on that effect on Patreon in 2018.
Each mammalian rod outer segment consists of a stack of ∼1500 distinct discs enclosed by the plasma membrane. Approximately 60% of the dry weight of the disc membrane is protein, of which, opsin comprises 90% of the protein content. There is not a lot of mitochondria in this area at all.
Remember all opsins are "loosely" covalently bound to Vitamin A to operate in humans. Hence, the retinal-bound opsin, rhodopsin forms a large structural component of the rod disc membrane. These components are even larger in the outer retina where melanopsin controls the quantum release of melatonin release from the pineal after 4 hours of dark. This is the major quantum mechanism that controls mitophagy and autophagy signaling.
7. When mitochondria are absent or poorly functioning the game of evolution is to try to recycle ATP faster than it does in the TCA cycle. How does this happen? It uses the pentose phosphate pathways. So when a tissue is defective for some reason or an older generation of the operating system is in use, these are the pathways that do better with GNCs creatine.
Did you hear that correctly Bitcoiners and bro science folks. Youre using fiat or ETH to run your Bitcoin node. That is what using creatine means in biology.
8. All G-coupled receptors are linked to the circadian mechanism in humans. Rhodopsin used in the eye is a G protein-coupled receptor comprising 348 amino acids, with a rich glycine and serinecomponent. This is the very same serine and glycine amino acid components that link them to the speed in the PPP (and in glycolysis). The PPP is the major way cells regenerate the major reductive moiety called NADPH you learned about years ago in the EMF 4 blog post. This is how life did it before the TCA cycle was used due to oxygen. Note below the thermodynamic implications of using older pathways. They have to rely on non visual photoreceptors more.
9. Tissues with poor oxygneation cannot use the TCA or urea cycle. This is critical in tissues that cannot use the TCA or urea cycles because this is a backdoor way for the cell to augment informational quanta transfer using H+ pulled from the serine cleavage system.
What are the cells that have to live this way? Cells that do not have a lot of mitchondria, or cell whose mitochondria is not operational. They are RBC’s, Muller cells and every single embryonal stem cell uses glycolysis and the PPP by nature’s design.
None of them have high oxygen contents. This keeps a lid on their growth rates. There is NOTHING pathologic about these cells that have to rely on gluconeogenesis. The key point in understanding is that when cells use gluconeogenesis for biosynthesis exclusively they MUST use glycolysis and the PPP for biosynthesis. What determines their use? The amount of oxygen present in the tissues.
10. This is where you may remember David Sinclair paper about pseudohypoxia, NAD+ and aging I mentioned in December of 2013 on the blog. Sinclair was talking about cells losing the ability to use the TCA and urea cycle as they age so they all seemed to have a common phenotype of having low NAD+ and pseudohypoxia.
He called it a cardinal feature of aging and disease. When cells that use the TCA cycle are oxygen deprived they age faster.
The Bitcoiner bro who are addicted to creatine better think about that line above carefully. If they do not they need to make a multisig for the kids because they will follow the fate of Jobs, Allen, and Hal Finney.
It turns out in Sinclair's 2013 paper he misread the tea leaves of Nature. The skeptic may say he took financial advantage of it.
As cells age, they become less able to use the TCA and urea cycle because autophagy loses its efficiency, due to a loss of redox power. When autophagy becomes faulty, sleep becomes poor as a marker for aging, and as a result, a cell loses control of atoms of deuterium buried in the PUFA in the mitochondrial membranes and membranes in cells.
You heard about this mechanism in the May 2018 webinar. This is a huge big deal folks. Why? What are the collateral effects of this mechanism?
Is this how cells make and create Ultraweak-biophotons they use to direct cells to a mitotic division? Yes. Is this the basis of the research of Fritz Popp work on ELF-UV light.
11. Richard Young did the seminal experiments on the retina. The deuterium critics have no clue how this complex dance operates because they do not understand how information is transferred via the quantum spin state of protons and electrons to Orbital Angular Momentum (OAM). Biophysics controls this process not biochemistry.
Moreover, they have no idea what the OAM is used to do in your cells or blood. The next few ideas link my Vermont 2017 talk to the one I gave on the skin last week. This is a story of how deuterium does things people never anticipated to help mitochondria and cells self-regulate their own behavior under the power of the Auger effect (UV light). UV light is critical in controlling ECT flow in mitochondria several ways as this series has shown.
Now you do and I am showing you how it links to the physiology that controls melatonin creation and releases in the mammalian retina. In fact, this quantum mechanism is so powerful that Mother Nature decided to use it kingdom-wide in our clade and on every surface of their body plans.
12. The rhodopsin turnover rate in the human retina parallels the degree of aerobic glycolysis found in many different species in mammals. The rhodopsin turnover rate matches the Vitamin A and D cycles in humans almost perfectly. I showed a slide of this in Vermont.
This is why unsupplemented Vitamin D levels are great proxies for defects in Vitamin A cycles in the brain and retina. This makes your unsupplemented Vitamin D3 level a great proxy for what is really going on in your skin and eyes mitochondrial matrix. The next part of the puzzle is not well known.
13. Photoreceptors have a relatively low rate of turnover in lower vertebrates. This is not true in humans. In lower vertebrates there is a different system in operation that uses a temperature dependent mechanism. This is another clue from Nature that the problem links to the H+/D effect in tissues. Think Shannon thereom.
Recall physics dictated that higher temps favor H+ bonding in aqueous environments versus D bonding in water.
As temperature increases, the non-pathologic Warburg effect becomes temperature-dependent. In mammals the story is exactly the opposite.
The rate of turnover in the mammalian retina is astounding and this is why mammals became warm-blooded. Lower vertebrates where not.
Mammals are 200 million years old they used heat release from their mitochondria to precisely control the flow of H+/D in the matrix and cytosol to control growth and metabolism of the retina just by using light and temperature and oxygen concentrations in the eye. This was the core message I delivered to "Uberman."
This is the basis of the CT 4 and 6 blogs written over a decade now. All of these reasons are why I made the educated guess years ago that melanopsin had to be present in the skin/fat of mammals. In December of 2017, I was proven correct on my guess. Light controls this process. Not bioelectricity as Levin wants you to believe.
14. Since melanopsin is present in the eye, arteries of the skin and fat mass this becomes a critical point in understanding how the skin becomes the gatekeeper of deuterium flows from the blood plasma versus the tissue. Remember phototaxis is well known in the leaves of plants. Most third graders know that leaves grow toward light and can change their angle of inclination of growth toward sunlight based upon the type of sunlight present. Very few people realize that the RBC’s in mammals do the very same thing as leaves. This maybe why aneurysms form in arteries because RBC function differently when they are out of sunlight. Arteries should have laminar flow in the center of a vessel and why blood flow is more turbulent towards the artery wall. Sunlight causes the entire arteriole to migrate toward the sunlight of UVA light. Sunlight can directly affect the RBC’s in the center of your blood vessels to act just as leaves do to collect IRA and UVA light as a form of animal phototaxis.
15. Recall UV spectrum in sunlight heats mammalian skin up the most significantly. IR light in sunlight is considered cold light energy on a relative basis but it is the initial light of the sun that builds the EZ in tissues and our blood.
Remember, via chemistry’s laws that heating favors H+ in hydrogen bonding over deuterium bonding, so organisms can use their body heat as a fractionation method to control growth in tissues. This helps you understand further why mammals evolved warm bloodedness.
Heat is a powerful physical tool in controlling the flow of different isotopes of hydrogen in your cells. It turns out UV light raises the temperature more than any other light waves in sunlight.
16. Having the innate ability to uncoupling your protons gradients helps keeps deuterium in the blood plasma because blood moves so rapidly, it can diffuse its heat like a radiator, but tissues do not have the same ability. This relative difference is all that is needed to control where isotopes of hydrogen should be found. When deuterium is trapped in the arterioles of the skin is can be pressurized by sunlight in the UV range and the chiral heat effect to pinch deuterium in the blood vessels coming to the surface, while at deeper levels H+ accumulation is favored in our tissues. Compression of H+ or deuterium allows the body to make a continuous UV spectrum from the isoform of hydrogen trapped in both tissues.
The UV spectrum is not equivalent because of the chiral heat effect. In the blood, the spectrum of light extends deep into the UVC range, and this frequency matches the optical absorption spectrum of the EZ in the blood. Recall this is built by the water and IRA light initially from the sun. When this phenomenon occurs in the blood plasma, the EZ can grow further to absorb light rays into the UVC range to further energize blood plasma to carry more light energy and information in the ophthalmic artery distribution of the retina. The flow of information is more important in tissues that cannot use the TCA or urea cycle. This helps the areas of the retina that have poor blood flow. This circulatory pinch of hydrogen allows deuterium and hydrogen to become a creator of full spectrum UV spectrum light creators via an unusual nuclear effect specific to hydrogen on the periodic table. This photic phenomenon extends the size of the EZ in the blood and vascular space to become something more than just a battery or capacitor as Pollack has shown in his studies on water. According to Pollack he just took my criticism of his work from 2013 and found out DDW has an even larger EZ than what he found in his 2010-2013 experiments.
17. The NIR light addition to blood allows water in our bodies to transform into an optical resonator. This means it can operate like a molecular mirror. This mirror can then be used to optical resonator to create tiny lasers at our skin surface or in our ophthalmic artery which feeds the retina. Recall that NIR light knocks off NO to make Hb stay in its +2 state and this is the state that binds oxygen. This is how the decision tree operates to run the TCA cycle over the PPP.
That UV light created by this mechanism is then used to regenerate melatonin, dopamine, and build many more substances in quantum thermodynamic fashion. This is how every non visual photoreceptor in you regenerates. Look at the slide below.
This system is amazing when you see how the quantum system is organized to support the semiconductive circuits of the central retinal pathways I laid out in last years Vermont talk. How it links to the skin is also quite remarkable. You might want to watch that Vermont video 2018 when it goes live here on Patreon.
We can see the wisdom of information quanta by nature when we carefully examine the anatomy of the photoreceptors in our eyes. I showed some of Dr. Wunsch slides in Vermont in 2017 but I could not get into this level of complexity with that audience because they were not facile with the science and they were not mitochondriacs who understood what Krebs bicycle was. I am hoping to change that this year. You have to understand how quantum thermodynamics differs from classical thermodynamics to understand the process fully.
18. In the retina information from light is the key resource that determines the anatomy. The organization of the retinal cells involves the highly compartmentalized cellular configurations, with the confinement of mitochondria to the inner segment, absent from the outer segment.
The dense aggregation of mitochondria in the ellipsoid region of the inner segment reflects the considerable reliance of this portion on oxidative energy from the TCA/urea cycle.
Evidence that supports these ideas was the finding of high concentration of malate dehydrogenase (an enzyme involved in the TCA cycle) in the primate photoreceptors inner segments.
The malate result revealed a level 30 times higher than the outer segment of the photoreceptor. Malate needs fumerase to be completely free of deuterium to add water to it to support the functioning of the inner retina. This tells the wise person nature had to build a light-based control system to control the flow of H+/D if any retina was to operate with an aspect of light from the sun.
I think the momentum of light within the visible spectrum is key to understanding how our eye works. I began to put all the pieces together 18 years ago.
Now you can see information processing in the eye and skin really begins with H+ and deuterium fractionation occurring immediately in the surfaces of the retina and skin. This helps explain why nature really built the retina in the way she did.
For those of you who don't know the retina appears to build inside out. This has confused biologists for ages because none of them understand light well. It is backward because mitochondrial use of oxygen is a GOE event life had to deal with. She used our light absorbing biomolecules to solve the GOE riddle. The same idea is true in the skin's physiology.
19. Key point in the thread. This is why my periodic table hacks mattered.
Since this was true in the retina, I knew that it had to share metabolism with several pathways that worked with different oxygen levels.
Oxygen as an atom of matter creates complexity just by its presence or absence. Read that again. Oxygen is your biobot in quantum biology. Its uniqueness is the key to understanding it. It is paramagnetic.
Atoms can and do act as nanomachines in cells. Theses quantum machines in cells are built toward specifics found to the environment it is working in. A machine for building a house might not be capable of dismantling it.
The edges of your biology, the integument, the gut, the eyes tell a different story than the center of the organism through the morphogeneic lens. These boundaries aren’t just dividing mindlessly, they’re deciding what they can become of the light they sense. They are not bots, they are quantum computers who use light to make bioelectric bets.
20. I hypothesized that we should see data that lactate would be higher in areas where the PPP and glycolysis are used in the retina. I believed strongly in 2003 the same thing had to be true in the skin because of their shared embryology. Do we have any evidence of this? Yes we do.
Contrary to conventional biochemical wisdom, the measured fractions of lactate dehydrogenase (LDH) used in glycolysis was significantly LOWER in the inner segment where the cones are located as compared with the outer segments of the retina where melanopsin and Vitamin A are used.
This tells you cone vision needs lowered oxygen tensions because the light they work with is less powered than the blue light that melanopsin works with.
Look at the circulatory system of your eye. You'll see the message Nature gave me.
21. This is why the fovea/macula has a POOR blood supply. I showed those pictures last year in Vermont (above). How does the retina accomplish these thermodynamic gymnastics? It did exactly what the RBC did in evolution. It eliminated mitochondria from the cone cells while restricting blood flow to make sure no oxidative metabolism from the TCA/urea cycle could occur there. Any place mitochondria are located, deuterium, the heavier isotope of H+ must be sparse, and vice versa. This is tied to the quantum thermodynamics of the tissue in question.
The quantum machines in our cells in different tissues are built toward specifics found within the environment the cell is optimized to working in.
The exclusion of mitochondria from the photoreceptor outer segment necessitates its reliance on glycolysis/PPP for cellular energy production, while still permitting information transfer from sunlight via protons with the H+ isoform in the retina and into the small structures of the brain mentioned above. There is a deep lesson here for the mitochondriac about how and why the retina where built as they were to work with hydrogen to make UV light inside our body to drive photonic programming of physiology. This is how information quanta is created and moved in the central retinal pathways to affect your brain and CSF pathways to build the world wide web in your head called your mind.
22. So if your brain improves on creatine........youre not really human. You are not using the TCA fully on the surface of your brain. This means you are a B, C, or D compared to the way Nature built you to work.
Once you see it and understand it for yourself then you'll know why I warned you if you see a benefit to creatine and use it a lot, you are digging a huge hole on the suface of your brain and you might now get out of it easy.
23. @threadreaderapp make a roll
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1. ANSWER: In ALAN contexts, blue light suppresses melatonin, which normally inhibits AVP and cortisol, leading to unchecked vasopressin release during "light stress." This causes a reactive hyponatremia in the posterior pituitary, activating brain osmoreceptors and RAAS, raising blood pressure and stress hormones, which fragment sleep and impair daytime recovery. They also chronically degrade the mitochondria in these neural tracts.
2. Now for the dirty details.
Precise Mechanisms of Sodium Regulation in the Brain and Circulatory SystemSodium (Na+) homeostasis is tightly regulated to maintain osmotic balance, blood pressure, and neuronal function, with disruptions like hyponatremia (serum Na+ <135 mEq/L) directly impacting sleep via arousal, cognitive fog, and fragmented rest. The brain acts as the central sensor and regulator, while the circulatory system executes adjustments through hormonal and renal pathways.
Brain's Role in Sodium Sensing and Control: The hypothalamus, particularly osmoreceptor neurons in the supraoptic and paraventricular nuclei, continuously monitors plasma osmolality and Na+ levels via stretch-sensitive ion channels. When hyponatremia occurs (e.g., from ALAN-induced vasopressin overrelease diluting blood Na+), these neurons trigger arginine vasopressin (AVP, or antidiuretic hormone) secretion from the posterior pituitary.
AVP promotes renal water reabsorption via aquaporin-2 channels in the collecting ducts, conserving water but exacerbating dilutional hyponatremia if unchecked. In the brain, low Na+ also activates the subfornical organ and organum vasculosum of the lamina terminalis (circumventricular organs lacking a blood-brain barrier), which integrate signals from baroreceptors and chemoreceptors to modulate thirst and salt appetite. Chronic hyponatremia impairs neuronal excitability, leading to symptoms like headaches and insomnia, as it alters membrane potentials and synaptic transmission.
Circulatory System Integration with Hormones: In the periphery, low Na+ (hyponatremia) is sensed by renal juxtaglomerular cells, triggering renin release, initiating RAAS: renin converts angiotensinogen to angiotensin I, then II, which stimulates aldosterone from the adrenal cortex to enhance Na+ reabsorption in the distal nephron and potassium excretion. This raises blood pressure to restore volume but can cause nocturnal hypertension, disrupting sleep architecture (e.g., reduced REM). Cortisol, released from the adrenal cortex in response to stress signals (including ALAN and hyponatremia), amplifies this by promoting Na+ retention via mineralocorticoid receptors and enhancing sympathetic activity, increasing heart rate and arousal. Vasopressin interacts with cortisol and RAAS; for instance, AVP potentiates cortisol's effects on water balance, while cortisol feedback inhibits AVP in healthy states, but ALAN disrupts this, leading to unchecked stress responses. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) counterbalance by promoting natriuresis (Na+ excretion) when blood volume rises, but in hyponatremia from SIAD (syndrome of inappropriate antidiuresis), this balance fails, perpetuating low Na+ and sleep disturbances like frequent awakenings.
3. So Emily, what you should do is see the AM sunrise every AM. Drink DDW water and add high-quality salt to the water, and within 2-4 weeks, you will sleep much better. These slides support the tweets, and the last one with the D20 water spectrum really hits the mark.
A couple of points: Not all human cells have mtDNA. See adult blood cells. This is a big deal when you consider their absorption spectra. 200-600 nm light with a sharp cut-off. Also, blood still transforms energy into UPEs. And since blood fills 20% of our CO to the CNS, this also has implications. The retina and gut increase their blood flow with light use and feeding. Feeding is a light-based phenomenon since all food webs link back to photosynthesis.
In humans, light stress does not force mitochondria to react exactly the same way as infection (no ATF4 surge, different folate handling), but there are partial overlaps in ISR activation, 1C remodeling, and mtDNA signaling.
This suggests UV light acts more as an external folate depleter for DNA protection/photorepair, while infection is an internal ATF4-orchestrated defense. If environments lack natural light controls (as in modern human life), it should exacerbate mismatches in folate biology. For deeper dives, I'd recommend reviewing the ATF4-UV papers for experimental details.
Folate as a Light-Responsive Switch: My patreon has made this point over and over again, natural folate (not folic acid) is photosensitive, degraded by UVB, and shows seasonal lows in summer (higher at low latitudes, with gender differences showing men have lower levels). This would act as a "switch" for mitochondrial/genome control, linking to melatonin/tryptophan pathways and neurotransmitter synthesis (e.g., serotonin, dopamine). In low-light/artificial blue light environments (e.g., indoors), folate stability increases unnaturally, disrupting methylation/DNA synthesis and contributing to diseases like Alzheimer's, Parkinson's, or diabetes (via melanin quenching loss and superoxide buildup). People with MTHFR and COMT defects are supersensitive to ALAN and a LACK OF SUNLIGHT. This is echoed all throughout my decentralized photo-bioelectric thesis: light refines folate via photosynthesis/food webs, but artificial setups bypass this, leading to transgenerational effects.
No Seasonal/Light Controls: absent natural light cycles (e.g., constant artificial light), retinal/CNS signaling should be expected to dysregulate—e.g., excess folic acid fortification (since 1996 in North America), which overloads 1C pathways, causing cognitive haze, sleep issues, or neural migration problems in lit environments. This photonic effect is completely missed in centralized medicine and is really missed in functional medicine, which pushes for excessive folate use with SNPs. These people need more sun and less ALAN, not drugs.
Black Swan Mitochondriac View: Melanin (from UV-absorbing aromatic amino acids) quenches mitochondrial superoxide, protecting against neurodegeneration. Blue light destroys melanin and heme proteins, amplifying risks from ALAN and a lack of sunlight which aligns perfectly with UV's mitochondrial stress but without the adaptive folate restriction seen in infection.
2. Why is this tweet important to the jabbed? If you follow the work of @Kevin_McKernan you'll find in his blogs many mentions of pseudouracil and jab injuries. Then you look at my blogs on jab repair, and you'll notice I recommend Tropical relocation as the best risk reduction for the compliant. WHY?
Did you know that in humans, UVR depletes folate in skin and blood, inducing S-phase arrest, affecting uracil misincorporation (frame-shift mutations), and sensitizing apoptosis in keratinocytes. This isn't "damage" but a permissive environment for seasonal phenotypic changes, e.g., increased melanin production to protect folate stores. When you understand the photorepair mechanism, you will see this is how humans can block the DoD and BigHarma death mechanism from uracil replacement induced by the jabs. @MdBreathe None of the COVID experts have this sophistication. They are still pushing detox answers when it is crystal clear that redox biology is the path for the Savage trying to stay alive and away from disease.
3. Individuals with MTHFR C677T (thermolabile variant) are indeed supersensitive to light/folate fluctuations, as the mutation impairs folic acid conversion to 5-MTHF. High folic acid may select for this allele evolutionarily, acting as a "genetic time bomb" by promoting unmetabolized buildup and altering DNA/RNA biology.
People who have this SNP and took the jab have no choice but to move. If they do not, they will be taken out to Taper the Ponzi. This variant requires higher folate for stability, making carriers vulnerable in low-UVR (winter/indoor) settings, where blue light further degrades melanin (a superoxide quencher), exacerbating mitochondrial stress.
If Einstein was correct that energy = mass times the speed of light squared (E = MC2), then how did biology make all life from that simple equation? As I looked up, the sun hit me in my eyes. I realized the link, right there. I had to reverse Einstein’s equation to see how life made sense of the chaos on our planet, to create life from it. E = MC2 is a simple math equation using simple variables we all know.
Truth Bomb #2: Life is energy and energy is life according to this equation.
It also implies that the equation can also be reversed mathematically. The “Commutative Laws” say you can swap numbers over and still get the same answer. A + B = B + A. Biologic sciences have pretty much ignored E = MC^2 for much of the last 108 years since its discovery. It has been felt to be the domain of subatomic physics and of theoretical physics, and astronomy. Physicists and chemists have always read Einstein’s masterpiece equation from left to right. This helped them explain the massive power generated from the nuclear fission of atomic blasts. As a surgeon, I realized there is were no nuclear explosions occurring in cells to generate energy. I reasoned, biology could not use the reaction that way, so life had to find another way to do it. I thought, that maybe, life at its origin on the chaotic Earth, sought order from the environments it had to endure to survive. If that was correct, then all biology must start with the speed of light, squared and not with energy. I felt I had to reverse Einstein’s equation in my head to figure the riddle out. It made sense because today we know all life makes energy from the sun or from electrons in our mitochondria. Plantlife uses the photons or electrons of the sun to make its energy efficiently. Animals use electrons to make fuel in the mitochondria in the form of ATP.
The M, the ‘mass’ part of the equation brings in the elements of space/time and gravity from physics. This is a topic biology rarely deals in. This is where the riddle got complex for me. This implies the way the mitochondria account for energy has to include a very precise timing procedure as a part of energy generation. I knew from mitochondrial biology that is precisely what the “Rolex” in our head does at the SCN by responding to the magnetic field of the Schumann resonance of the Earth.
But there is more.
Food is information of light from the sun. It is also energy. This means that info and energy are linked. It turns out they are linked via the concept of mass.
Shannon took the vague concepts of information and pinned them down to what its essence was all about.
He asked what was the minimum requirement needed to create a message that could still be deciphered well.
The equation he came up with looks identical to Boltzmann's equation for entropy. This means Information truly links to thermodynamics.
Boltzman gave us the statistical explanation of the second law of thermodynamics. In 1877 he provided the current definition of entropy,
In 1948 Shannon figured this out by mathematically learning how to measure the information in the messages
Shannon realized that the quantity of the message had ZERO to do with its true meaning.
Physicist John Wheeler extended Shannon's ideas further.
Wheeler tells us every particle in the universe emanates from the information locked inside it.
My idea at my KLC clinic: This idea has massive implications for mitochondrion who deal exclusively with light, electrons, and protons in cells.
Wheeler’s ideas have been expanded recently by Vopson (dark energy non-believer)
His paper says that not only is information the essential unit of the universe but also that it is energy and it has to have mass.
To support this claim, he unifies and coordinates special relativity (1905) with the Landauer Principle (1961)
Landauer predicted that erasing even one bit of information would release a tiny amount of heat, a figure which he calculated = mtDNA is a heat engine
If information is energy, Information, once created has to "finite and quantifiable mass."
This connects information directly to energy. E-mc^2
When information is lost in the system there has to be a change in mass in the system..............
These ideas fueled the EMF 2 blog post at jackkruse.com
2. It amazes me how ignorant the paradigm is about AM sunlight. AM sunlight is filled with high intensty red light and a smaller amount of blue light. This is why the color temperature of AM sunlight at sunrise is around 1600K and it is 16,000 K at sunset. High intensity red light in the AM is the light that Nature uses to stimulate testosterone release in men. UV light is a potent "off switch" for testosterone action in the blood. It amazes me that this PEER reviewed article has no clue that AM SUNLIGHT is the circadian controller of testerone level in MEN.
They want to use fake light.........to do the job of the sun.
Ridiculous.
The use of light therapy dates back to ancient civilizations, going as far back as the ancient Egyptians and Indians, who used sun- light (heliotherapy) for healing and promoting health. The therapeutic use of light energy was more fully appreciated in the late 19th century when a Danish physician-scientist, Niels Ryberg Finsen, demonstrated the benefits of red and blue light in the treatment of lupus vulgaris and was recognized with the 1903 Nobel Prize in Medicine and Physiology. In 1960, the L.A.S.E.R. (Light Amplification by Stimulated Emission of Radiation) by Theodore Maiman was invented, based on theoretical work by Albert Einstein in 1917.
This brought renewed attention to the therapeutic light energy field. The monochromatic, coherent, and collimated nature of lasers led to immediate interest in their biologic effects. In 1967, Endre Mester, a Hungarian physician-scientist, reported that low-dose laser treatments were capable of promoting wound healing and hair regrowth in mice. He termed this phenomenon photostimulation and went on to demonstrate the efficacy of this treatment in human patients with skin ulcers. medicalnewstoday.com/articles/31296…
3. When a human lives in a poor environment loaded with Blue light and nnEMF it stimulates a type of cell death called 'ferroptosis'. Do you know about it? Most gurus have never even herd of it. This is why you must be careful who you allow to pack your parachute.
Ferroptosis is defined by the iron-dependent accumulation of lipid peroxides when heme containing photoreceptors undergo damage. Most people have no idea that this occurs in the blood (catalase), mitochondrial cytochromes, and th eP450 system. All of them containing heme (iron based) proteins that work with light. Ferroptosis is associated with the abnormalities I look for in peripheral blood smears at Kruse Longevity Center and it is genetically (DNA/mtDNA) and biochemically distinct from other forms of programmed cell death such as apoptosis, necrosis, and autophagy. It is linked to why many gas anesthetics are linked to neurotoxicity in people with neurodegeneration. It also is linked with people who are floxxed and have many other mitochondrial redox linked diseases.
It appears this new mechanism is driven by downstream inactivation of glutathione peroxidase 4 (GPX4, Yang et al., 2014). Peroxidase enzymes are ALSO ALL HEME containing proteins. I believe the fluoride in the inhalational or prescription drugs is ONE of the proximal cause of the iron-dependent accumulation of lipid peroxides because it causes a dielectric collapse in the metabolic water around these proteins in mitochondria. I also think this leads to melanopsin dysfunction in the circulatory system where the most heme iron-containing proteins exist in man. The tell tale sign is when retinol levels in the plasma rise sharply because the Vitamin A derivative is running free destoying photoreceptors as it goes.
The second critical spot they are found is in the mitochondrial membranes of man. This has not been studied as far as I can tell in 2019. The normal dielectric constant of water is 78 in bulk water but it has been shown to be 160 in metabolic water or EZ. I have been waiting for papers to link melanopsin dysfunction to a falling dielectric constant in the anesthesia literature but no luck on that so far. I strongly believe these mechanisms are linked. This is why Vitamin C by the IV route can help cases like this. It will not work by the oral route.
Mitochondrial cytochromes are all heme-containing lipid proteins. This would cause acute colony failure of the photoreceptors there. I bet it would alter catalase in the cell as well which quenches free radical signal H202 as well. Catalase is another heme-containing protein. All heme-containing proteins seem to be red light chromophores as well. Hemoglobin is the main red light chromophore porphyrin in our blood. Hemoglobin has a strong ability to absorb light between 250-600 nm. UV light spectra go from 250-399nm in man. The word porphyrin is derived from the Greek word which stands for purple. Purple light is UV light color in the solar spectrum. Again here you see the link back to UV and IR light in these disease mechanisms. B12, folate, melatonin, riboflavin, serotonin, dopamine, glutathione are just a few of the photoreceptors destroyed by ferroptosis. This is why photobiomodulation seems to help in some of these disorders, in my opinion. It helps reverse cell death from this mechanism. Few people are making these links in the literature.
The classical view of cell death has long assumed that, once initiated, the dying process is irreversible. However, recent studies reveal that recovery of dying cells can actually occur, even after initiation of a cell suicide process called apoptosis. This discovery raised fundamental key questions about which forms of the cell death process could be reversible and how reversal is mediated. Recent study results reveal the first evidence that ferroptosis is reversible and they have suggested strategies to enhance its reversibility. We are now using those ideas in helping our clients out at Kruse Longevity Center. bio.biologists.org/content/8/6/bi…
1. Today's lesson: Your longevity experts are RETARDS.
If you know you know. This is the lady below that shows you every longevity expert out there is FOS. She is and was the ultimate wellness rule breaker who lived 122 years and 164 days. Longer than anyone in recorded history.
2. Her daily routine:
↳ Smoked 2 cigarettes daily until age 117
↳ Ate 2 pounds of chocolate per week
↳ Drank Port wine regularly
↳ Doused everything from the Sea/land in animal fats and olive oil
She also took up fencing at 85. Rode her bike until 100. Walked until she was 110. She only quit smoking because she went blind and could not see her cigarette to light it. She was the opposite of this rich moron below.
3. The Decnetralized Science Behind It
Her mitochondrial colony were exceptional. She sat out in her flower garden every day of her life. She was a young woman when the Eiffel Tower opened and was present. She was there for its 100th anniversary as a guest of the French government. Studies on her found she had mitochondrial epeigenetic variants that enhanced cellular photo repair and maintenance.
She was the first human who showed us that environment trumped our nDNA and diet. But centralized science continues to miss this lesson and you pay that toll every day with their evidence based advice.
None of you realize it. How can I say this?
Did you know that recently a paper was published in Nature Medicine that was a massive analysis from the UK Biobank on this topic. Do you know what it revealed? It revealed the lesson Ms. Calment life; that our environment – the "exposome" of everything from air pollution to workplace light stress packs a bigger punch on how you age and die than your diet or DNA ever could. It tells us why all our longevity advice is horribly flawed.
1. This interaction is governed by the Chiral-Induced Spin Selectivity (CISSS) effect, where spin-polarized photons or electrons preferentially match the protein's chirality. In photosynthesis, this spin selectivity may guide exciton transport through protein complexes. If a biophoton's spin aligns with the protein's symmetry, it can trigger excitation or release; otherwise, the signal may be lost, suggesting spin could be nature's way of encoding selective bio-communication.
2. Mitochondria convert food into electrons via the electron transport chain, where cytochromes (especially cytochrome c oxidase) pump protons out, reducing oxygen to water. Proton tunneling, not just bulk diffusion, enables this rapid proton movement (over 10³ protons per second). ATP production peaks during awake hours and initially rises during sleep onset due to free fatty acid (FFA) release, but drops sharply in REM sleep to support a quantum state for brain recycling.
During uncoupling in deeper sleep, mitochondria release infrared heat, condensing surrounding water and coupling to quantum processes.
This mirrors spintronics, where electron spin, manipulated by electric and magnetic fields, stores information, much like mitochondria control electron spin for energy and life processes. Free radicals, with unpaired electrons spinning in the same direction, play a key role, defying the singlet state (paired spins) governed by the Pauli exclusion principle. This quantum spin manipulation underscores mitochondria's unique bioenergetic role.
3. When electrons with the same spin are excited by electric or magnetic fields, they enhance quantum processes in chloroplasts and mitochondria, which use Fe-S redox complexes as electromagnetic compasses to gauge environmental needs. These organelles act as quantum heat pumps, generating infrared light modulated by free radical signals to drive energy and signaling via the MINOS water layer. Water, with its high dielectric constant, breaks symmetry by separating charges and shrinks when heated by infrared, imprinting environmental signals as an ionic plasma. Its hydrogen bonding network acts as a quantum measuring device, recording the state of entangled electron pairs in free radicals. Mitochondria release monochromatic infrared light to entangle electrons and protons, akin to the double-slit experiment, while skin filters sunlight (optimal at 270 nm UV) before mitochondrial processing, reflecting a quantum-coupled design in evolution.
2. Decentralized Answer:
My thesis leverages first principles in your question to me about LPR because light as energy, POMC as a UV switch, melanin as a charge modulator all link to propose that sunglasses disrupt UV-driven biology, reducing melanin and charge, and potentially causing LPR via glycation and neural crest effects. The UV-POMC-melanin link is solid; the LPR and charge extensions are cutting-edge hypotheses needing research.Sunglasses,
UV Light, and Melanin Production: Principle: Light is electromagnetic radiation, and UV photons (e.g., 280–315 nm UVB) carry energy that excites molecular chromophores in skin cells, triggering biochemical cascades. POMC (proopiomelanocortin) expression is a photochemical process driven by UV light, as confirmed by studies (e.g., Slominski et al., 2018) showing UV-induced upregulation in keratinocytes and melanocytes.
Mechanism: UV photons activate POMC transcription, leading to α-MSH production via the melanocortin 1 receptor (MC1R) pathway. α-MSH stimulates melanogenesis, producing melanin, which absorbs and dissipates UV energy, protecting tissues. Sunglasses Effect: Sunglasses with UV400 protection block 100% of UVA/UVB. If UV is the sole trigger for POMC translation, blocking this spectrum halts the signal. This reduces α-MSH and melanin synthesis. The extent depends on exposure time, but chronic use could significantly lower baseline levels, especially in low-pigment individuals. The claim holds, sunglasses directly reduce melanin by cutting the UV-POMC- α-MSH pathway.
3. Ciliary Ganglion and POMC Disruption: Principle: The ciliary ganglion regulates pupil size and lens accommodation via parasympathetic innervation (95% of its neurons target the ciliary muscle). Light spectra influence autonomic signaling, and neural crest cells (originating from POMC-expressing regions) migrate to form pharyngeal and laryngeal structures. Mechanism: UV light, absorbed by retinal and skin chromophores, modulates POMC processing into its 10 peptides (e.g., α-MSH, ACTH). Sunglasses alter the light spectrum reaching the eye, potentially mimicking non-native electromagnetic fields (nnEMF) by shifting the input from natural UV/IR to artificial blue light. This disrupts POMC translation, affecting neural crest-derived tissues, including the pharyngeal pouches. Sunglasses mimic a ciliary ganglionectomy (surgical removal). Sunglasses functionally alter light input, which indirectly influences ganglion-mediated responses and POMC signaling. The nnEMF mimicry is plausible because blue light (400–500 nm) from screens differs from UV (280–400 nm) in energy and penetration, potentially misaligning cellular clocks and POMC processing.