QT#17: SWINGING ON THE SPIRAL: TIME

 

Few of us realize the liquid crystals in us create time using light.  Time and space are modes by which we think and experience reality but neither are conditions in which we live on Earth.  We live by swinging on the spiral arm of a galaxy constantly moving through space .

Ever since the derivation of the theory of relativity, physicists have thought they have done reasonably well in understanding time; however, biologists are still waiting for a comprehensive theory of timing in living systems:  they remain waiting for a corpus of “laws” describing how cells and organisms can precisely initiate and terminate processes at specified times because they are focused on the nuclear genome and not the mitochondrial genome.  Time perception is critical to mitochondrial biology but it is not especially important to the nuclear genome because the energy provided by the mitochondrial genome allows time to manifest in living things. This deficiency in biology is particularly acute in developmental biology, where complex mechanisms of various paces and durations must be orchestrated to solve huge developmental problems such as the one faced by the fertilized egg: how to become an organism using energy/information and electric and magnetic field to direct and power morphogenesis.

Animal development is, in fact, nothing but time. From the cell cycle to the beating of the heart, our own lives are composed of a multitude of microscopic and molecular oscillations. For developmental biology, the study of causal relationships implies the examination of two time points: inducing the cause and looking at the effect. In QED, cause and effect is blurred because of the uncertainity principle.  In biology, cause and effect “appear” to be linked because of how time is perceived.  We are generally ignorant of the temporal rules governing this transformation. Light and aromatic amino acids form those foundations.  Whereas the rules of a Swiss watch involve a timing mechanism that uses a uniform unvarying tempo to translate rapid oscillations (seconds) into longer periods of time (hours), the rules of the developmental clock of animals are much more complex because they use light and light is non linear in the violet part of the visible spectrum. The animal clock is made up of a variety of counting mechanisms that follow varied temporal rules at different frequencies and often run in parallel without any “apparent” interaction with each other, because their linkages are via molecular resonance. The goal of the developmental clock is not simply to mark off time, but to integrate and unify the myriad temporal signals received from throughout the organism.

However, the frequencies and amplitudes of most, if not all, developmental clocks are robustly determined within the same species, suggesting that these are genetically encoded devices being linked and controlled by resonance instead of being produced by the system itself, as an “emergent feature.”  I have always believed time is an emergent property of life because time emerges from the complexity of light the force carrier of the electromagnetic force. Today, the “old paradigm of biologic time (Franz Hallberg) is dominant in the published literature, but as Max Panck said, things change in science one funeral at a time.  Morever, if the “belief” is true that time is encoded in our DNA (it’s not), what are the genetic balance wheel, hairspring, and gears, and what are the specialized tools that are needed to elucidate the intricate workings of the genome? There are many possibilities to consider here, but I will discuss two.

 

 

The first one concerns clocks generated by mechanisms in “trans”, generally based on the postulate made in the early 1950s by Alan Turing (mathematician, philosopher, and inventor of the concept of the computer), who argued that the diffusion of substances with activation, repression, and retroactive potentials can generate intrinsic oscillations in space and time. The literature has begun to decipher some of these ideas and more are likely to come in the near future.

The second possibility involves mechanisms in “cis”, using the linearity of our genetic material itself, our chromosomes, to measure time; an admittedly elegant solution, but one that severely lacks both experimental and theoretical support. Chronobiology is stuck on these two options because they do not realize that time is a superposition of many possibilities. This is why they ignore the mitochondrial genome. This genome creates many possibilities when small changes occur to it. When we disrupt it with anesthesia timing is completely altered, we observe it and we measure it, but we do not understand the implications for man or his diseases. This will change with the coming age of quantum biology. The old guard expected some help from the human genome sequencing and related high-throughput technologies, but they got stonewalled because it destroyed constructs that we inherited from Watson and Crick. I reject most of their thesis about biology.

 

 

Modern epigenetics data has blown up much of Darwin’s thesis from 1859 but few biologist will admit it today because it is akin to removing the binding from a book.  All organizing principle are afloat now in molecular genetics because of the new insights of epigenetics.  So is science and life.  Every end is a new beginning in understanding and learning with respect to nature’s wisdom.  Darwin’s supporters today are still trying to hold the theory together but the concept of timing and energy is 100% tied to energy collection and generation and distribution in the cell. They have no Earthly idea that energy and information processing are coupled by light.

There is little doubt that the mechanisms in ‘trans’ will be advantageously studied in this context. Time-lapse proteomics and metabolomics, adapted to minute amounts of material such as cohorts of less than a thousand cells, would certainly show significant recurrences and, perhaps, allow the temporal algorithms underlying developmental clocks to be uncovered.  But trends in protein or metabolic movement can just describe the cellular processes and it won’t explain it.  The explaination will take a mind filled with innovated thoughts to link them back to the fabric of nature’s laws.  Today’s developmental chronobiologists believe that a reductionist approach to clock mechanisms will give us the key answers.  In fact, we just gave three people a Nobel Prize recently for discovering the biologic molecules involved in the circadian mechanism.  For example, the tightly regulated timing in the successive appearance of whiskers on the nose of a rodent would likely be deciphered if we could microdissect the whisker field like a chess grid, and submit each square to full protein content analysis.

On the other hand, the challenge in identifying ‘cis’ processes would be to use several species showing graded variations in clock parameters, such as in the frequencies of the same clock, and to find correlations with the “cis organization” of DNA segments through a large-scale approach. Such correlations, if any, could reflect the existence of linear time-measuring devices, from the mere duration of transcription to more complex processes such as progressive transitions in the chromatin state. However, that is easier to say than to do; a genuine “casse-tête” for bioinformaticians.

 

 

I believe based upon what we know today about epigenetics, it is seriously pretentious to try to extract the fourth dimension, time, out of our DNA/RNA structure when we still lack complete understanding of the other three dimensions of our world. But the human quantum computer does not need complete data sets to jump to conclusions. That is what innovation and imagination are useful for in complex problem solving. This science is the privilege and the difficulty of working with embryos: The spatial construction can be understood only in the light of time. The irony of this idea, is that light is what creates time.

 

 

This concept continues to trip up biologists because they are ignorant of the queerness of the physics of light. Similarly, evolutionary genomics will likely teach us what happened during phylogenetic times, and our ontogenic clocks may be revealed by global comparative analyses.

 

 

Chronomics is on the way, but only the unripe mind will think it is the be all end all in the discussion of what time really is.

Time allows us to see what we have become, even when we miss it. The liquid crystals inside of us build this library. Time is erased for some of us, because we cannot use sunlight and water to build the crystals properly to manage our time. Sometimes we erase people and family, and walk away from the shadows creeping up on us. Sometimes you must give up on people, not because you do not care, because they do not care enough for themself by making the correct choices.

Spiral out…………..

QT #16: WHERE DOES ELF-UV COME FROM?

 

So do we glow when sunlight hits the skin? Yes, we do. What kind of light do we glow with? ELF-UV light manifests in our blood plasma = do we gain or lose electrons when this occurs? We lose electrons and give them to other anions in our blood. Sulfated amino acids are added to many proteins and lipids in our blood under the power of sunlight. Sunlight increases sulfhydryl groups which are the major anions in our blood plasma.

 

 

Our tissues glow because when an electron is delocalized light is given off and that light produces change without atomic change because it changes the topologic charge of atoms in our skin proteins because UV light causes a loss of electrons in out tissues.  This mechanism is what causes release nitric oxide from the arterioles in our skin to change the topology or femtochemistry of the surface of the skin when it is irradiated by IRA and UVA light.  The change in femtochemistry results in attochemical changes in deuterium in our blood plasma.

Full spectrum sun contain UVA/B light which is capable of altering the topologic charge of nitric oxide (NO).

UVA light releases the most NO into our blood.  IRA light is how the exclusion zone is built initially in sunlight in our plasma.  Both of these frequencies penetrate below the epidermis to where the arterioles of our skin.

The key thing to comprehend is there is no way to satisfy the octet rule for both atoms in NO because of their valence shell electron state. The structure is a double bond with three non-bonding electrons on N and four on O but really one of the electrons on N is not localized to N but the entire molecule.

Formal charge = electrons in ground state – (non-bonding electrons + 0.5 * bonding electrons)

Formal charge for N = 5 – ( 3 + 4 * 0.5) = 0 (there are two bonds so four electrons are involved in bonding)

Formal charge for O = 6 – (4+ 4 * 0.5) = 0

Sunlight alters that balance of charge on our surfaces.  What does it do?

It creates the triplet state of free radicals because of the effect on electron quantum spin.  Every surface in our body has this mechanism available if the sun is allowed to interact with it.  If the sun is absent this will not occur and it will lead to collateral damages.   Where else is electron spin altered?   MITOCHONDRIA.  This is where the critical ROS and RNS signals are made.  These signals affect a third cycle in us that controls the sulfated amino acids.  This is the sulfated amino acid cycle contains cysteine methionine and homocysteine.  This cycle is altered because of the changes in free radical creation by the light our skin does or does not experience.

Full spectrum solar exposure of the skin increases sulfhydryl groups in the blood plasma.  This increases the anions present in our blood.  Sulfur amino acids are a kind of amino acids which contain sulfhydryl groups, and they play a crucial role in protein structure, metabolism, immunity, and oxidation. Recent studies have demonstrated the oxidation resistance effect of methionine and cysteine, two of the most representative sulfur amino acids, and their metabolites.

Methionine and cysteine are extremely sensitive to almost all forms of reactive oxygen species MADE IN THE MATRIX, which makes them antioxidative and critical redox switchs that tell us about TCA and urea cycle kinetics.  They can both be used to tell us when the matrix is slowed by deuteration.

Moreover, methionine and cysteine are precursors of S-adenosylmethionine, hydrogen sulfide, taurine, homocysteine,  and glutathione. These products are reported to alleviate oxidant stress induced by various oxidants and protect the tissue from the damage. However, the deficiency and excess of methionine and cysteine in our diet can affect the normal growth and longevity of animals.

 

 

It is well known that oxidation from free radicals of the cysteine thiol groups occurs in all stressors in humans.  This results in defective glucocorticoid receptor (GR in pic above)  function and it affect ligand and DNA binding in cells.  This implies that in a 5G world where the toplogy of the skin will be affected, cysteine and methionine hacks will be quite important to understand and use when one gets afflicted with electropollution type diseases like autoimmunity, sepsis, and cancer.   To understand how these sulfated amino acids operate you must understand how the sun works in your skin.  I discussed this in the Vermont 2018 talk now available for purchase to Patrons and the public.

Vitamin D3 supplement pills don’t and can never give you triplet state being described here because you need the light stimulus on the skin to get it.  You also need skin in the game to generate the light pressure on your skin and arterioles to enable the chiral effect.   Sunlight exposure of the skin, works in unison to sulfates the cholesterol anion substrates in the skin and blood from the sulfated amino acids so that cholesterol can become Vitamin D3 via various steps between the skin, kidney and liver under the power of UVA and UVB light.

 

 

KEY POINT ALERT:

UVA light helps in performing this task because of the action of activated NO in the skin.  NO inactivates cytochrome 4 while IRA light allows the ATPase to spin freely with fewer electrons needed from foods/fat due to the action of NO on ECT.  UVA light inhibits or slows electron chain transport flow on the inner mitochondrial membrane.   With this knowledge are you still afraid of black lights indoors?  You should not be.  It might be a great hack for you depending upon your N = 1 context.

 

 

Nitric oxide (nitrogen oxide, nitrogen monoxide) is a molecular, chemical compound with a chemical formula of NO that is a colorless gas under standard conditions. Nitric oxide is a free radical—i.e., its bonding structure includes an unpaired electron with a specific electronic spin state. It is a practically important intermediate in the chemical industry. In addition, some are unavoidably produced during combustion of fossil fuels in power plants and automobile engines, with an excess of NO being created when there is present more air or higher temperatures than needed for efficient and complete combustion of the fuel. More oxygen and higher temperatures in a cell favor H+ bonding.

 

 

They lower deuterium bonding in the skin. This is very important because it is the key mechanism of how and why deuterium is found in the high concentration of the blood plasma in the irradiated skin by the sun. In skin thermal temps are raised most by UV/IR light and oxygen is increased by UV light striking the skin alone.

 

 

Not only does skin make it with the powerful sun but so does the atmosphere in a quantum fashion. It is also produced naturally by the extremely high air temperatures produced along the path of lightning in thunderstorms.

Now stop here.  Did I not tell you in the past on previous blogs that the inner mitochondrial membrane can generate the same voltage as a bolt of lightning in the “What powers life and death blog years ago?”  Yep.

30 million volts is possible.

It was found that NO acts through the stimulation of the soluble guanylate cyclase, which is a heterodimeric enzyme with subsequent formation of cyclic-GMP. Cyclic-GMP activates protein kinase G, which causes reuptake of Ca2+ and lowers the intracellular calcium by the opening of calcium-activated potassium channels. This is highly protective in high nnEMF environments. 5G will block this effect in the skin. 5G will also destroy the covalent bond between melanopsin and Vitamin A.  This will demolish the entire circadian mechanism in all the peripheral clock genes.

This is why 5G risks will ramp up mitochondrial diseases linked to the melanopsin/retinol system.  Melanopsin also uses calcium as a secondary messenger.  This creates another risk of nnEMF in destruction of the melanopsin mechanism.  nnEMF alters calcium flows and this is the signal that makes free radicals in the matrix for proper quantized signaling.

 

 

The fall in concentration of Ca2+ ensures that the myosin light-chain kinase (MLCK) can no longer phosphorylate the myosin molecule, thereby stopping the cross-bridge cycle and leading to relaxation of the smooth muscle cell in our skin arterioles allowing more RBC’s loaded with porphyrins to continue absorbing UVA light to keep this action of NO working properly to keep deuterium inside of our arteries where it belongs.  Deuterium concentration in the blood plasma is how the body normally creates ELF-UV within our blood plasma to activate cell water to become an exclusion zone.  This is a topologic charge effect that must occur endogenously.

Nitric oxide, is also known as the ‘endothelium-derived relaxing factor’, or ‘EDRF’, is biosynthesized endogenously from L-arginine (urea cycle), oxygen, and NADPH by various nitric oxide synthase (NOS) enzymes. Reduction of inorganic nitrate may also serve to make nitric oxide in our gut. The endothelium of blood vessels uses nitric oxide to signal the surrounding smooth muscle to relax, thus resulting in vasodilation and increasing blood flow so we can collect a lot of UV light from skin irradiation. How does hemoglobin fit into this blood UV story?

Two important biological reaction mechanisms of nitric oxide are S-nitrosation of thiols and nitrosylation of transition metal ions. S-nitrosation involves the (reversible) conversion of thiol groups, including cysteine residues in proteins, to form S-nitrosothiols (RSNOs). S-Nitrosation is a mechanism for dynamic, post-translational regulation of most or all major classes of protein in all living things. This is why the ubiquitination series has so many blogs and threw so many new details at you.  They were foundational for this blog.

Sunlight controls protein turnover via ubiquitin marking and nitrogen flow in cells using this mechanism.  Methionine is needed for this step no matter the protein being made by a cell.  The second mechanism, nitrosylation, involves the binding of NO to a transition metal ion like iron or copper in your cells.  In CPC #25 you saw how this process is broken in sepsis.

Methylene blue, IV Vitamin C, and glucocorticoids in low doses can improve the function of sulfated amino acids in people with mitochondrial damage who do not get enough sunlight.  The sulfated amino acids are the critical optical switches in many neurotransmitter and glucocorticoid receptors.  They are also critical in DNA function.  This has been shown in many diseases like sepsis in many papers on PubMed.  Sulfur and iron clusters are found in the mouth of every cytochrome protein. Did you also know that cytochrome C oxidase is also a heme protein that has 4 red light chromophores embedded in its atomic structure?   This is why IRA light exposure is a critical part of solar exposure and control of apoptosis.

In this nitrosylation function, NO is referred to as a nitrosyl ligand. Typical cases involve the nitrosylation of heme proteins like cytochromes, thereby disabling the normal enzymatic activity of the enzyme when it becomes necessary in cold environments where sunlight is poor.  This was the key point I made in the Cold Thermogenesis 6 blog years ago.

Nitrosylated ferrous iron is particularly stable, as the binding of the nitrosyl ligand to ferrous iron (Fe(II)) is very strong. Hemoglobin is a prominent example of a heme protein that may be modified by the NO free radical by both pathways: NO may attach directly to the heme in the nitrosylation reaction, and independently form S-nitrosothiols by S-nitrosation of the thiol moieties. There are other heme proteins you will soon learn about that refine this process even further.

Hemoglobin absorbs light at 280 nm (UVC) and 3 other IR frequencies. Maybe now you can see why they link to NO function via the 42% red light in our sun.  The addition of sunlight and seasonal ketosis keeps the TCA and urea cycle clear of a lot of RNS and ROS from broken kinetics in both cycles due to a loss of control of hydrogen isoforms from cell membrane damage.

The sun is designed to increase the mammalian battery using UV/IR light and cold for humans with bad environments.  The Quantlet was designed with this idea in mind.  The best idea is not to rely on any man made device, but to rely on sunlight with a seasonal ketosis regimen in humans to make metabolic cell water devoid of deuterium in the matrix.  Deuterium needs to be kept in the blood to make UV light in us endogenously that programs the proteins in us because it passes its information and energy to water that surrounds every protein in us.

 

 

 

 CITES:

Dr. Kruse talk June 2, 2018 Shelburne Farms.