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I was just out in Malibu with Mr. Rubin and one of his friends, interviewing me for a movie we are making about me and Quantum Biology.  We sat down two days ago and did a three-hour podcast that will be part 3 of the Tetragrammaton series.  The goal of part 3 is to go deeper into the implications of what was said between Rick, Huberman, and me. Part 3 was done without Andrew.  Bill Gifford sat in his place, and he is an award-winning health journalist.

SO WHAT DID WE TALK ABOUT?

Can we see the evidence of light toxicity in the skin before it afflicts the brain?  Yes, we can.  People often forget that the skin and brain come from the same tissue layers in the human embryo.  Because of this linkage, your skin and your eyes tell your decentralized physician to look deeper into your health to see how badly you are afflicted with light toxicity.  See this thread and read my comments for the details.   HYPERLINK

Do you know the implications of the last post above about breast cancer and Vitamin D and sulfation? What happens when you add sunlight to a skin? Melanin becomes eumelanin because of the addition of the sun. Did your experts know that? Did you see the color of all human hair, skin, and eyes is made from this sulfated semiconductor? Do your experts know how this all works in the human mammal? I’m just warming up, folks.

What makes melanins so unique and so attractive to science these days?

The list of arguments is a long one. From the viewpoint of physicochemical properties, all melanins share:

(a) a broadband absorption spanning the entire spectral range of the visible domain

(b) a permanent electron paramagnetic resonance (EPR)d signal denoting a stable paramagnetic character.

An unpaired electron can change its electron spin by either absorbing or emitting a photon of energy, denoted by hv, such that the resonance condition, hv = the change in Energy is obeyed. This leads to the fundamental equation of EPR spectroscopy.

Electron Paramagnetic Resonance (EPR) is the study of direct transitions between the electronic Zeeman levels of the ground state. EPR is a magnetic resonance method under suitable microwave stimulation, enabling the unpaired electrons by their magnetic moment.  The basic concepts of EPR are analogous to those of nuclear magnetic resonance (NMR), but the spins excited are those of the electrons instead of the atomic nuclei.

(c) hydration-dependent semiconductor-like behavior.  For example, eumelanin conductivity increases in water because it conducts electricity via ions and electrons.

(d) efficient dissipation of electromagnetic energy as heat.  Melanins can absorb massive amounts of light and get rid of it quickly without damage to the system.  Water with a high dielectric constant helps facilitate this.

On the chemical side, most melanins display:

(a) antioxidant properties, both as an H-atom donor and as a reducing agent;

(b) metal chelation and binding of organic compounds

(c) redox behavior.

In addition, melanins are bioavailable, biocompatible, and biodegradable, thus representing the most promising candidates for biomedical applications in optical signaling in the condensed matter physics world of science.

Melanin has many of the same semiconductive abilities we see in cytochrome c oxidase, which is also a semiconductive protein (above).  That protein is responsible for water creation in the mitochondrial matrix. Water creation and alteration by the mitochondrial matrix is how the DC electric current is stepped down to the precise amperage to create the regenerative drafts used in mammalian tissue regeneration found by Robert O. Becker’s experiments..

Melanin is the critical tissue in all mammals. It allows for tissue engineering and regeneration via nanotechnology operations in the cell via a combined diagnosis and therapy (theranostics) action with our stem cell supply. Melanins are also critical in creating the bio-photon spectrum needed to run the specificity of biomolecules in the cellular system of control. The source of the electromagnetic wave spectrum has to match the absorption spectra of biomolecules to keep the system far from equilibrium so coherence and entanglement are possible.

WHAT IS INFLAMMATION IN THE MAMMALS FUNDAMENTALLY?

It is from a lack of sun or too much light at night.  This is the primary decentralized cycle in all of biology.

Eumelanin is a form of melanin and conducts electricity – albeit weakly – in its natural state. Researchers first discovered that the polyindolic pigment was a semiconductor in the 1970sand suggested that this behavior comes from energy bands associated with a non-localized empty molecular orbital within the eumelanin polymer chain.  All free radicals are paramagnetic because they have unpaired electrons. So are all the melanins in mammals.  This makes them the ideal wide band gapped (WBG) semiconductor to absorb them.  This again points out how modern biology is lost in the woods.  They believe ROS/RNS is terrible when, in fact, they are critical in how non-linear optical signaling controls biochemistry in cells by creating the right spectrum in bio-photon release from tissue-level metabolism controlled by mitochondria.  When melanin is missing, chaos in tissues is created = inflammation.  That is how inflammation manifests in you and every mammal on this planet.  This is how modern neolithic disease is being made in the USA at alarming rates.

So, my patrons, I hope you are beginning to see why Nature wants to limit deuterium in the mitochondrial matrix now.  Could its carburetor function be linked to water chemistry that is quantized to the amount and spectral density of biophoton release in the matrix by metabolism?

I think so.

A lack of POMC, degraded melanin, and a matrix not making water is all a sign of a mammal in deep need of the sun to begin its melanin renovation Rx.

Well, it turns out that deuterium in the mitochondrial matrix is controlled differently in every body tissue because each tissue needs a specific regenerative current to differentiate stem cells to rebuild tissues anew.

The reason is simple: deuterium concentration allowed into the mitochondrial matrix is how a cell controls metabolic rates in different tissues. No two tissues have the same physiology.  Therefore, metabolic rates have to vary in these tissues to be thermodynamically efficient.  This creates the spectrum of the VUV-IR-A light used to manage the biochemistry in that specific tissue.   Not all tissues have the same metabolic rates because of their physiologic needs. This means the metabolism of a mitochondrion produces its unique spectra.  A unique spectrum means the matter in these tissues must also have individual absorption spectra.  This should raise the question, how does the matrix in differing tissues get more deuterium? What type of WBG semiconductors should we expect there?  What is the gating mechanism?

The answer is the type of melanin adjacent to the uncoupling proteins of mitochondria that generate heat from metabolism.  Remember, all haplotypes produce varying amounts of heat via uncoupling efficiency.   The thermodynamics here are also linked to how badly degraded the melanin is in the tissue system.  A big clue to this mystery is if ROS/RNS production is driving biomolecules of inflammation higher or lower:  HS CRP, haptoglobin, homocysteine, lowered glutathione, procalcitonin, etc.  This heat is liberated into the surrounding water to dampen the current in the electrical conduction pathways found in cells.

The recently released Owen Sheasby podcast illuminated this effect.

The further one goes from the equator; the more uncoupling humans need to use to control the regeneration current in a tight ampere range. Equatorial light is the most powerful light on Earth, and this is the light human mammals evolved under.  That system is a powerful melanin stimulus for the skin.  At higher latitudes, cold temperatures stimulate more robust frequency endogenous light generation.   Moreover, as a result, more heat is produced, and melanin in our interiors becomes a better electrical conductor.  Any excess heat is thermalized directly to water so the system can remain far from equilibrium.   The slide at the beginning of this blog post shows this effect.

The closer the equator one lives, the less uncoupling one needs because the sun provides all the ingredients for self-regulated autophagy and apoptosis, which is controlled by ferroelectric currents in the cell that are dampened by melanin biology. Why is ferroelectricity the key to this process?

Iron’s toxicity is mediated by sunlight, and few people seem aware of it. Please recall the first steps of heme synthesis in mammals begin in the mitochondria.  This was proven by papers from Simcox JA, Mitchell TC, Gao Y, et al.  In Rubin, Kruse, Huberman Part 1 & @ I told you hemoglobin was the second big innovation in evolution after chlorophyll.

Heme synthesis begins its first step in mitochondria. If you have a circadian mismatch disease tied to melanopsin dysfunction by definition you are blue light toxic or nnEMF toxic and this causes a defect in mitophagy and ruins the iron cycle in humans. This immediately affects the liver clocks, too.   This leads to fatty liver disease.

People in centralized healthcare often forget heme synthesis occurs partly in the mitochondria and partly in the cytoplasm. This is precisely how the TCA and urea cycle are built in us too. The process begins in the mitochondria because one of the precursors is found only there. Since this reaction is regulated in part by the concentration of heme, the final step (which produces the heme) is also mitochondrial.

People with defects in iron always have a blood dyscrasia (anemia) at some level and it usually bleeds into fertility and thyroid hormone creation too, because of its link to AM sunlight deficiency. These pathways are proximal to the melanin-building pathways as the slide shows below.  In Part 3, I get into it with Bill about how melanin degradation and bleeds backward into this pathway via hypoxia.  This is a catabolic effect  All nnEMF cause hypoxia in humans and drives this catabolism of endogenous melanin to lead to interior destruction and a lack of wound healing.

Remember, purple light = UV light and it creates oxygen in our venous blood and this drives anabolic pathways to make melanin via POMC and alpha MSH.

Purple light in sunlight ALSO stimulates RBC synthesis in humans. Blue light causes RBCs to break down sooner and live a shorter life than they can. What is the color of the main breakdown color of heme? It is the complementary yellow color of bilirubin. Yellow is the complement of purple, and orange is the complement of blue in the color wheel.

An analogy to explain this idea is how paragliders use the thermals on Mount Blanc to ride high up into the atmosphere. The sun heats the air at the mountain’s base, and the heat rises to carry the gliders to very high altitudes.  This allows them to ride the thermals almost at no energy cost. The only price needed is the solar input that drives the temperature variations. If you were a glider who wanted to go further than anyone else has ever gone, you’d need to add an engine to your back that could work to power a fan to move you further. If you did this, you’d have to have a solution for the altitude problem. Why? As we go higher, oxygen is not as expected, and neither is temperature.  This is why the circadian mechanism measures them in their optical lattice clock mechanism. I explained this to Mr. Sheasby in his podcast and the Tetragrammaton part 3 podcast.   This is why the human retina consumes more oxygen than any tissue in the human body.  Modern eye researchers and clinicians do not explain why the choriocapillaris does what it does.  I realized it immediately as the source of why obesity happens when the periphery of the retina is destroyed by blue light.  This also occurs when melanopsin is at its highest density in human tissues. The choroid sits adjacent to the retinal pigmentum epithelium on its densely fenestrated side to act like a radiator to absorb heat. A thickening of the choroid is the first sign of impending obesity in humans (Pics below).  BOOM

This also explains why fat people now have lousy bones and why the mechanical stress of weight no longer makes Wolf’s law factual in centralized biology.

Metabolomics network studies show that the kinetic isotope effect (KIE) of deuterium affects the metabolism of L-lysine, L-glutamine, and L-serine.  This is why linoleic acid loaded with deuterium affects bone metabolism at its core.  Pass that fact on to the food gurus.  They remain ignorant of biophysics.  Be careful who packs your parachute, folks.

As such, you’d need a mechanism to alter the fuel and oxygen mix to be oxidized to power your flight. This is very similar to what a car has to do with its carburetor. The higher you go, the more pseudohypoxic you get, so you must alter the fuel source to maintain your flight.  The third through fifth citations below highlight this.

Mitochondria are hydrogen-fueled engines, so deuterium concentration and production is critical in biology.  This explains the title of this paper.  Deuterium-depleted water stimulates GLUT4 translocation in the presence of insulin, which leads to decreased blood glucose concentration​.  I still chuckle at the food gurus ranting about seed oils and never realizing they are deuterium bombs.  https://pubmed.ncbi.nlm.nih.gov/34510301/

The UCP-2 proteins were innovated for this reason. It controls the fuel-oxygen mix in mitochondria. It is a carburator for deuterium/H+ flow. The more deuterium that flows in, the more anions in the TCA cycle are bound to the substrates because of the kinetic isotope effect (KIE) of deuterium. One deuteron binds 96 H+ protons in the matrix.  This slows the spin rate of the TCA cycle. That has an indirect effect of raising and lowering methionine in its metabolic cycle, causing a collection of heavy metals.  This is how melanin detoxes heavy metals and does not use endogenous glutathione.  When someone has heavy metal toxicity, it is a sign to me, as a decentralized clinician, that they have a vast POMC problem and they need more sunlight to renovate melanin inside the affected tissue.  Chelating with exogenous agents is a losing strategy of functional medicine.  The reason it’s so popular is because of the revenue it generates.

SUMMARY

How do you know your clinician is genuinely a decentralized mitochondriac? The whole world will tell you they are nuts, and you should not follow what they tell you. Be wise enough to know that the paradigm does not like truth-tellers. They are bad for business.

Is melanin a perovskite material with unique biophysical abilities that centralized biology has ignored at your peril?  You bet your ass it is.   What else doesn’t centralized science know?  Biophysics controls all the biochemistry in their books.  If you do not understand what light is doing you don’t understand decentralized biochemistry either.  They are light ignorant.    Biomacromolecular pigments, such as melanin, play an essential role in the survival of all living beings as I told Rick and Andrew. Melanin absorbs sunlight transforms it into heat and deposits the energy in water and proteins at the electronic level to build a dissipative system.  This step is crucial for avoiding damage to skin cells. Light absorption produces excited electrons, which could either fall back to ground states by releasing the heat (photothermal effect) and/or light (photoluminescence), or stay at higher energy levels within its lifetime period, which can be captured through external electronic circuitry (photovoltaic effect).   In published studies that no one in centralized biology reads, it has been demonstrated that the combination of melanin with halide perovskite light absorber in the form of a composite exhibits high absorbance from the UV to NIR region in the solar spectrum. And the hybrid displays significantly reduced photoluminescence and minimized density of residual excited states (verified by photovoltaic measurement) owing to the enhanced considerably nonradiant quenching by the melanin.

As a result, the composite shows an ultrahigh solar-thermal quantum yield of 99.56% and solar-thermal conversion efficiency of ≈81% under one-sun illumination (AM1.5), which is superior to typical carbon materials such as graphene (≈70%). By coating the photothermal composite film on the hot side of thermoelectric devices, a 7000% increase in output power as compared to the blank device under illumination is observed.   Mammals are experts in collecting the sun using this technology woven into the fabric of NATURE.  Get your skin in the game of the sun.

HYPERLINK

Please remember blue light induces hypoxia in cells, and this stimulus causes melanin to break down into L-DOPA, dopamine, adrenalin, and noradrenaline.   Every biochemistry textbook printed has this pathway, but most centralized PhDs and clinicians have no idea how it links to melanin biology.  How much crowd wisdom is there when most of the crowd is afflicted by nnEMF and blue light, and their frontal lobes have been emptied of melanin/L-DOPA/dopamine anyway?

Did you know that cephalopod ink is 70% pure melanin?  Do you know why?  https://www.youtube.com/watch?v=ohZsX5-qAD0

More sun = more water production by the mitochondrial matrix = more mitochondrial melatonin production = less chance of leptin resistance = less chance of neolithic disease.  Any light at night causes leptin resistance = Blue light at night is the worst offender = because it makes melatonin vanish = causing leptin resistance = mitochondriac, and melanopsin wisdom and proves the food guru fail……

LIGHT’S EFFECT > FOOD EFFECT

All food is, at its core is matter created downstream from sunlight—photosynthesis wisdom on display.    When the world moves away from your biological necessities, becoming fearful is fruitless. That’s not the point, given the dire situation. It’s learning how to control your fear, harness it, and use it as fuel to change your conditions of existence. Fear shouldn’t shut us down; it should wake us up to increase the fidelity of our awareness and focus to overcome the present challenge we face and crush it.

Stand for what is right even if you are standing alone. There is a fine line between challenging yourself and overwhelming yourself. Changing paradigms is not for the weak of heart or mind. This type of transformation takes hold of you. Invades you. Soon it owns you. You want to be free of them, but you never will be. A prolonged movement on the right way is better than overwhelming speed on the wrong path, and this is why you enjoy the chaos of being overwhelmed. You must become the change you seek in this world now.

Part 3 of Tetragrammaton is epic.  I hope you all enjoy it once Mr. Rubin is done editing it.

HAPPY HALLOWEEN!

CITES

1. Pullman, A., and Pullman, B. (1961). The band structure of melanins. Biochim. Biophys. Acta. 54, 384–385. doi: 10.1016/0006-3002(61)90389-4

2. https://www.popsci.com/eumelanin-conduct-electricity/

3. https://www.sciencedirect.com/science/article/abs/pii/S0166432821004861

4. https://www.frontiersin.org/articles/10.3389/fendo.2022.927576/full

5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5881424/

6. https://twitter.com/DrJackKruse/status/1718950743674163200

Schwarzschild’s equation is used to calculate radiative transfers.  These are energy transfers that occur via electromagnetic radiation through any medium in local thermodynamic equilibrium that both absorbs and emits light radiation.

The general theory of relativity states that in particular, the curvature of spacetime is directly related to the energy and momentum of whatever matter and radiation are present.

Einstein’s general theory of relativity can be summed up in just 12 words:

Space-time tells matter how to move; matter tells space-time how to curve.

This also implies that light energy responds to the action of matter.

The Schwarzschild equation and the Schwarzschild radius are related concepts in the theory of general relativity, which describes how gravity affects space and time. The Schwarzschild equation is a mathematical solution to the Einstein field equations, which describe how the curvature of space-time depends on the distribution of mass and energy. Noether’s theorem solves the energy requirements of the bending of space and time.

I actually talked about that here in this podcast but I think few people really understood where Uncle Jack was driving you.

Many smoothed brain thinkers believe everything is just about energy with respect to the mass equivalence equation.  They do this because they have a rudimentary understanding that equation.  This concept offers us nothing, as I’ll explain below.

WHY THE OWEN SHEASBY PODCAST NOT YET RELEASED WILL MATTER DEEPLY TO THOSE WHO REMAIN IN THE DARK

If you consider the mass-energy equivalence relationship, E= mc^2 you might be led to this conclusion. However, what this equation really tells us is that matter is not conserved in Nature.  It is a shocking because it tells us that mass can be converted to energy.  It does say how but Nature allows for it.  In other words, E=mc^2 tells us something deep about mass that has huge implications for biology. That’s why it’s useful to the mitochondriac. However the concept that everything is just energy gets us nowhere in terms of understanding our world. It is essentially a statement of existence. The fact that the universe exists and is full of energy is an empirical fact. It is not explained by the concept of energy. Similarly, the laws of physics are ultimately empirical, and they are also not explained by energy. Energy is essentially an accounting tool that helps us solve problems. This is what leptin is in biology.  Melanin however, is a lot like Noether’s theorem.  It tells us a lot about the mass in the system and how much light can be absorbed into the system. The physics is given in the nature and character of the fundamental forces that describe how things interact.

Life is basically about electricity and magnetism that come from light in a system. Think about the tests done by your centralized doctor in the form of an EKG, EEG, and an EMG. All show the electrical and magnetic potential of our organ systems. Anything and everything electrical stems from the phenomena of charge. No one seems to have a clue why this relationship in nature exists, but physics tells us it is true. Atoms are made up of 3 parts: Protons have a positive charge, neutrons are neutral, and electrons have a negative charge. Here is the interesting part: Electrons have the equal and opposite charge of protons, but an electrons atomic mass is 1/1836th that of a proton.   This is a huge difference in mass.  Thusly, charge of these particles is the main variable with respect to their atomic mass. Atomic mass links to the thermodynamics and energy needed in the system because mass determines the size and shape in protein lattices. The charge of the lattice is determined by the protons and electrons in the system.  Electrons delocalize most often because they are not encumbered by the mass as protons are.  This points out why deuterium is a problem in mitochondrial biology.  The mass of the lattice determines the how the speed of light can travel in our tissues.  It also determines the frequency of light emitted.  This is the basis of how a semiconductor emits light = LED.

The speed of light is variable in a substance when it becomes encumbered by electrons.  This is why size and shape alter the thermodynamics of things made up of electrons and protons.  Light only interacts with electrons via the photoelectric effect.  Thusly, electrons are exicted and powered up by light.  Light instantaneously interacts with matter to create the fastest pathway through tissues.  This directly links tissues to Fermat’s principle.  Light does not interact with protons or neutrons and has to go around them.  This increases the distance that light must travel and it creates tiny delay’s in tissues at the quantum level.  Just because the distance increases does not mean the path is longer in all cases.  That small delay creates a signal that denotes biologic time in a cell.  That delay is observed in the telomere length of a cell.  What moves atoms or things made up of atoms?  Light is capable of this fundamental task and nothing else can.

How light is captured and travels in our tissues is how time manifests in biology = melanin biology.

On the flip side; energy and momentum are quantities that will crop up in the analysis of virtually all physical systems that exhibit such symmetries.  Noether’s theorem says that every symmetry implies a conservation law is present and acting and that link is always to energy in the system in question.

For mammals, melanin controls that process.

THE PICTURE STORY ABOVE SHOWS YOU CENTRALIZED SCIENCE STILL HAS NO IDEA HOW FAR AHEAD MY MEMBERS ARE IN THE STORY OF LIGHT AND MAMMALS.

Understanding the physics of organisms is the only way to resolve this chasm in knowledge.  

Light has a universal speed limit at 186,000 miles an hour in space where matter is sparse compared to space-time.  Inside a cell matter is not sparse. Light travels 30 centimeters in one nano-second. The only way to increase its energy/power is to increase its frequency and this is why endogneous light production is a key feature improvement in mammals. That change in energy can alter the electric and magnetic fields associated with the atomic lattice present in cells where matter is present. When those fields are altered, so are the interactions that can occur with specific light frequencies. The frequency of light determines the current and the force of the current. The DC current is what determines wakefulness and sleep.  Current is the flow of electrons or protons inside the matter of cells and is measured in amperes.  During daytime the DC current is present and at night it is absent in the brain when we sleep.

Magnetic fields are produced by the motion of electrical charges inside of tissues.  A fundamental property of magnetic fields is that they exert forces on moving electrical charges.  Magnetism is best seen in cells by the free radicals they create as they move electrical charges inside of cells.

Magnetism outside of cells is best visualized by putting a magnet under a paper and throwing iron filings on the paper. You can see the field the magnet generates by looking at the pattern of the iron filings. If you throw away the filings and add new iron filings the exact same pattern will emerge showing you that the magnet, and not the atoms of iron, determine the shape of the field of action.  This action is very similar to what the human body undergoes every night and day cycle.  Its molecules are disturbed by daylight constantly and are condensed back to their form at night.  Sunlight alters, disturbs, and un-condenses magnetic fields. Sometimes atoms in us are lost and we have to replace them from our environment.  We get a fresh supply of atoms from water, food, and from light. But thanks to the controlling forces within our cells, namely our mitochondrial electric and magnetic fields, new molecules and cells are rebuilt as before and arrange themselves in the same pattern as old atoms were.  They are recycled by autophagy and apoptosis in our colonies of mitochondria.

Current has another feature called electromotive force. This is the “push” behind the current and it is measured in volts. Currents in space flow differently than they do on Earth. This is a function of the plasma they exist in. Plasma is one of the four fundamental states of matter, the others being solid, liquid, and gas. A plasma has properties unlike those of the other states of matter. Plasma in space can travel multi-directionally.  Plasma’s inside the ionosphere can only flow unidirectionally.  The presence of a significant number of charge carriers makes plasma electrically conductive so that it responds strongly to electromagnetic fields. Like gas, plasma does not have a definite shape or a definite volume unless enclosed in a container or contained by an environment. Unlike gas, under the influence of a magnetic field, it may form structures such as filaments, beams and double layers. In space, current flows in all directions because space is essentially a vacuum filled with double layered plasmas.  The ionosphere itself is a plasma.  Sunlight must traverse that plasma to get to mammals.

On Earth, within the ionosphere where life exists, energy flows unidirectionally from the sun to the surface of the Earth.  This flow controls the quantum yield of photosynthesis which forms the basis of the food webs on Earth.   Current only flows when a source of electrons is connected to a conductor that contains fewer electrons.  This is why lightening (another plasma) flows from clouds to the Earth’s surface and not into space. This allows flow from things with a higher electron density to one with a lower density of electrons. If there is no conductor present between these density changes in electrons, there is only a hypothetical charge of flow we call the electric potential.  That potential is measured in volts.

An electric field forms around any electric charge and we can now imagine them with unrivaled precision.  That implies that any other charged object if it has an opposite polarity, will be attracted. If the charge is similar they will be repelled. The charge differentially is reflected in the distance between the two densities. The distance between to charged particles is called an electric field. The field is the region of the space of this plasma in which an electric charge can be measured. This is measured in volts per unit of area. All electric fields are associated with magnetic field actions by Maxwell’s laws. We can distinguish electric fields from magnetic ones easily today.  This was not true in our recent past.

Charge is poorly understood by most people. Understanding of magnetism, by most, is atrocious. Magnetism is an intrinsic property of atoms that manifests in two polarities. Any flow of electrons is accompanied by a combined electric and magnetic field around the current of flow of electrons. Those two fields are always at 90-degree angles to one another. As electrons flow, they disturb other electrons around them in these fields.  Just as a current produces a magnetic field, a magnetic, when it moves in relation to a conductor, induces a current. Magnetic fields are measured in Gauss.  Both fields are determined by lines of force and they indicate the direction and shape of the field locally between particles. Both fields power declines with distance but their influence over charged particles is infinite.

SUMMARY

General relativity has acquired a reputation in centralized scinece as a theory of extraordinary beauty.  Why?  Subrahmanyan Chandrasekhar has noted that at multiple levels, general relativity exhibits what Francis Bacon has termed a “strangeness in the proportion” (i.e. elements that excite wonderment and surprise). It juxtaposes fundamental concepts (space and time versus matter and motion) which had previously been considered as entirely independent. Chandrasekhar also noted that Einstein’s only guides in his search for an exact theory were the principle of equivalence and his sense that a proper description of gravity should be geometrical at its basis, so that there was an “element of revelation” in the manner in which Einstein arrived at his theory just by thinking about the Universe.  Other elements of beauty associated with the general theory of relativity are its simplicity and symmetry, the manner in which it incorporates invariance and unification, and its perfect logical consistency.  But there is a problem.

Reconciliation of general relativity with the laws of quantum physics remains a huge problem in modern science.  As a mitochondriac you must hold open the idea that Einstein is wrong in some of his assumptions.  Why?  Mother Nature operates quantum mechanicallly 100% of the time.  I trust her more than Sir Albert.  Not only that, Einstein also doubted his own work when he introduced the cosmological constant.

Quantum mechanics is the science of probabilities, biology is the study of the improbable which only makes sense from the perspective that the living state is only probable using reactions that appear statistically improbable.  The power in that sentence is immense and highlights the difference in understanding between the decentralized and centralized science.

WHY DON’T I TRUST A SCIENTIST I REVERE?

He is centralized in his ideas.

You should know that the Einstein field equations are nonlinear and are very difficult to solve. Einstein used approximation methods in working out initial predictions of the theory. But in 1916, the astrophysicist Karl Schwarzschild found the first non-trivial exact solution to the Einstein field equations.  This was called the Schwarzschild metric.

This solution laid the groundwork for the description of the final stages of gravitational collapse, and the objects known today as black holes. In the same year, the first steps towards generalizing Schwarzschild’s solution to electrically charged objects were taken, eventually resulting in the Reissner–Nordström solution, which is now associated with electrically charged black holes.   In 1965 -75 Einstein’s predictions in general relativity were proven again correct when quasar black holes were found to exist in nature.  This tells us his theory has deep predictive value, but it still does not jive with quantum mechanics…….the science of biology.

In 1917, Einstein applied his general theory of relativity to the universe as a whole, initiating the field of relativistic cosmology. This is where I think he went off the rails.  In line with contemporary thinking, he assumed a static universe, adding a new parameter to his original field equations—the cosmological constant—to match that observational presumption.  By 1929, however, the work of Hubble and others had shown that our universe is expanding. This is readily described by the expanding cosmological solutions found by Friedmann in 1922, which do not require a cosmological constant. Lemaître used these solutions to formulate the earliest version of the Big Bang models, in which our universe has evolved from an extremely hot and dense earlier state. Einstein later declared the cosmological constant the biggest blunder of his life.  He knew there was a fly in his own ointment.

Why does all this matter to us, as Black Swan mitochondriacs?

In the study of heat transfer, Schwarzschild’s equation is used to calculate radiative transfer (energy transfer via electromagnetic radiation) through a medium in local thermodynamic equilibrium that both absorbs and emits radiation.  I use this daily when I am calculating what the effect of nnEMF is on me in a particular zipcode when I am traveling.  I am on my way to Europe today.

When solar radiation is scattered it creates the phenomena that makes the sky appear blue to your brain.   For example, scattering from clear skies reflects about 32 W/m2 (about 13%) of incoming solar radiation back to space.

Visible light is also reflected and scattered by aerosol particles and water droplets (clouds). Neither of these phenomena have a significant impact on the flux of thermal solar infrared through clear skies.

You need to be bathing in that light chronically.  If you do not and use man made light to bath in I would expect one of two things to afflict you:

1.  A mitochondrial disease inflicted by the SCN on your colony of mitochondrial in some tissue linked to the leptin melanocortin pathway because of how our system is built to work in decentralized fashion.  People forget that the ipRCGs are directly wired to the SCN.

2.  A mental disorder or neurodegenerative condition because of how the leptin melanocortin pathways wire directly to the habenular nucleus without any synapses.  Today’s blog helps explain why  ALL MENTAL ILLNESSES links to the physics of light.  If you have one of these diseases or you know someone who has a history of these diseases,  you should immediately jump to the conclusions at some level in their life or their transgenerational existence, that their cells lines have been afflicted by horrible choices around light to ruin the neurotransmitters created in their brain.  They do not have a chemical deficit that requires a pharmaceutical deficit.  They suffer from a solar light deficit and/or an artificial light addiction present day or night or both.

Smedley Butler was the most decorated Marine in US history, Yet he wasn’t proud of his work. He called himself a “gangster for capitalism.”  After retiring in 1931, he toured the country, giving an explosive speech:

War Is A Racket!

What defines a racket?    An enterprise that is “conducted for the benefit of the very few, at the expense of the very many.”   War perfectly fits this definition:  Millions are maimed and killed so a few thousand can make an untold fortune

Wars are waged not for democracy or peace but for the *business interests* who profit wildly during wartime. The young men who kill and die aren’t told why they’re being marched off. Instead, they’re shamed into it.

Who profits from war, exactly?   Butler lists them:  “Munitions makers. Bankers. Ship builders. Manufacturers. Meat packers. Speculators.”  War supercharges the profits of specific industries, as their products are now demanded and bought by the ultimate spender: the government

There’s no overlap between those who fight the war – and those who profit from it. Butler reported that “21,000 new millionaires and billionaires” were minted during WW1. He asked:   “How many of them dug a trench? How many of them went hungry in a rat-infested dug-out?”

Soldiers in WW1 often got no money on “payday.”  Soldiers had to pay for their “accident insurance.”   They had to fund their own “ammunition, clothing, and food” through compulsory “liberty bonds.”   When the payday came, most soldiers got nothing in hand.

But corporations made untold fortunes in WW1. International Nickel Company’s profits jumped by “more than 1,700%.”  The US government spent billions of dollars on “airplane engines that never left the ground!”

The shoe manufacturers were suddenly in a “business with abnormal profits.”   They sold the US government 35 million pairs of shoes in WW1. General Butler writes his regiment had “only one pair” per soldier. At the end of the war, 25 million pairs were left unused.

The US army was convinced by some businessmen that “colonels shouldn’t ride in automobiles, nor should they even ride on horseback.”   6,000+ buckboards – four-wheeled carriages driven by a large animal – were sold to the government   “For the use of colonels!”   Never used

War takes ordinary men and makes them killers. Butler saw how men were taken out of “fields and offices and classrooms”  And trained to become very good at mass murder. When the war ended, they were “discharged” and told to become normal again – a reversal impossible for many.

The psychological damage of war  War gives young men “tremendous excitement.”  When the survivors return, they’re suddenly cut off from it.  These extreme swings drive some of them insane. Butler saw many veterans of WW1 in government hospitals – they were “mentally destroyed.”

How to end the racket of war?  I think the answer is to adopt Bitcoin.  Bitcoin makes war unaffordable for governments.

Those asked to fight, kill, and die should vote for the war. Butler:  “Only those who would be called upon to risk their lives for their country should have the privilege of voting to determine whether the nation should go to war.”

Concerning war, never mistake activity for achievement.

CITES

https://memod.com/jashdholani/the-rule-bending-ex-marine-hired-to-turn-the-us-in-4085

My new place in El Salvador will highlight the effect of art and light on health.  This blog will help you understand what is driving this decision process in my choices.

The “regressive evolution” of mammals today on Earth is spawning interesting new ideas for decentralized science for us that are unique.

I believe the first Hominid TBI that told the melanin story of mammals is when ancient Neanderthals lost sunlight and became modern humans.

Only wise modern humans who can see the loss of human superpower around the melanin sheets in their heads happening at breakneck speed will survive this “backward evolution”.  Wisdom for today’s mammals is born inside their melanin sheets inside their skulls.  Wisdom makes you the most adaptable creature in a rapidly changing environment.  What is changing fastest today?  The light we live under is the answer.

Let us take a walk back in history to understand what decentralized science is signaling.

Light is the creative “Source” in the universe.  To some “backward evolution” may imply a loss of complexity, misleading you to believe, that evolution has a goal of creating more complex forms. It doesn’t mean this.   However, evolution merely favors features that make a poster “more fit” for a particular current environment and this is based on the redox status of the non-visual photoreceptive system.

Consider cave-dwelling fish in Mexico below.

The cave-dwelling form of the Mexican tetra cannot see, and uses its eye sockets as repositories for fat. Credit: Barry Mansell/Nature Picture Library

Look at the fish.  Implications of the picture?  What you do isn’t what you think. Let me explain the creative process buried at the core of life.  The evolutionary process doesn’t retrace its steps in “regressive evolution”.  It just appears to those who do not carefully observe the process.  You have to go deeper than the facade of just seeing a fish with no eyes.  Cave-dwelling creatures have frequently undergone “regressive evolution”,  due to their unique light environment.  Remember fish are not mammals, but mammals have fish/amphibian OPN5 in their brains.  This creates a lesson for mammals to learn.

These fish have lost their eyes because they are not needed in dark environments. But eye loss in cavefish, for example, doesn’t mean an exact return to a primordial ancestor without these organs. The eye remnants remain.  They are atrophic and lie in wait until the light, the “Source code” returns.  Instead, processes that previously produced the eye stop partway through the process, leaving a vestigial eye overgrown with skin.  The decision to lose their eyes was a thermodynamic one.  With food so scarce in caves, the animals have to save their energy—and being sightless gives them a major energy boost​ so they can adapt to a low food environment.  This teaches us there is a huge link between light and food.  The link is thermodynamically driven.

I believe the same process occurred in the primate clade of mammals in Africa 2-4 million years ago to explain our species today.

To a surface thinker of today with low dopamine fueling their frontal lobe circuits, due to degraded melanin sheets in their skulls, things can look like they’re going into reverse when they aren’t. The eye didn’t go in reverse. It just stopped going forward.  Might human creative be the result of the same process in the chimp family?

Might it even be more complex today compared to our own genesis?

I believe this is exactly what is happening to human mammals today.  They are no longer moving forward, and their epigenetic toolbox which relies on UV light to drive mitosis, is also regressing.  What does that imply?  The cavefish doesn’t face this now because it is not a mammal and it is protected fully from man’s use of artificial light.

​What is happening to mammals that aren’t in Nature and are subject to man-made light?  Now gorillas are getting obese in zoos?  Yep.

Was Michelangelo’s David truly perfection 520 years ago in stone?  I do not think it was because his eyes and brain case where smaller than his ancestors.

​As humans have degraded the melanin sheets inside their skulls with the use of clothing and indoor dwelling with fire use they have become more creative. Look at the relationship of fire to melatonin. As fore became more popular among Neanderthals in caves their melatonin levels would have dropped.  This would have driven their blood sugars and insulin levels higher and this would have made their larger brains a real thermodynamic drag on their biology.

Who was affected by this most?  Mammals are and neanderthals were mammals.  We still see this in nocturnal mammals today.  See the link above.  Neanderthals likely went extinct over this change in light use in caves.  Could the use of fire inside of a cave to survive have given birth to homosapien creativity as we lost 125 grams of brain tissues?

I believe creativity, like autism, is a regressive evolutionary creation. Creativity manifests as a regressive change of melanin degradation to dopamine in the frontal lobes.  Autism is regressive creation in the diencephalon derivatives giving us a spectrum of change.  With respect to creativity, this regressive change has had a positive connotation which can best be seen in the Louve in Paris.  Melanin degradations created various levels of dopamine in our frontal lobes that lead to new creations on Earth.  There is a deep evolutionary lesson here.

​If this lesson offends the artist in you, good.  What did I say above?  Cave-dwelling creatures have frequently undergone “regressive evolution”,  due to their unique light environment. Mammals react just as the fish do because the OPN 5 in their brains.

Tell me, when did “human paintings” show up on Earth?  They showed up when humans went inside caves and brought fire with them to light the dwelling and they made pictures of their world on a stone wall.  They left UV-IR-A light and used alien light (fire) to light their world.  Fire is capable of destroying melatonin and melanopsin to degrade melanin.  Few see the implications as I do, but ultimately it makes sense why diseases like autism and Alzheimer’s afflict modern homo sapiens whose brains are shrinking further.

Cave art, generally, the numerous paintings and engravings found in caves and shelters dating back to the Ice Age (Upper Paleolithic), roughly between 40,000 and 14,000 years ago. The first painted cave acknowledged as being Paleolithic, meaning from the Stone Age, was Altamira in Spain.

People forget our history with light and how it is linked to our brains.  I will remind you of what you conveniently forget.  The story is right in front of your eyes.  Every day I see shrinking brains on MRI and CT scans of modern humans who have created a life around manufactured light.  It reminds me of the cavefish all the time.

Around 40 000 years ago Neanderthals went extinct.  Have you ever asked yourself why a hominid with 125 grams more brain tissue than you went extinct at Northern latitudes?  Might that answer be a lack of sunlight to fuel that brain with big eyes?  Might that brain have caused them problems when the sun’s power vanished and they began to use fire too?

I told you that the eye is the on-and-off switch of the brain.  Did you know that their Neanderthal eye socket was much larger than ours?  Is this a clue to the light story here?  Are we the result of the cognitive devolution of the Neanderthals?

For more than 350,000 years, Neanderthals inhabited Europe and Asia until, in a sudden change by evolutionary standards, they disappeared around 40,000 years ago when they faced 1000  year cooling period associated with a lack of sunlight. This was at around the same time the anatomically modern human Homo sapiens emerged from equatorial Africa where the sun was stronger. Neanderthals never got to Africa.  The story of light and lack thereof is all around our history if you look for it.

When DNA gets passed down through the generations, it gets shuffled into new arrangements that can be used to build a sort of timeline.  And this timeline suggests that the DNA entered the most northern Neanderthal gene pool roughly 100,000 years ago.

The scientists were initially skeptical of the patterns they saw in the DNA data because it said centralized science was wrong about the “Out of Africa” time line of modern homosapiens.

The most recent Neanderthal data findings challenges the current narrative that human migration out of Africa took place around 50,000 years.  In fact it raises the possibility that an earlier movement of human explorers did occur to cause the mixing of the species.

Centralized science believes Neanderthals could withstand the cold, but much new  evidence does not support this.  Few of their skeletons are found above the 51st latitude.   In fact, they got their name as a homid because the Valley of Neander is the highest latitude where most of their bones have been found in Germany.

​Neanderthals had heavier fur coats than modern humans they were covered with animal skins as the climate got colder.  This would have changed how melanin operated in their skins and brain. Neanderthals are now also thought to have processed animal hides and crafted clothing that could have covered up to 80 percent of their bodies. Do you think this had no effect on their disappearance given what I said to Rick and Huberman?  Like humans, they are thought to have covered their feet too.  Might this have affected their ability to ground as the sun got weaker?  Now we also believe other sensitive body parts, like their gonads were covered too.  Do you think this had any effect on their fecundity?  Funny how modern humans in artificial light are also now struggling with the same issues do not you think?

​

Another recent breakthrough was the discovery that Neanderthals may have been capable of “symbolic thought”. In my opinion, this shows something else that has already occurred in modern humans.  A regressive evolution began to cause them to lose 125 grams of brain mass when the light diminished on Earth and at the 51st latitude. In 2018, researchers announced they’d discovered evidence of cave paintings from 65,000 years ago—the oldest artworks of their kind. This art was described as abstract nature.  I find it funny that modern abstract human art began in Paris with Pablo Picasso after he locked himself inside after a friend committed suicide.  Both changes in art abstraction came with losses of sunlight.  Few see what I see.

This Neanderthal finds continue to fuel debates among scientists about how complex their mental capacities truly were, but I’d bet they were every bit as wise as us when the sun was shining.  Their candle dimmed when the sun dimmed because they had more eye mass and brain tissue to illuminate.   I think creativity is a regressive trait due to a loss of melanin because dopamine is made from it during hypoxic states.  A lack of UV light causes a pseudohypoxia.

Thoughts to ponder this AM as I look at some art to buy for the Ark down in Salvador……………..

Marie Antoinette was a story about melanin loss wasn’t it?

SUMMARY

Everything has beauty, but not everyone sees it for what it really is.  Observing nature in her raw form taught me that her many realities hidden behind a wall of perception.  That vision is created not just what we see, but what we hold to be true.  I learned from Nature that it is ideal to hide your best secrets; this is why I like seeing people when they can’t see the real me.  You might begin to watch the world around you with glittering eyes because the greatest secrets are always hidden in the most unlikely places.  I watch nature in her raw form at every sunrise.  I never miss these lessons.

CITES

https://en.wikipedia.org/wiki/Neanderthal_1

Post translational time stamping is present from cyanobacteria to mammals.  All organisms have evolved timing mechanisms to adapt to environmental changes in order to optimize survival and improve fitness for an environment. To anticipate these regular daily electromagnetic cycles of light and dark, many organisms manifest near 24-h cell-autonomous oscillations that are sustained by transcription–translation-based or post-transcriptional negative feedback loops that control a wide range of biological processes. With an eye to identifying emerging common themes among cyanobacterial, fungal and animal clocks, some major recent developments in the understanding of the mechanisms that regulate these oscillators and their output need to be discussed. These include roles for antisense transcription, intrinsically disordered proteins, codon bias in clock genes, and a more focused discussion of post-transcriptional and translational regulation as a part of both the oscillator and output.

Circadian rhythms in every organism are cell autonomous, appear to have arisen only a few times in evolution, and can be driven by one of a few lineage-specific but otherwise highly conserved central oscillators. While oscillators driving bacterial and plant clocks are distinct from each other and from other known clocks, fungal and animal cells share circadian oscillators of conserved regulatory architecture: transcription-translation feedback loops (TTFLs) comprised of two parts.

Specifically, 1) a positive arm with a heterodimeric complex at its core that behaves as the activator of the system, promoting the transcription of 2) one or more components of the negative arm, which when translated inhibit the activity of the positive arm.

WHAT IS THE TTFL?

Transcription-translation feedback loop (TTFL) is THE cellular model for explaining circadian rhythms in behavior and physiology. It is widely conserved across species, and the TTFL is largely auto-regulatory with the assistance of the sun & moon and dark periods on Earth, in which transcription of clock genes is regulated by their own protein products. This implies that light and dark control genetic expression and not the other way around. The TTFL is a negative feedback loop, in which clock genes are regulated by their protein products. Generally, the TTFL involves 2 main arms: positive regulatory elements that promote transcription and protein products that suppress transcription. When a positive regulatory element binds to a clock gene promoter, transcription of DNA proceeds, resulting in the creation of an mRNA transcript, and then translation proceeds, resulting in a semiconductive protein product. There are characteristic delays between mRNA transcript accumulation, protein accumulation, and gene suppression due to translation dynamics, post-translational protein modification, protein dimerization, and intracellular travel to the nucleus. Across species, proteins involved in the TTFL contain common structural motifs such PAS domains, involved in protein-protein interactions, and bHLH domains, involved in DNA binding.

The two overarching areas characteristic of circadian systems in general: 1) the negative arm and its regulation of the core clock; 2) the control of output by the positive arm and its environment.

In ALL mammals the heterodimeric BMAL1-CLOCK complex positively regulates expression of negative arm component genes, the Periods and Cryptochromes(encoding PER1, PER2, PER3, CRY1 and CRY2), that combine with CK1 and several other proteins to make the repressive complex that depresses BMAL1-CLOCK activity and alters periodicity of the mammalian clock which alters its accuracy.  Remember all circadian clocks are flow meters for entropy in a cell.

Solar light input into mammal TTFLs begins with dedicated non visual photoreceptors that elicit signaling that acts to induce (in fungi and mammals) or reduce (insects) the amounts of negative arm proteins mentioned above. In broad outline, Output occurs when the positive Arm heterodimer binds to DNA and activates expression of genes whose products do not impact the TTFL.  The key take away is the clock gene actions are PROXIMAL to DNA translation and gene activation.  This tells you that light inputs controls gene expression in mammals and it is not the other way around.  Altering your genome will not improve your illness or disease if the light and dark environment is repair first.

HOW DOES TIME STAMPING WORK BY LIGHT AND DARK WORK?

Once enough modified protein products accumulate in the cytoplasm of a cell, they are transported into the nucleus where they inhibit the positive element from the promoter to stop transcription of clock genes. The clock gene is thus transcribed at low levels until its protein products are degraded, allowing for positive regulatory elements to bind to the promoter and restart DNA transcription. The negative feedback loop of the TTFL has multiple properties important for the cellular circadian clock. First, it results in daily rhythms in both gene transcription and protein abundance and size, caused by the delay between translation and negative regulation of the gene. The cycle’s period, or time required to complete one cycle, remains consistent in each individual and, barring mutation, is typically near 24 hours. This enables stable entrainment to the 24 hour light-dark cycle that Earth experiences from the sun & moon.

Additionally, the protein products of clock genes control downstream genes that are not part of the feedback loop, allowing clock genes to create daily rhythms in other processes, such as metabolism, within the organism. Light and dark cycles are the decentralized controllers of the TTFL.

THE TTFL USES MELANIN TO ELECTROCHEMICALLY TIME STAMP YOUR CELLS. This occurs in the retinohypothalamic pathways anterior to the SCN and it modifies what the SCN signals to all the other molecular clock genes it links to in tissues.

WHY IS MORNING LIGHT SO CRITICAL TO GET RIGHT?

CSP-1 (conidial separation 1) is a morning induced transcriptional repressor with a phosphorylation gated half-life is a key cog in driving EVENING gene expression in mammals.  If you do not get AM sun your evening genomic expression will be AWRY.  People have forgotten that leptin is released by fat cells and can only enter the hypothalamus under darkness after 4 hours. This should happen at night time. It cannot happen when CSP-1 is not created by AM light.  These are the new recent insights into how circadian clocks in your eye and skin achieve phase-specific gene expression.  This is how and why leptin resistance exists.

The negative element of the core circadian feedback loop is the frq or frequency gene.  The frequency (frq) gene controls the morning-specific rhythmic transcription of a sense RNA encoding FRQ segment.  As a result of this action, a long noncoding antisense RNA, qrf, is rhythmically transcribed in an evening-specific manner.  It has been reported in the literature that the qrf rhythm relies on transcriptional interference with frq transcription and that complete suppression of qrf transcription impairs the circadian clock.  The biological function of qrf transcription and its impact on the circadian clock are not understood in centralized science because centralized science has no light controls at night in labs.

CSP-1 expression is induced by light and glucose, and this finding suggests a rhythmic coordination of qrf transcription with metabolism.  Because it is light and glucose we know POMC, ACTH, and melanin are the key to understanding CSP-1 biology.   It also means that artificial light during the day or night is especially toxic when you know this is how the mechanism operates.

There are three type of melanins in humans and only one ACTH in humans. All three are used to time stamp the atomic lattice of cells to create an internal map of space time domains to be accurate measuring sticks for the flow of entropy inside of cells. This links melanin biology to Noether’s theorem directly.  You have blogs on all these ideas now and it is time for you to link them all to comprend what I have been teaching your for 20 years.  Light causes modern diseases.

These 3 melanins are ALL extended heterogeneous biopolymers composed of molecular subunits with ambiguous macromolecular topology to modern centralized science. In the literature, an electrochemical fingerprinting technique has been described for melanin, which suggests that natural melanin pigments which contain indole-based tetramers seem to be always arranged into porphyrin-like domains to capture light and measure it in some way useful to the system.

Spectroscopy and density functional theory calculations suggest that sodium ions undergo occupancy-dependent stepwise insertion into the core of porphyrin-like tetramers in natural melanins at discrete potentials that time stamp the internal atomic lattice that allow it to act like a clock to measure the flow of entropy in the cellular system accurately just using light and dark as the feedback loops. It is fully decentralized because light and dark control this process. One is not more important than the other. A loss of melanin implies a loss of accurate time keeping inside the cell or tissue.

Lastly, in humans, the TTFL is a limit cycle, meaning that it is a closed loop that will return to its fixed trajectory even if it is disturbed by its environment, maintaining the oscillatory path on its fixed 24-hour period. It appears this is only true if the melanin structures it uses on surfaces and endogenously remain intact and are chronically replaced and renovated. If the endogenous electrochemical time stamping mechanism is damaged, the TTFL loses its periodicity and chronic modern disease results without any alteration to the DNA or RNA of a cell. These are diseases do not mimic genetic diseases like Tay Sach’s. These diseases are far more common than mutational diseases of DNA which are relatively rare. It means our circadian mechanism is open to the environment, and as such is not subject to calories measurement for metabolism because calories only is useful in closed thermodynamic loops.

CITES

1. Aronson BD, Johnson KA, Loros JJ, Dunlap JC. (1994) Negative feedback defining a circadian clock: autoregulation of the clock gene frequency. Science 263:1578-1584.

2. Belden WJ, Larrondo LF, Froehlich AC, Shi M, Chen CH, Loros JJ, Dunlap JC. (2007) The band mutation in Neurospora crassa is a dominant allele of ras-1 implicating RAS signaling in circadian output. Genes Dev 21:1494-1505.

3. Bell-Pedersen D, Shinohara ML, Loros JJ, Dunlap JC. (1996) Circadian clock-controlled genes isolated from Neurospora crassa are late night- to early morning-specific. Proc Natl Acad Sci U S A 93:13096-13101.

4. Cheng P, Yang Y, Heintzen C, Liu Y. (2001) Coiled-coil domain-mediated FRQ-FRQ interaction is essential for its circadian clock function in Neurospora. EMBO J 20:101-108.

5. Dunlap JC. (1999) Molecular bases for circadian clocks. Cell 96:271-290.

6. Froehlich AC, Liu Y, Loros JJ, Dunlap JC. (2002) White Collar-1, a circadian blue light photoreceptor, binding to the frequency promoter. Science 297:815-819.

7. Gallego M, Virshup DM. (2007) Post-translational modifications regulate the ticking of the circadian clock. Nat Rev Mol Cell Biol 8:139-148.

8. Larrondo LF, Olivares-Yanez C, Baker CL, Loros JJ, Dunlap JC. (2015) Circadian rhythms. Decoupling circadian clock protein turnover from circadian period determination. Science347:1257277.

9. Baker CL, Loros JJ, Dunlap JC. FEMS Microbiol Rev 2011

10.  Transcriptional interference by antisense RNA is required for circadian clock function.

Xue Z, Ye Q, Anson SR, Yang J, Xiao G, Kowbel D, Glass NL, Crosthwaite SK, Liu Y.Nature. 2014 Oct 30;514(7524):650-3. doi: 10.1038/nature13671. Epub 2014 Aug 17.

11.  Molecular Regulation of Circadian Chromatin.

Zhu Q, Belden WJ.J Mol Biol. 2020 May 29;432(12):3466-3482. doi: 10.1016/j.jmb.2020.01.009. Epub 2020 Jan 16.

12.  Koike N, et al. Transcriptional architecture and chromatin landscape of the core circadian clock in mammals. Science. 2012;338(6105):349–354.

13.  Li N, et al. The frequency natural antisense transcript first promotes, then represses, frequency gene expression via facultative heterochromatin. Proc Natl Acad Sci U S A. 2015;112(14):4357–4362.

14.  Xue Z, et al. Transcriptional interference by antisense RNA is required for circadian clock function. Nature. 2014;514(7524):650–653.

POMC arose over 500 million years ago by an insertion of the melanocortin sequences into a prepro-endorphin gene. Evidence for this comes from structural identities with other opioid precursors in both the NH2- and COOH-terminal regions of POMC.

The phenomena of pro-opiomelanocortin (POMC) as a hormone precursor emerged gradually over time as observations slowly filled in pieces of the puzzle. Long before the concept of hormone precursors was realized, the bronzed skin color described by Addison in his patient with adrenal insufficiency (“melasma suprarenale”) gave perhaps the first hints of a connection between the hypothalamic, pituitary, adrenal (HPA) axis and skin color. A similar link between the pituitary and pigmentation came from the studies of Allen in 1916 and Smith in 1916 who both noted that immersing tadpoles in pituitary extract made their skins darker. In humans too, large doses of porcine pituitary extract also appeared to cause pigmentation in 1954, with this active extract of the pars intermedia of the pituitary henceforth termed “melanocyte stimulating hormone” or MSH.

In 1932, Cushing extended his clinical reports of a polyglandular syndrome caused by basophilic adenomas of the pituitary by linking this finding with adrenal hyperactivity. In the 1930s, work by Ingle and Kendall in the 1930s showed that administration of large amounts of “cortin,” a purified adrenal extract, produced atrophy of the adrenal cortex in rats. Importantly, they found that administration of the “adrenotropic principle” of the anterior pituitary was effective in preventing adrenal cortical regression following treatment with cortin. The first hints of a behavioral angle to POMC biology came from studies by Ferrari in the 1950s, when “stretching-yawning syndrome,” a bizarre crisis of muscular tone, occurred following central administration of MSH. Many other studies assessing the effects of central α-MSH on motivational processes followed, but it was not until 1976 that Panskepp observed for the first time that this peptide decreased food intake using light alone.  What else might POMC do in a modern world run by artificial light now?  Today, you get to see another perspective centralized science missed.

Viewed from the comfort and assured knowledge of the modern centralized molecular world, these observations and interventions could be considered overtly simplistic. However, I believe that these classic decentralized observations should be regarded as essential building core evolutionary building blocks, not only for our understanding of POMC peptide processing, but also for the work which subsequently tied together these seemingly diverse peptides.

Is this why did I had a ubiquitnation & mitochondrial series before the Quantum Engineering series on Patreon?

Yep.

In mammals, a master clock localized in the suprachiasmatic nucleus of the hypothalamus synchronizes cellular clocks in other central nervous and peripheral tissues with each other and with external time. At the molecular level, these clocks are based on an interregulatory network of clock genes, including the 3 Period genes (Per1–3), that control circadian rhythms (CRs) by rhythmic orchestration of 5–10% of the cellular transcriptome in a post translational tissue-specific manner.  CRs time stamp genes after they are translated and cause diseases.  I relayed this last month to the government of El Salvador in a speech I gave there.

Transcription-translation feedback loop (TTFL) is a cellular model for explaining circadian rhythms in behavior and physiology. Widely conserved across species, the TTFL is auto-regulatory, in which transcription of clock genes is regulated by their own protein products. Rev-erba is one and so is NF-kappa beta.

THIS IMPLIES TIME STAMPING CAUSES CHRONIC NEOLITHIC DISEASES.

What can we use as an example to see if light stress on out largest organ causes diseases below?

I posted the video above to show you how centralized edicational materials still miss the obvious elephant in the room.  The lights used in surgery can cause the problem.  the lights on laparascopic cameras are all high intensity blue lights, and it is already well know that other parts of the electromagnetic spectrum used in medicine can cause this problem without any previous surgery.  Look at the picture below that I lifted from the video to show you how their own video on this topic misses the elephant in the room on adhesions.  I even mentioned this to Huberman during my podcast when I told him everytime I open a skull I now worry about what I am doing because of my understanding.

Have you ever heard of adhesions of the gut?

Abdominal adhesions commonly form after intra-abdominal surgery, radiation, and inflammatory processes in humans. In a subset of patients, adhesions lead to problematic symptoms such as abdominal pain, bloating, and bowel obstruction. The mechanisms of adhesiogenesis are not well understood by centralized science but are believed to involve mesothelial surface disruption with subsequent fibrinocoagulative and inflammatory signaling processes. I believe the reason centralized science has missed the boat on adhesions is because aberent light causes it. It is a biophysical disease at its core.  Melanin in your omentum is a big deal to the gut clocks below.  The melanin in the omentum links to the POMC genes in the skin of the rectus sheets on your abdomen.

WHAT ARE ADHESIONS?

Abdominal adhesions are fibrous bands that span two or more intra-abdominal organs and/or the inner abdominal wall (i.e. peritoneal membrane) which typically form after abdominal surgery. Adhesions may also form secondary to inflammatory conditions of the abdomen in the absence of prior abdominal surgery or as a sequela of abdomino-pelvic radiation. Although the majority of patients with intra-abdominal adhesions remain asymptomatic, a clinically significant subset of patients will develop “adhesive disease”, a symptomatic state ranging from mild and/or vague to highly distressing and even life-threatening symptoms.

Considering the fact that adhesions have no characteristic laboratory features and are not readily visible by currently available imaging methods, many cases of adhesive disease will go undiagnosed for prolonged periods of time, causing medical providers to find themselves in a diagnostic and therapeutic quandary. Patients, consequently, after extensive non-diagnostic testing and empiric treatments, may not only experience protracted symptoms and adverse medical outcomes, but can also suffer from significant emotional distress or demoralization, which in turn may be misdiagnosed as depression, anxiety, or a functional bowel disorder.  This topic was going to be the headliner in 2019 in Vermont.  That never happened.

WHAT IS THE LIKELY DECENTRALIZED CAUSE OF ADHESIONS?

Irradiating human skin with blue light in frequency bands that causes both type of blue light toxicity is likely the cause of abdominal adhesions. People with autoimmune conditions are at increased risk of adhesions and keloid formation on their skin. The link between all these conditions is the chronic irradiation of human skin with artificial blue light devoid of IR- A and UV frequencies with blue light. One must remember that isolated blue frequencies activates the blue light hazard in mitochondria powered by melanopsin signaling that cause pseudohypoxia in mitochondria. When will centralized medicine learn how light stress not from sunlight ruins mitochondrial biology?  Melanin is a key battery in the skin and deep inside of our systems.

This type of isolated light irradiation can set up adults for epithelial cancer, myopia, low dopamine diseases, diabetes, and skin cancer as they age and their heteroplasmy rates grow larger faster as they age into adults formats. If you destroy the battery you have no energy left for health and disease is the result.  Could it also be the cause of adhesions?  Might this mean adhesions in the gut are a warning signal that surgeons should be paying attention to in patients?

It is for me.  When i see arachnoid webs in the brain I know what it means to my patients.

Women with keloids on their cesarean scar have been found in prospective studies to have increased adhesions between the uterus and the bladder and between the uterus and the abdominal wall. This certainly supports my theory and my ideas on this topic. This is cited below.

In mammals, a master clock localized in the suprachiasmatic nucleus of the hypothalamus synchronizes cellular clocks in other central nervous and peripheral tissues with each other and with external time. At the molecular level, these clocks are based on an interregulatory network of clock genes, including the 3 Period genes (Per1–3), that control circadian rhythms (CR) by rhythmic orchestration of 5–10% of the cellular transcriptome in a post translational tissue-specific manner. This tells us that most human disease is not DNA/RNA based, it is mitochondrial based because circadian disease phenotypes mimic those of chronic diseases in centralized healthcare. Circadian biology and oscillations time stamp genes after they are translated and cause modern chronic diseases. How does it happen in humans?

Transcription-translation feedback loop (TTFL) is a cellular model for explaining circadian rhythms in behavior and physiology. It is widely conserved across ALL species, & the TTFL is auto-regulatory, in which transcription of clock genes is regulated by their own protein products. Rev-erba is one and so is NF-kappa beta.  I’ve written about both of these things in the past on my blogs.

Rev-erbα, a nuclear receptor and circadian clock component, is a mediator of microglial activation and neuroinflammation in the connection between the CNS and human gut.

I believe people who get adhesions (Crohn’s, UC, SIBO patients) all have destroyed Transcription-translation feedback loop destuction due to an altered circadian mechanism. I propose that such a mechanism can be found within the molecular control of circadian rhythms and “Clock” gene biology and a lack of melanin in some key places in the spinal cord that connect the gut to the CNS.

All melanin’s can create a toxin when they breakdown in human tissue.  For example, neuromelanin can reversibly bind and interact with amine containing neurotoxins, (e.g., MPTP(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine is an organic compound. It is classified as a tetrahydropyridine.) MPTP augments their actions in the terminal, eventually leading to the instability and degeneration of melanin-containing neurons due to oxidative stress and mitochondrial dysfunction.

In particular, a lack of neuromelanin and POMC translation by a lack of UV light appears to confer susceptibility to chemical toxicity by providing a large sink of iron-bound, heme-like structures in a pi-conjugated system. This system seemingly allows for stabilizing interactions including pi-stacking, sodium inclusion,  as well as ligand binding to iron in cells. Given the progressive accumulation of neuromelanin components with aging. it seems melanin degradation corresponds with an apparent decrease in dopamine synthetic pathways in man.  This raises an immediate question of whether melanin can also create or is capable of binding dopamine, the primary functional monoamine utilized in gut enterocytes and its corresponding gut neurons, should be raised by centralized research.  To date, it has not been.

A number of physiological processes demonstrating circadian variation have been shown to involve ‘Clock genes’ in the suprachiasmatic nucleus (SCN), which then entrains a similar set of Clock genes in peripheral tissues such as the heart, brain, spleen, lung, liver, skeletal muscle and kidney. The intrinsic time-keeping system influences activity, such as sleep, temperature regulation, rates of metabolism, immune responses, blood pressure and hormone secretion. The function and availability of mediators involved in the inflammatory response, fibrinolytic and anti-coagulation pathways are all under the tight control of the molecular Clock system. These include IL-6, PAI-1, fibrinogen, fibroblasts and TNF-α. I am making the educated guess that disruptions in the ‘Clock system’ are central to the causal pathway of adhesion formation here.  I am also implying this symptom is a gateway disease to many other diseases linked to altered cellular time stamping in humans.

The transcriptomic analysis of hippocampus from Rev-erbα-/- mammals has revealed a predominant inflammatory phenotype results in mammals and it suggests it comes from a dysregulated NF-κB signaling due to circadian dysfunction at its core.  When one considers that melanin derivatives are always found in pathologic specimens it is not hard to come up with this linkage.

DEEP DECENTRALIZED SCIENCE THEY ARE MISSING

The brain gut connection requires pristine circadian rhythm control to stay healthy. Loss of Rev-erbα in primary astrocytes of the spinal cord of mammals had no effect on basal activation of the neurons that innervate the gut but do potentiate the inflammatory response to lipopolysaccharide (LPS). In vivo, Rev-erbα-/- in a mammalian model has exhibited enhanced hippocampal neuroinflammatory responses to peripheral LPS injection, while pharmacologic activation of Rev-erbs with the small molecule agonist SR9009 suppressed LPS-induced hippocampal neuroinflammation. This explains to us how a loss of circadian control allows the LPS of the microbiome to lead to a disease phenotype just with a loss of circadian control post translationally of DNA.  This means DNA alteration is not the cause of a majority of modern human disease.  This is 180 degrees from the current centralized perspective.

Rev-erbα deletion due to a loss of clock gene control clearly influences gut enterocyte function and neuronal health in a coordinated fashion. When this link breaks it makes the formation of adhesions post surgically much more likely. Lab experiments done have shown when gut neurons are conditionally cultured on media from Rev-erbα-deficient primary gut-glial cultures, it exacerbates oxidative damage in cultured neurons that innervate the gut. Rev-erbα-/- mammals have not only shown gut dysfunction in these models but they also exhibited significantly altered cortical resting-state functional connectivity. This finding tells me that many central neurological diseases maybe masquarding in centralized medicine clinics as circadian diseases of the Transcription-translation feedback loop(TTFL).

One neurologic disease in particular intrigues me with its skin & gut connection is ALS. ALS patients tend not to show up in low latitudes and they tend to be quite pale because they lack UV exposure POMC requires for translation of melanin. In human ALS, abnormalities have been found in mitochondrial structure, mitochondrial respiratory chain enzymes, and mitochondrial cell death proteins indicative of some non-classical form of programmed cell death.  In ALS patients this happens in the spinal cord, skin, and their gut in pulsatile fashion over timescales.  This is a hint to me that it might be a disease of time stamping of the TTFL masquarading as a neurological disease.

The creation of MPTP, which is lipid-soluble, readily penetrates the blood—brain barrier and enters the brain cells. Because it is amphiphilic, it is captured into acidic organelles, mostly lysosomes, of astrocytes. MPTP itself does not appear to be toxic, but its oxidized product, 1-methyl-4-phenylpyridinium (MPP+), is toxic. This has been linked in Parkinson’s Disease but I think it might link to ALS because the toxic MPP+ could affect defective mitochondria in neurons in the anterior motor horn from circadian rhythm damage in the gut. These malfunctioning mitochondria might contribute to neuronal death in ALS through the biophysical entity called the mitochondrial permeability pore (mPTP) activation.

The major protein components of the mPTP are enriched in mammalian motor neurons which also have abundant POMC genes. Early in the course of disease in ALS humans seem to present with mutant superoxide dismutase-1 enzymes in their mitochondria. The mitochondria in motor neurons undergo “trafficking abnormalities” which results in dramatic remodeling of mitochondria in ALS patients that results in the formation of mega-mitochondria (larger size) and coinciding with increased protein carbonyl formation and nitration of mPTP components. Anything that enlarges is a thermodynamic sign to me.   In fact, lab experiments in nocturnal mammals have shown that genetic deletion of a major mPTP component called cyclophilin D which has robust effects in ALS by delaying disease onset & phenotype and extending survival of the anterior motor neurons.

When this process is disrupted the MPP+ action it appears to destroy the mPTP in a cascading manner in the spinal cord mitochondria and spreads like an infection would in the anterior motor neurons. I think the circadian disruption in the anterior motor neurons causes a paralysis like effect that we normally see in REM sleep. In ALS, the circadian disruption shows up when we are awake and it has gone unrecognized as a completely disrupted rhthym disorder because of how we perceive the disease and we have not looked at the data carefully enough. I happen to have one person with this disease who is doing something no one else has done with this diagnosis. He is improving his solar redox and improving mtDNA function by living in the tropics adjacent to a flat beach. So far he is doing a lot better than other ALS patients who aren’t paying attention to their light stamping problem.  In fact, I believe some of these patients diseases are made worse when they travel outside of time zones.  That seems to make the diseases more aggressive.

I think this model in mammals explains why anterior motor neurons can be destroyed in isolated fashion in the spinal cord when the circadian rhythms are disrupted in the nerves that innervate the gut but link back to their embryologic origins. The inflammatory cascade could start out in the splanchnic nerves below but as the spinal cord anterior motor neurons loses REV-erb alpha it could create an inflammatory cascade of LPS induced damage to “infect” other adjacent motor neurons by destroying their clock gene TTFL’s. This is how ALS might be progressing in these patients.

The Rev-erbα, mPTP in mitochondria, and TTFL should be thought of as as a key biophysical link between the circadian clock control and neuroinflammation in the CNS.  People forget that the spinal cord is part of the CNS and so is their skin. Nerves link the gut to both.

Look more carefully at the picture above then you did in QE #47.  Note the skin is on the left of the picture and it is our largest organ and it has a somatotopic organization to the ENTIRE spinal cord and to our internal organs by way of nerves.

The Quantum Enginnering #47 blog has the key metric of why the eye, skin, PVN, and DLF of the brain stem sleep and pain areas give the input into celiac plexus to cause gut problems via the microbiome. The implications of this connection are massive in many other diseases besides bipolar disorder. I told you that there and I am doubling down on it here.

WHAT DID I SAY IN QE #47 AGAIN ABOUT THIS PROCESS?

I said, “The dorsal longitudinal fasciculus (fasciculus of Schutz) is a periaqueductal (area around ventricular system Aq above) ascending and descending fiber system arising from the hypothalamus and terminating to the autonomic nuclei of the pons and the medulla, conveying autonomic fibers from the brain to the gut in humans.  It also conveys pain messages and is important in the sleep pathways of humans.  These are usually altered in bipolar patients as well because of a lack of melanin in these areas.

The dorsal longitudinal fasciculus is found within the dorsal brainstem tegmentum. It passes through the periaqueductal gray matter and contains both ascending and descending fibers. The ascending fibers pass from the reticular formation (sleep region/insomnia) passing to the hypothalamus thus transmitting information related to the viscera in the thorax and abdomen.  THIS IS HOW THEY PASS THE ANTERIOR MOTOR HORN CELLS AND THE GUT VISCERA!

People who travel a lot across time zones or people who use a lot of blue light or nnEMF at night or day in their cities are going to have massive sleep disturbances because they lack charge density in this spot.  They mimic people with mental disorders like bipolar patients because they have broken the same rules of Nature.  I view insomnia as a mental disorder in my decentralized medicine framework.

This topologic neuronal surface is a critical barrier to the brain health of humans.  This is the pathway where metabolic syndrome, poor sleep, and fatty liver all come from fundamentally.  This pathway could be in many blogs but I left it out this detail.  Why?  You already thought this stuff was too hard.  Why add another level of complexity with neuroanatomy?

Many of these same findings are found in diabetics, bipolar disorder, and those with sleep disorders like insomnia.  Patients with bipolar disorder tend to have all these symptoms at times that vary based on how defective their FM antennae are in their eyes & brains.”

DOES ANYONE SEE THOSE LINKS NOW IN THIS BLOG IN THE SERIES?

Now, go back and look at the lipofuscin blog in this series.  That chemical comes from melanin degradation and is always associated with aging and light stress.  Dopamine is made in the eye several ways by sunlight and it can be made in the gut by your microbiome due to the link to melanin. People forget that bacteria release 5000 times more light than eukaryotic cells and this light is capable of making dopamine from the aromatic amino acids in the gut. This is why serotonin and phenylalanine and tyrosine are stored in the enterochromaffin system in our gut.

The more and more you look into its biology, I feel more confident in saying that light is the most powerful drug for living systems. The light release is more important than the fuel in the diet for our health outcomes because food has light information built into photosynthesis. This stimulus leads to light release to start the optical signal cascade in the gut using aromatic amino acids as the mover in the GI tract. When you are blue light/nnEMF toxic you cannot repair the gut or sleep issues at all. This is why many people get gut adhesions without having had any surgery.  The same thing will be true for pain thresholds and opiate use. I can tell you this. Your gastrointestinal system will never function optimally in a circadian mismatch (melanopsin/encephalopsin dysfunction) and that will bypass however good a diet is.

The study linked below in cite 6 is a longitudinal study on TBI following college football athletes across a sports season.
•Nanopore 16S rRNA sequencing of gut microbiome reveals changes after head injury.
•Serum biomarker GFAP increased during the competitive period of the season.
•S100β and SAA blood levels were positively correlated with Eubacterium rectale.
•Gut microbiota is suggested as a future biomarker for diagnosis following head & neck injury.

The blue light hazard/nnEMF links the gut to the brain, heart, and vascular damage leading to neurodegeneration that causes protein folding issues in blue light-damaged tissues as cites 4 and 5 show. Few are making these links in diseases like adhesions and ALS.

But I am.

CITES
Van Goor H. Consequences and complications of peritoneal adhesions. Colorectal Dis. 2007 Oct;2(9 Suppl):25–34.
Menzies D., Ellis H. Intestinal obstruction from adhesions; how big is the problem? Ann. R. Coll. Surg. Engl. 1990;72:60–63.

Sjogren syndrome and abdominal adhesions.Could they be related?

Background: Sjögren syndrome is a chronic systemic inflammatory disorder (classified as an autoimmune disorder) characterized by lymphocytic…

egojournal.eu

https://www.bmj.com/content/362/bmj.k3549

Blue light-induced retinal lesions, intraretinal vascular leakage and edema formation in the all-cone mouse retina – Cell Death & Disease

Little is known about the mechanisms underlying macular degenerations, mainly for the scarcity of adequate experimental models to investigate cone cell death. Recently, we generated R91W;Nrl−/− double-mutant mice, which display a well-ordered all-cone retina with normal retinal vasculature and a…

Alterations to the gut microbiome after sport-related concussion in a collegiate football players cohort: A pilot study

Concussions, both single and repetitive, cause brain and body alterations in athletes during contact sports. The role of the brain-gut connection and …

sciencedirect.com

The auditory nerve transmits auditory information up a series of nuclei to the cortex where perception occurs. These nuclei include 1) cochlear nucleus, 2) superior olivary nuclei, 3) lateral lemniscus, 4) inferior colliculus, and 5) medial geniculate nuclei.

Melanin pigment is normally present in the outermost layer of the retina of the eye, the inner ear adjacent to capillaries in stria vascularis near hair cells, and vestibular organs. In the skin, it is in the basal layers.  In the gut, it is found in the enterochromaffin cells.  Significant reduction in melanin pigment in mammals is associated with embryonic miswiring and disruption of visual and auditory functions. This has implications for human diseases like autism which usually affects all sensory inputs to the thalamus.  In this way, it mimics what I wrote about Autism in this series in QE#45.    The consequences for the visual system include abnormal development of the retina and misrouting of optic pathways into the brain impairing visual acuity, eye movement, and stereovision. Lack of melanin pigment in the inner ear is associated with greater susceptibility to noise damage and poorer localization of sound in space.

Auditory sense in mammals is unique in another way and may be critical to why melanin exists where it does.  Unlike other cells within the brain, hair cells within the Organ of Corti of the cochlea do not have axons. Neurons within the spinal ganglion have peripheral axons that synapse at the base of the hair cell soma. These axons make up the auditory nerve. Most (90%) of auditory nerve fibers receive their input from the inner hair cells. Thus, the inner hair cells facilitate a majority of auditory processing.  My bet is this arrangment is how sound waves are converted to light waves that the auditory nerve can process.

The melanin sheets in the ear are proximal to the auditory nerves.  When melanin is hypoxic it can break down into noradrenaline and dopamine.  The mammalian auditory brain stem, and in particular the medial nucleus of the trapezoid body (MNTB) (Wynne and Robertson 1996), receives extensive adrenergic input.  This tells me that the sheet in the cochlea is creating neurotransmitters by melanin degradation in the auditory pathways as the slide below shows.

The mammalian auditory brain stem receives profuse adrenergic innervation, whose function is currently poorly understood by centralized science.  Noradrenaline increases high-frequency firing at the Calyx of Held synapse during development by inhibiting glutamate release.

The calyx of Held synapse plays an important role in the auditory system, relaying information about sound localization via fast and precise synaptic transmission, which is achieved by its specialized structure and giant size. During development, the calyx of Held undergoes anatomical, morphological, and physiological changes necessary for performing its functions. The large dimensions of the calyx of Held nerve terminal are well suited for direct electrophysiological recording of many presynaptic events that are difficult, if not impossible to record at small conventional synapses. This unique accessibility has been used to investigate presynaptic ion channels, transmitter release, and short-term plasticity, providing invaluable information about basic presynaptic mechanisms of transmission at a central synapse.

DECENTRALIZATION ANSWER to why all senses have melanin sheets between them and the environment?

Why does the spiral cochlea have this huge melanin sheet?  Melanin shows up in mammalian tissue because of the melanin concentration hormone.  Melanin-concentrating hormone (MCH) was originally isolated from salmon pituitaries (think of Huberman fish gaff on melanopsin now) where it induces the aggregation of melanin granules in melanophores, which results in pale skin color. MCH sequence is conserved in ALL MAMMALS analyzed to date, including mice, rat, rabbits, and humans. In mammals, the neurons that synthesize and release MCH are present mainly in the hypothalamus and nearby areas.  Is the cochlea near the hypothalamus?  No.  But the melanin stimulatory hormone is very prominent in the brainstem and the cochlear is very close to that.  Lack of melanin pigment in the inner ear is associated with greater susceptibility to noise damage and poorer localization of sound in space.

I think a relative lack of melanin in different areas of the cochlea is the cause of misophonia.  Misophonia is a disorder in which certain sounds trigger emotional or physiological responses that some might perceive as unreasonable given the circumstances. Those who have misophonia might describe it as when a sound “drives you crazy.” Their reactions can range from anger and annoyance to panic and the need to flee.  If your centralized health professional doesn’t know about misophonia, they may take all that information and try to fit it with something they do know about. Here are some diagnoses you might hear before a health professional finally acknowledges your misophonia:

Melanocytes are distributed in the stria vascularis and spiral ligament regions and recent evidence illustrates the distribution of melanin in the human cochlea with the lower relative amount of melanin observed in the basilar turns compared to apical turns.  Sensorineural hearing loss caused by presbycusis (old age heteroplasmy), maternal-fetal rubella infection, aminoglycosides, and noise exposure disproportionally impacts the basal turn with variable losses of spiral ganglion and hair cells reflected in a down-sloping audiogram.  Melanin is sparse in those regions.  The location of melanin and its known function as a free radical scavenger may explain some patterns of sensorineural hearing loss and highlight that melanin has special abilities in the sensory pathways of mammals.

Might it have to do with the binary code of biology and the fidelity of sound that I raised in the Kruse for Dummies lecture?  I believe it does.  Look at how many areas sound inputs are sent.  If we are built to semiconductor sound waves this implies we need a big equalizer in our ear no?

Since this synapse is massive in all mammals it has been studied.  What do we know?  Researchers have studied multiple mammal species and to the extent that a comparison is possible, the time course for development embryologically matches earlier experiments performed in rats, cats, mice, or gerbils, suggesting that the development of this synapse is highly conserved across all mammalian species. There is another surprise.  The essential steps to build hearing occur largely before the onset of hearing, supporting the view that sensory activity does not play a major role in the formation of this synapse.  So the sound stimulus is unnecessary to morphology.  This is a clue that morphology likely links back to the binary code in morphogenesis.

Do you know what the Calyx of the Head is in humans?  It is the big equalizer mentioned above.

Function. The calyx of Held is a part of the auditory system, connecting the globular bushy cells (GBCs) of the anteroventral cochlear nucleus to the principal neurons of the medial nucleus of the trapezoid body (MNTB).

Most of the MCH-positive fibers in mammals have been detected throughout the brainstem and the cochlea is very close to it in mammals. Interestingly, there was a profuse MCH innervation of brainstem areas that are involved in the control of REM sleep.

The calyx is a giant glutamatergic terminal formed by the main axon of globular bushy cells (Fig. 2, GBC). These cells have their cell body in the cochlear nucleus contralateral to the MNTB and receive large axosomatic terminals from the auditory nerve (endbulbs of Held).

The calyx of Held is probably the largest synaptic terminal in the brain, forming a unique one-to-one connection in the auditory ventral brainstem. During early development, calyces have many collaterals, whose function is unknown.

During embryonic and postnatal development, the calyx of Held undergoes a significant transformation in order to possess morphological and functional properties necessary for performing its major role in relaying acoustic information from the environment to our brain.  

SUMMARY

The implication of this blog are that hearing, tinnitus, and acoustic changes can all be changed by solar exposure on the skin.  If this is true is there evidence that heavily melanated human skin leads to less acoustic disease?

There is. There is a ton of data I provided you below.

Many studies have shown that blacks have a 40%–70% lower prevalence of hearing loss than do whites.

In a previous cross-sectional study, Lin et al. (below in cites) demonstrated an association between certain Fitzpatrick skin phototypes and lower odds of hearing loss among Hispanics, which they suggested might be due to differences in melanocytes between darker-skinned and lighter-skinned individuals. Melanocytes are known to be present in the inner ear, and results from evolutionary studies have suggested that darker-colored individuals tend to have more internal (nonskin) melanin. Furthermore, studies in humans have demonstrated a positive association between number of melanocytes in the skin and in the inner ear.

Melanocytes have antioxidant functions that might serve to protect against reactive oxygen species that are associated with the death of inner ear hair cells in noise-induced hearing loss . Furthermore, cochlear melanocytes serve as intermediate cells in the stria vascularis and are important in the generation of the endocochlear potential.  All this tells me that getting a tan is a great way of maintaining your acoustic system and lowering your risk for both acoustic diseases like tinnitus and misophonia, ocular diseases like retinopathy and thalamic diseases like autism.  Get your skin in the game.  Decentralize your biology to get back what you’ve lost.

CITES

https://optimalklubs.com/kruse-for-dummies-general/

J Kil, GH Kageyama, MN Semple, LM Kitzes, Development of ventral cochlear nucleus projections to the superior olivary complex in gerbil. J Comp Neurol 353, 317–340 (1995).

K Kandler, E Friauf, Pre- and postnatal development of efferent connections of the cochlear nucleus in the rat. J Comp Neurol 328, 161–184 (1993).

BK Hoffpauir, JL Grimes, PH Mathers, GA Spirou, Synaptogenesis of the calyx of Held: Rapid onset of function and one-to-one morphological innervation. J Neurosci 26, 5511–5523 (2006).

VC Wimmer, H Horstmann, A Groh, T Kuner, Donut-like topology of synaptic vesicles with a central cluster of mitochondria wrapped into membrane protrusions: A novel structure-function module of the adult calyx of Held. J Neurosci 26, 109–116 (2006).

DK Morest, The growth of synaptic endings in the mammalian brain: A study of the calyces of the trapezoid body. Zeitschrift Anat Entwicklungs 127, 201–220 (1968).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4521893/

Lin FR, Maas P, Chien W, et al.. Association of skin color, race/ethnicity, and hearing loss among adults in the USA. J Assoc Res Otolaryngol. 2012;13(1):109–117.

Lin CS, Zak FG. Studies on melanocytes. VI. Melanocytes in the middle ear. Arch Otolaryngol. 1982;108(8):489–490.

Dubey S, Roulin A. Evolutionary and biomedical consequences of internal melanins. Pigment Cell Melanoma Res. 2014;27(3):327–338.

Wolff D. Melanin in the inner ear. Arch Otolaryngol Head Neck Surg. 1931;14(2):195–211.

LaFerriere KA, Arenberg IK, Hawkins JE Jr, et al.. Melanocytes of the vestibular labyrinth and their relationship to the microvasculature. Ann Otol Rhinol Laryngol. 1974;83(5):685–694.

Nofsinger JB, Liu Y, Simon JD. Aggregation of eumelanin mitigates photogeneration of reactive oxygen species. Free Radic Biol Med. 2002;32(8):720–730.

Meyskens FL Jr, Farmer P, Fruehauf JP. Redox regulation in human melanocytes and melanoma. Pigment Cell Res. 2001;14(3):148–154.

Henderson D, Bielefeld EC, Harris KC, et al.. The role of oxidative stress in noise-induced hearing loss. Ear Hear2006;27(1):1–19.

Takeuchi S, Ando M. Inwardly rectifying K+ currents in intermediate cells in the cochlea of gerbils: a possible contribution to the endocochlear potential. Neurosci Lett. 1998;247(2-3):175–178.

For a long time, there has been a guy running around the world advocating wearing yellow clothing to block radiation.  Is this pseudoscience or might there be something to this?  You might even run across this pamphlet from time to time.

What is a possible mechanism for this observation in Nature? Many people do not know when I look into the eye of a patient with an ophthalmoscope one of the things I am looking at is the macula lutea. The macula contains the fovea where color vision is the sharpest. “Lutea” is yellow in Latin. This area collects yellow carotenoids to decrease the visual blur that is induced by blue light because blue light is the high frequency of light and it is the frequency that bends the most for the macula to handle. Yellow is the complementary color of blue.

In nuclear reactors, the heavy water that contains spent fuels emits Cherenkov radiation. The frequency spectrum of Cherenkov radiation by a particle is given by the Frank–Tamm formula. Unlike fluorescence or emission spectra that have characteristic spectral peaks, Cherenkov radiation is continuous. Around the visible spectrum, the relative intensity per unit frequency is approximately proportional to the frequency. That is, higher frequencies (shorter wavelengths) are more intense in Cherenkov radiation. This is why visible Cherenkov radiation is observed to be brilliant blue. Cherenkov radiation is a form of energy that we can perceive as a blue glow emitted when the electrically charged particles that compose atoms (i.e. electrons and protons) are moving at speeds faster than that of light in a specific medium. Ironically, most Cherenkov radiation is in the ultraviolet spectrum—it is only with sufficiently accelerated charges that it even becomes visible to our retina; the sensitivity of the human eye peaks at green, and is very low in the violet portion of the spectrum. This helps explain this scientifically. Anyone who calls it pseudoscience without examining it for themselves should not be listened to.

HERE IS WHAT THE RADIATION LOOKS LIKE INSIDE A NUCLEAR REACTOR

DOES SCIENCE PROVIDE A POSSIBLE ANSWER FOR THIS OBSERVATION IN NATURE?

Can Gold be used as nnEMF radiation shield for melanin protection?

Now for more science related to this idea.

In 1988, this was published in the NY Times and I remembered reading it.  Remember gold emits a yellow color because of Einstein’s relativity equations.

What was in the article I read in 1988 in New York City?

I was dental school in 1988 and I was learning about class 5 gold foil dental reconstructions and came across this article back then.

GOLD, one of the heaviest chemical elements, is the basis of a new lightweight plastic foam under development as a radiation shield.

Scientists at Texas A&M University have found a way to intersperse gold atoms with other atoms in the long molecular chains that make up polymers. By bubbling gas through the gold polymer, it can be expanded into a light foam that reportedly shows great promise as a shielding agent against neutrons and other types of radiation.

Dr. John Fackler, director of the program, said the new polymer combines gold with triphenylphosphine, a compound of carbon, hydrogen, and phosphorus, in a form that may be suitable for making anti-radiation garments.

The polymer is 11 percent gold by weight, and the gold atoms in the substance efficiently scatter or absorb most forms of radiation, including X-rays. Chemically incorporated into a polymer, gold is less poisonous than other heavy metals that also block radiation.

Metallic gold is not poisonous, but when incorporated into compounds it may be. Dr. Fackler said that because gold is chemically very stable, it tends to revert to its native state from some of the compounds it forms. ”We often have trouble with shiny, yellow metallic gold precipitating out of liquid compounds – just what refiners want, but the opposite of what we want,” he said.

The gold polymer the Texas group has developed looks like plain white plastic, Dr. Fackler said, but it emits a yellowish glow when exposed to ultraviolet light.

SUMMARY

Many might find this shocking but there is a lot of science behind these claims about the color yellow and the atom of gold.  One of my former members in the mining industry could not believe this when I share it with him during a consult I did on him in 2015 about his melanoma risk.

Above you see a series of bis(thiocyanato)gold(I) complexes with Au−Au interactions show luminescence in the range from 500 to 670 nm.  These frequencies include the blue light frequencies that cause the blue light hazard in the human retina. This picture below from Alexander Wunsch, MD show this effect.

The series of salts correlates emission energy with the reciprocal of the Au−Au distance. As the Au−Au distance increases, the emission energy decreases. The ligand system provides no framework for the Au−Au interaction. The emission energy seems totally determined by the Au−Au distance.

So when I am in a country where I cannot opt out of the new TSA scanners I reach into my computer bag to protect melanin in body.  I usually take it 30 minutes before flight.  Last time I had to do this was in Germany when I went to speak at Flowfest.  I posted about this hack on Instagram.

Gold therapy, while not commonly used in the treatment of RA today, is still available in oral capsule form as Ridaura (auranofin). The injectable forms—Myochrysine (aurothiomalate) and Solganal (aurothioglucose)—are no longer manufactured but they can be compounded by a pharmacy.  Below is my travel jacket I wore to Europe the last time I went there. The jacket is definitely not a fashion statment.

Jason Bowden Smith, a former entrepeneur member who was a mining industry executive, was with me in Mexico 4 months before the Germany talk and I told him about the jacket hacks and the gold hack and why I was doing it to go to Europe.  Here is the picture taken that morning at 8:34 AM on January 4, 2018.  He just did not believe what I shared with him.  That maybe explains why reality unfolded as it did.

The gold salts and clothing are expensive hacks to protect melanin, but I think my health is worth the expense.  I first mentioned this effect to Jason Bowden Smith  in a consult in 2016.  He was from Australia and had a very challenging medical history.  We did a few consults when he was alive & during a consult I told him about these effects for long flights to mitigate TSA scanners, cosmic/gamma radiation exposure, and WiFi toxicity from passenger use around him.

Gold therapy can induce an internal Yarkovsky effect  (below) for melanin protection.  People who have had melanoma and who still are afraid of the sun should be told about this mitohack.  Very few of my clients needed this.  Unfortunately he did need the advice and he got it.  UInfortunately, he believed a lot of the propaganda that is floating around in Australia even today about the sun.

Jason took a lot of circumpolar flights in his life.  I thought this was linked to his REAL melanoma & thyroid risk and I told him about POMC and melanin.  I told him a lot of what you’re learning now in this blog series a long time ago.  In fact, Jason was with me in a meeting the night before my clinic opened in New Orleans in December 2018 to talk about a business opportunity about this very topic since he had deep connections with gold miners in Australia.  My nurse, Chantal was present at this meeting.

Anyone who was with me in Germany knows I did not feel well when I was in Germany because they had recently turned on 5G in the city I was speaking in.  I distinctly remember Jason mocking me before my talk when I took my clothes off and laid in the sun to get ready to speak.  He kind of pissed off my nurse who was with me at the event.  He just did not believe that something on the surface could have that big an effect on our mitochondria below.  I told him that the gold/yellow can protect quantum coherent process happening with 1/2 nuclei spin magnetic moments in our colony of mitochondria to maintain quantum coherence.  I told him everything that is important in quantum biology happens on the surface before it changes the matter inside of us. I told him that in June of 2018 I was goning to unleash this in Vermont.  I did.  Here is the slide from that event.

I spoke in Germany right after the Vermont event on July 6th, 2019.  Something else happened at that talk that others can verify. The meeting organizer subtracted 45 minutes from my talk and only gave me 15 minutes to speak. Matt Maruca and Jason were both there also as a speaker and they saw this go down.  He made me a bet that there was no way I could do a nnEMF talk for the German biohacking community in the 15 minutes.  I went and powered up in the sun, drank one liter of DDW, and laid shirtless for two hours before my talk and missed many talks doing so.  Matt then got a red LED stop clock and put it in his lap to show me my time to see if I could do it.  Notice the first slide in the talk.

I finished the talk at 14:59 and everyone who was at the event was astounded I got the talk done in such a short time frame.  The talk was so good that the Q & A lasted two hours outside the event when I was ushered off the property because the event was closing. Jason Bowden Smith spent that two hours in the sandpit of the event with me trying to ask me more about this science.  It was the last time we met live in person and we never spoke about it again.  He died soon after it.  I feel that he never called me back to speak about things because he felt foolish that he had an answer from 2016 and thought it was a joke.  Generally I don’t joke around on consults.  I am all business.

Below this was me in Germany live on the stage during the Q&A before it spilled outside.  That jacket was tailored to be infused with gold microfiber threads hidden in the silver etchings, hence the reason I bought it and wore it.  I still have this jacket today.

What is the Yarkovsky effect?

The Yarkovsky effect is defined as a thermal radiation force that causes objects to undergo semi-major axis drift as a function of their size, orbit, and the COLOR of the material properties in the matter that makes up the object in question.

Melanin has a massive Yarkovsky effect inside of cells because of its color.  so anything you can do to reflect and deflect incoming radiation should help protecrt you melanin sheets.

The Yarkovsky effect is hard to predict, though. Scientists have to know the asteroid’s mass, size, and shape. They also need to know the patterns of light and dark on its surface, because lighter colors reflect more sunlight, while darker colors absorb more.

The best measurement of the Yarkovsky effect so far is on an asteroid named Bennu. The effect has altered Bennu’s position by about a hundred miles in just a dozen years.  So when you hear something that sounds ludicrous.  Remember it is the height of ignorance to say it is pseudoscientific without looking deeper at the issue before making a decision.

Just because something’s logical, doesn’t mean it’s not wise. Something can make sense in and of itself, but when tested against reality yield an undesirable or inefficient outcome. Being seduced by impractical logic is antithetical to wisdom, you just feel smart despite being wrong.  Sometimes chosing comfort over wisdom might kill you.

CITES

1.https://artsci.tamu.edu/news/2023/02/texas-aandm-mourns-loss-of-distinguished-professor-emeritus-john-fackler.html

2. A version of this article appears in print on Sept. 6, 1988, Section C, Page 11 of the National edition with the headline: SCIENCE WATCH; Gold as Radiation

3. https://pubs.acs.org/doi/pdf/10.1021/ja00310a028

4. https://www.instagram.com/p/CsJcPQUM2a9/

5. https://forum.jackkruse.com/threads/dog-health.27663/#post-321327

Supraventricular tachycardia SVT is a broad term for a number of tachyarrhythmias that originate above the ventricular electrical conduction system (Purkinje fibers).  read the link below to learn about SVT.  This rhythm is usually the first symptom in melanin degradation of the cardiac plexus.  I showed you this picture in Quantum Engineering #47 for the first time.

https://www.ekgstripsearch.com/SVT.htm

In ACLS codes we use adenosine via IV push to rid the heart of this detrimental rhythm when the patient is not symptomatic.  SVT can lead to rapid cardiac standstill.  We are seeing this more commonly now due to the spike protein inflammation of the heart by mRNA vaccines.  I believe this was behind the demise of Demar Hamlin and JJ Watt.

IS THERE NOW EVIDENCE THAT INTENSE RED LIGHT can do THE same thing using the PER circadian gene?  Does this imply that red light is a drug equivalent?

YES, it does.  The picture above shows you this.

Is there more to this circadian story you need to know?  YES.

You know my answer and you should know what Dr. Tina Kuru says about this………..Red light is a drug equivalent to adenosine use.  This is a message Big Pharma wants buried from centralized MDs.

In this paper below in an effort to find out why red intense light can do this, researchers developed a photonic strategy using optogenetics to protect the heart using intense light to target and manipulate the function of the PER2 gene which is expressed in a circadian pattern in the part of the brain that controls circadian rhythms.  (Sounds like something Dr. Kruse would suggest no?)

You do know that sunlight is made of 42% intense IR-A light huh?

By amplifying this gene to improve the periodicity of the cardiac clocks, the researchers were just using LIGHT PHOTONS to do this job; they found that it protected cardiovascular tissues against LOW OXYGEN conditions like myocardial ischemia, caused by reduced oxygen flow to the heart.  Dr. Kruse called low oxygen situations pseudohypoxia (low NAD+).  These are all associated with low NAD+ levels in cytochrome 1 and leptin resistance with low delta psi on the inner mitochondrial membrane = low redox power.

They also discovered that the light increased cardiac ADENOSINE, a chemical that plays a role in blood flow regulation.   Hey didn’t Dr. Kruse just do a massive post on ADENOSINE last week on his page?

Hey, isn’t leptin resistance a synonym for melanopsin dysfunction?  Isn’t melanopsin dysfunction a synonym for a melanin problem?  Yes, it is. Tell me again how that works Dr. Kruse?

Dr. Kruse Response:  Blue light and nnEMF liberate Vitamin A from our cells and cell membranes to raise its presence in the blood plasma and this lowers plasma levels of Vitamin C and Vitamin D.  This destroys melanin in the cardiac plexus and it degrades into adrenaline and noradrenaline that begins to stimulate the heart adrenergically.  It also has effects on the glylympaphatic system in the brain and on slow wave sleep.  When Vitamin A is liberated by non terrestrial light or trauma, we are inducing a light stress and this causes Vitamin A to becomes an aldehyde that becomes a wrecking ball for many non visual photoreceptors like melatonin, dopamine, NO, adrenaline, noradrenalin, L-Dopa, P-450 enzymes, RBCs, cytochromes, and melanin.

This wrecking ball action destroys the small molecule modulators of the mammalian circadian mechanism.  PER1 and PER2 are gears in that eye clock mechanism.  Once the molecular clock in the eye and peripheral clocks goes awry the implications for many neolithic diseases spiral out of control.  What are some of the Vitamin A proteins involved in this downward spiral?

They are called retinoic acid receptor-related orphan nuclear receptors or RORs for short.  The RORs have several isoforms too called RORα-γ.  These proteins are also under the transcriptional control of CLOCK/BMAL1 heterodimers.  CLOCK and BMAL1 are positive regulators of circadian gene expression, and PER and CRY are the NEGATIVE FEEDBACK LOOP regulators that operate under day and night cycles.

These are the positive and negative feedback arms of the circadian mechanism.  They must be coupled properly to terrestrial light to operate well and control all growth and metabolism, protein synthesis and hormone production and release.  It also controls receptor biology.  It controls EVERYTHING.  These are post transcriptional explosions that blow up the whole system of optical signaling and require the cell and mitochondrial to rebuild them all while our power plants are experiencing a brown out.  This is not ideal.

If they are not properly coupled to the light and dark cycles the eventual results is the extinction of both sides of the feedback loop.  That is how all human disease begins.  It is circadian biology that couples all the molecular clock genes in humans and the SCN of the eye drives the program and the major timekeeper.

Remember this lesson from the past:

Classic Paroxysmal SVT has a narrow QRS complex & has a very regular rhythm. … A rapid heart rate will significantly reduce the time which the ventricles have to fill. This is why degradation of melanin to adrenalin and noradrenalin is a real problem.  Carefully look at how melanin degrades on the top line during periods of hypoxia.  The chemistry in hypoxia goes from right to left.

The heart fills during diastole, and diastole is normally 2/3 the cardiac cycle. A rapid heart rate will significantly reduce the time which the ventricles have to fill and as a result this lowers cardiac output and oxygen delivery = hypoxia.  As a result of this the heart tries to beat faster to improve global hypoxia and this worsens the situation.  It fast forwards on itself.  The reduced filling time results in a smaller amount of blood ejected from the heart during systole. The end result is a drop in cardiac output & hypotension.

With the drop in cardiac output, a patient may experience the following symptoms. These symptoms occur more frequently with a heart rate >150 beats per minute as the ECG strip shows:

Shortness of air (S)

Palpitation feeling in the chest (S)

Ongoing chest pain (U)

Dizziness (S)

Rapid breathing (S)

Loss of consciousness (U)

Numbness of body parts (S)

The pathway of choice for SVT in the tachycardia algorithm is based on whether the patient is stable or unstable clinically.

The symptoms listed above that would indicate the patient is unstable are noted with the letter (U) in a code situation. This can present outside a code situation when someone has a very low redox state because of a very poor environment linked to blue light and nnEMF toxicity. This mimics adrenal fatigue and brainstem pathology, sleep disorders, and eating disorders I wrote about in the QE#47 blog.  Stable but serious symptoms are indicated with the letter (S) above.

Insert any 3G-5G city or environment = an acute or chronic adenosine problem. What fucks up sleep ultimately at the dorsal longitudinal fasiculus? Problems with adenosine at the brain stem level. This is why ACLS algorithms for advanced caridiac life support uses adenosine to treat acute mitochondrial failure in the heart that results in SVT cardiac rhythms……..guess what drug is used for cardiac tachycardias in ACLS?

ADENOSINE via IV push = a DEFECT IN PER 1 or PER2.  SOUND FAMILIAR?

How do you like me now…………?

Do you still think tech use and abuse is safe and has no side negative effects for the heart of your blood vessels?  That damage can be found early in your brainstem by the DLF where glylymphatic drainage occurs.  How about your eye clock or the molecular clocks in your skin.  These are all places where melanin, melatonin, melanopsin and leptin are.

Adenosine building up occurs normally during the day when red light is powerful as we live and is one thing that drives us to feel sleepy during the night. Then while you sleep, the adenosine is cleared out by the glylymphatic system in the brainstem at the perivascular spaces, leaving you refreshed and ready to go in the morning… for most people. This does not happen in those with sleep apnea.  Those with OSA have circadian mediated glylymphatic failure of AQA 4 in the brain stem due to lowered periodicity of PER1 & PER2 (above pic).  I can see the widened perivascular spaces on 3 Tesla MRI images at the DLF.  This is how decentralized medicine is practiced.  Today, most people that have a version of EHS that affects adenosine at the brainstem level which causes their sleep destruction and hypoxia via this mechanism. This mimics adrenal problems (PVN) and causes wild symptoms doctors cannot explain.

Who else can get these problems sans a technology addiction?

if you follow your genetics from 23 and me…

There is a genetic variant in the adenosine deaminase (ADA) gene that decreases the clearance rate of adenosine. People who carry the variant may get more slow-wave, deep sleep at night, but they also may need to sleep a little longer o feel refreshed the next morning.  These people are at high risk of neurodegeneration and for normal pressure hydrocephalus and glylymphatic failure.

What is the decentralized diagnosis that your centralized sleep MDs will never resolve for you?

Check your genetic data for rs73598374 (23andMe v4, v5; AncestryDNA):

C/C: normal clearance of adenosine

C/T: reduced clearance of adenosine, more deep sleep but may feel sleepy when waking up

T/T: reduce clearance of adenosine, more deep sleep but may feel sleepy when waking up.

How do you like me now?

Intense RED LIGHT via PBM/LLLT is the first step I like I use at Kruse Longevity Center for melanin renovation of the cardiac plexus that I wrote about in QE #47.  It is always cardioprotective.  The red light of the sun is better than my fake red light panels.  Shocking huh?

It shocks only those who are not on the path of becoming a decentralized Black Swan Mitochondriac.

If you do not listen to me you might wind up needing a shock from a defribrillator sometime in your life from tech abuse or from excessive spike protein build up in and around these areas in your body.  See my blog on Demar Hamlin or JJ Watt for more detail.

When you know better you do better.

CITES

https://www.sciencedaily.com/releases/2019/08/190808115052.htm

Today you get to see see what melanin looks like on MRIs of some of my patients.  

Melanocytes are normal, neural crest-derived cells present in the human leptomeninges (pia and arachnoid membranes) primarily at the base of the brain, the posterior fossa, and around the upper cervical spinal cord.  They are very close to cells with POMC expressed to some degree.

Meningeal melanocytomas are rare benign primary melanocytic tumors of the CNS that are derived from leptomeningeal melanocytes. They can occur anywhere along the neuraxis but are most commonly found in the spinal canal near the foramen magnum, as well as the posterior cranial fossa, Meckel cave, or adjacent to cranial nerve nuclei based on embryological movements.

Key point:  When these tumors are found in the trigeminal cave, then they are associated with a nevus of the dermatomes corresponding to the trigeminal nerve on the face. The benign dermal melanocytic nevus usually involves the ophthalmic (Va) and maxillary (Vb) divisions of the trigeminal nerve (CN V).  This again shows the neural create connections and the neuroplasticity pathways one should expect in melanogenesis from these movements in mammals.

Primary melanocytic tumors of the CNS can manifest as solid masses or as diffuse dissemination within the subarachnoid space. They range in histologic grade from benign to malignant, differentiating between the following entities:

• meningeal melanocytoma: benign mass-forming proliferation
• meningeal melanoma: malignant mass-forming proliferation
• meningeal melanocytosis: diffuse meningeal benign melanocytic proliferation
• meningeal melanomatosis: diffuse meningeal malignant melanocytic proliferation

Melanocytomas are more common in women (mean age 45-50 years old). A prolonged evolution of clinical signs of myelopathy or radiculopathy prior to surgical resection (from 5 to 10 years) has been documented.

I believe this is true because women tend to wear more clothing over their bodies due to cultural and societal reasons.

Approximately 100 cases of melanocytomas have been reported in the CNS (brain and spinal cord) since Limas and Tio coined the term “meningeal melanocytoma” in 1972. In the spinal cord, most cases of melanocytomas are found in the extramedullary intradural compartment, at the cervical and thoracic spinal levels. An intramedullary location as our case depicts is extremely rare, with only 24 cases reported before.

The unique paramagnetic properties of melanin result in a relatively specific MRI pattern for melanocytoma, consisting of iso- or hyperintensity on T1WI and iso- or hypointensity on T2WI, and with homogeneous enhancement.  The differences in MRI signal intensities relate to a variable degree of tumor melanization.

Paramagnetic means it is drawn to magnetic fields.  This is a clue why the tumor was in this location.

Definitive diagnosis is based solely on histopathological and immunohistochemical examination.

The distinction between melanocytoma and melanoma rests on the identification of cytologic atypia, mitotic activity, necrosis, and neural parenchymal invasion.

MIB-1 (Ki-67) labeling index seen in melanocytomas is low (0%-2%) while in primary melanomas is higher (2%-15%). Based on a proposition by Brat et al. the WHO classification assigns an intermediate grade to melanocytomas with increased mitotic activity and infiltrative growth that fail to meet all characteristics of malignant melanoma. In this case, MIB-1 (Ki-67) proliferation index was 5% and a definitive diagnosis of intramedullary Intermediate-grade melanocytoma of the thoracic spine was made.

CURRENT CENTRALIZED MEDICINE BELIEFS

Although classified as benign, meningeal melanocytomas may behave aggressively and a limited number may transform into malignant melanomas. Complete excision is the treatment of choice, however, this is often not possible as intra-operative hemorrhage may be severe. Furthermore, local recurrence has been reported even after gross total removal. Due to the risk of tumor recurrence even after complete excision, adjuvant radiation therapy is advised in cases of both complete and incomplete resection.  I no longer believe this.

EPIDEMIOLOGY

Peak presentation is in the fourth and fifth decades, although these tumors have been diagnosed in all age groups. Occurrence in children is very rare!

RADIOLOGY IMAGING

The patient presented after breast cancer resection with a 2-year history of progressive paraparesis, paresthesia, and dysesthesia in the left lower limb. Neurological examination demonstrated generalized hyperreflexia and clonus of the left foot.

The above MRI is done on a 1.5 Tesla magnetic and shows a solitary well-defined fusiform intramedullary lesion involving the spinal cord at the T8-T11 level, hypointense on T2WI, moderate hyperintense on T1WI, and presenting homogeneous enhancement of its solid component after gadolinium administration.

Lesion associates a cystic component in its cranial pole, and presents susceptibility artifacts in the T2WI-GRE corresponding to its melanin component and the presence of degraded blood products.

T2WI hyperintense per focal tumoral edema at the T5-T7 levels and conus medullaris is noted, suggestive of myelopathy.

OTHER IMAGES:

3 case questions are available

Q: The presence of hyperintensity on T1WI can be an important clue leading to a specific diagnosis, as happens in this case above. Which are the causes of T1 hyperintensity?

A: Melanin. Gadolinium. Fat. Blood forming proteinaceous substance. Some paramagneticstages of blood. Mineralization. Slowly-flowing blood. Calcium. (Pic below)

Q: What’s the most frequent T1WI appearance of meningeal melanocytomas?

A: Isointense or hyperintense depending on the amount of melanin content present.

Q: What’s the most frequent T2WI appearance of meningeal melanocytomas?

A: Isointense or hypointense depending on the amount of melanin content present.

The slide below reminds us that when we are looking for melanin loss we should see it missing in T1 weighted MRI images.

Radiological differential diagnosis includes:

• primary or metastatic malignant melanoma
• melanotic schwannoma
• melanotic meningioma
• melanoblastosis
• cavernous malformation
• astrocytoma
• ependymoma

Operation report:

Tumor resection was performed through osteoplastic laminectomy and under electrophysiologic intraoperative monitoring.  Tumor fragments were soft, brownish, and hemorrhagic.  Melanin tumors are always bloody because they are always associated with brisk blood flow due to their need for massive oxygen consumption.  This mimics what we see in retinal bleeds around the RPE and Bruch’s membrane.

PATHOLOGY SLIDES

H&E stained slides above show in sequence sheets and nests of cells with mild nuclear pleomorphism and prominent nucleoli; note the marked melanin pigment deposition. An immunohistochemistry study revealed positivity for melanocytic markers Melan A and HMB45. MIB-1 (Ki-67) proliferative mitotic index of 5%.

KEY BLOG POINT: This index clued me in that her previous breast cancer was likely related to this mass and its location.  She had a WiFi router under her bed in her apartment at the level of her mid-thoracic spine.

Meningeal melanocytomas are most commonly found in the cervical and thoracic regions (intrathecal-extramedullary). Within the spine, melanocytomas present as intradural masses, and maybe intradural extramedullary or rarely intramedullary. They are most commonly found in the upper cervical region, as melanocytes are most concentrated at this location. I believe the real reason is that this area is usually covered and not illuminated by sunlight.  Even more interesting is they are less common in the intracranial compartment because rarely do we lose all VUV-IR-A inside the brain.  We would most commonly see this in glioblastoma multiformans cases instead.

CITES

• 1. Louis DN, Ohgaki H, Wiestler OD, Cavenee WK, Burger PC, Jouvet A, Scheithauer BW, Kleihues P. The 2007 WHO classification of tumors of the central nervous system. (2007) Acta neuropathologica. 114 (2): 97-109. doi:10.1007/s00401-007-0243-4 – Pubmed
• 2. Karikari IO, Powers CJ, Bagley CA, Cummings TJ, Radhakrishnan S, Friedman AH. Primary intramedullary melanocytoma of the spinal cord: a case report. (2009) Neurosurgery. 64 (4): E777-8; discussion E778. doi:10.1227/01.NEU.0000341516.22126.AA – Pubmed
• 3. Liubinas SV, Maartens N, Drummond KJ. Primary melanocytic neoplasms of the central nervous system. (2010) Journal of clinical neuroscience: official journal of the Neurosurgical Society of Australasia. 17 (10): 1227-32. doi:10.1016/j.jocn.2010.01.017 – Pubmed
• 4. Czarnecki EJ, Silbergleit R, Gutierrez JA. MR of spinal meningeal melanocytoma. (1997) AJNR. American journal of neuroradiology. 18 (1): 180-2. Pubmed
• 5. G.Q. Hou, J.C. Sun, X.J. Zhang, B.X. Shen, X.J. Zhu, L. Liang, X.L. Zhang. MR Imaging Findings of the Intraspinal Meningeal Melanocytoma: Correlation with Histopathologic Findings. (2012) American Journal of Neuroradiology. 33 (8): 1525. doi:10.3174/ajnr.A2987 – Pubmed
• 6. Wagner F, Berezowska S, Wiest R, Gralla J, Beck J, Verma RK, Huber A. Primary intramedullary melanocytoma in the cervical spinal cord: Case report and literature review. (2015) Radiology case reports. 10 (1): 1010. doi:10.2484/rcr.v10i1.1010 – Pubmed
• 7. Brat DJ, Giannini C, Scheithauer BW, Burger PC. Primary melanocytic neoplasms of the central nervous systems. (1999) The American journal of surgical pathology. 23 (7): 745-54. Pubmed