QUANTUM ENGINEERING #10: HOW DO WE CAPTURE OF ELECTRONS/PROTONS

So in many of my podcasts,  I taught you about how the loss of negative feedback control in coupled biologic systems is the sentinel event for aging and disease generation.  When one side of a coupled system is lost the result with be extinction of both the positive and negative feedback loop.  This is why taking oral melatonin can lead to blindness by thinning of your retina.  It was also the reasons removal of the wolf from Yellowstone Park caused the topology of the rivers to change and cause many other animals to become extinct in the park.  

 I used the predator or prey in this analogy to make the point of how decentralization maintains control of feedback loops. If you alter the balance of predator or prey the result is always the EXTINCTION of both preadtor and prey. I have told you that in aging and neolithic disease generation NAD+ becomes altered in relation to the level of NADH. This can happen by several stimuli from the environment.  NAD+ and NADH operate just like predator and prey within the circadian mechanism.  If you get the light in your environment wrong you will destroy both NAD+ and NADH and you will never be able to control where electrons and protons are needed in cells.  If you disrupt NAD+ your circadian clocks can no longer OPERATE.  

^^^^This will become important when you review the end of this blog carefully.  

WHAT IS NAD+?  

It is how mammals capture electrons and protons from foods.

NAD+ serves as a crucial determinant of the abundance of other species of NAD such as the reduced form of NAD phosphate (NADP(H)). Alongside NAD(H), NADP(H) pools play crucial roles in REDOX maintenance, particularly as antioxidant cofactors (reviewed in Ying, 2008 and Xiao et al., 2018).  How it is destroyed or made inside a cell is one of the best measures of how the redox potential varies between the creative and destructive cycles in a decentralized fashion.  

PARPs are seen as one of the dominant enzymatic consumers of NAD+ within the cell.  Humans have 17 types of PARPs.  One of the 17 is called PPAR alpha.  It is the master regulator of fat-burning in mitochondria.  PPAR alpha upregulates CPT1, which controls the rate at which fat enters the mitochondria.  The rate at the entrance must marry to the timing of oxidation in the system to be burned properly.  Timing is critical in the ledger of life.  

You must have reserved or created 3 NAD+ to ride the fat-burning train to longevity.  Without it, you lose LIFE -time = longevity

PPARα, a transcription factor that modulates fatty acid metabolism, regulates substrate preference in organs with a high density of mitochondria.  (heart/brain/bone/immune system)

Three pathways of NAD+ biosynthesis within mammals have been identified: #1 is the Salvage pathway, #2 is the de novo, and #3 is the Preiss-handler pathway. 

During basal conditions of diurnal life, the salvage pathway is currently believed to be the dominant source of NAD+.  In recent times, evidence has been presented that all 3 NAD+ biosynthesis pathways can switch between (Zhang et al., 2019) and compensate for one another (Okabe et al., 2019) in mammals.

The de novo and Preiss-handler pathways are dependent on dietary derived vitamin B3 precursors.  

The salvage pathway seems to be most affected by the light and dark cycles of circadian biology.  The de novo pathway is also called the kynurenine metabolic pathway.  I've written about it in time crystal blogs in the quantum thermodynamic series here on Patreon.  The Preiss-handler pathway utilizes nicotinic acid (NA).  

The chronic loss of NAD+ is the critical sign of a loss of negative feedback control of the ubiquitin cycle when there is a light (photon) mismatch in the animal's environment. When this occurs the inner mitochondrial membrane does not oscillate at 100 Hz, fat burning doesn't operate well, and there is no alignment of the mitochondrion's IMJ's as seen below.  Our colony of mitochondria use this information to alter the rate of fat oxidation from winter to summer.  The sun informs the colony of mitochondria when to do this using charge and angular momentum of electrons and protons stripped from foods.  

What does this imply if we eat outside the seasonal photosynethic windows or under artificial light?  The mitochondria engine can become easily flooded with electrons and protons.  A flooded engine is an internal combustion engine that has been fed an excessively rich air-fuel mixture that cannot be ignited.  When a combustion engine gets flooded in this way an engine would make a tell-tale bogging sound and black smoke would come out of the tailpipe.  The black smoke also alters the ROS in the system.  Is there a clue in our blood that ROS is spiking inside the mitochondria?  Yes, there is.  

The problem with the flooded engine is too much fuel (electrons/protons and not enough oxygen = ROS drops.  This is why diabetics have no superoxide pulse at cytochrome 1.  

NAD+ is what captures electrons and protons in mitochondria.  If you are diabetic can you capture electrons or protons well?  

Electrons and protons are what sculpts the matter in cells.  Many people in biology think that only DNA can sculpt atoms to create life.  They always forget DNA only code for amino acids that create proteins.  There is another way we sculpt matter using NAD+.  NAD+ is how we get theses chiesels.

NAD+ changes in relation to the electromagnetic spectrum of light in a person's environment while they act to cause evolutionary changes via redox management.  How does this happen?

Angular momentum & charge are two conserved factors quantum mechanically that continue to confuse biologic scientists. If biology realized that the addition or subtraction of electrons and protons could change the solid-state function of proteins they'd realize finally why we do not need DNA/RNA changes to explain the small human genome.  The implications of this are massive and largely unknown in biology.  It means that the syntax of genes is vastly more complex than Darwinist believe.  It is more subtle and nuanced than any spoken language or genetic language known to man today.  The reason this is the case, is that genes themselves can be changed by alterations of the angular momentum and charges as electrons and protons move due to solar frequencies.  

DNA only codes for proteins and nothing else. DNA/RNA main purpose is to create a solid-state semiconductor that operates with the light of our star. The light of our star is the optimized electromagnetic signals mitochondria operate with.  Anything OTHER part of the electromagnetic spectrum changes angular momentum and charge and reduces the fidelity of information processing in our cells paving the way for disease propagation. NAD+/NADH couple respond to the change in light because they capture electrons and protons from hydrogen molecules in foods.  The type of hydrogen is critical in the physiologic function of NAD+/NADH in a cell.  If a cell is forced to deal with too much deuterium NAD+/NADH won't have many electrons and protons to capture.  That is a low energy state. That is what artificial light and artificial food cause in mitochondria. 

This lack of electrons and protons manifests via mitochondrial dysfunction. Acylcarnitines play an essential role in regulating the balance of intracellular sugar and lipid metabolism. They serve as carriers to transport activated long-chain fatty acids into mitochondria for β-oxidation as a major source of energy for cell activities = Dx mtDNA defects. No artificial light device (PBM/PEMF/UV) device has solved this issue.  The sun is the only answer that is APPROPRIATE in optimizing NAD+ function with the correct isotope of hydrogen stripped off of foods.  

Acylcarnitines are the black smoke created by a flooded mitochondrial engine in cells.  

A metabolic hallmark of mitochondrial diseases like obesity and diabetes is high circulating levels of acylcarnitines.
 The enzyme that controls fat flow into the mitochondria is called carnitine palmitoyltransferase (CPT1).  This enzyme takes a free fatty acid (palmitate) and transfers it (that’s the transferase part) to a chaperone molecule called carnitine.  Free fatty acids contain an acyl group on one end, so a molecule of fat attached to carnitine is an acylcarnitine.  

If you don’t care to memorize all of that, just remember that acylcarnitines are unburnt fuel.  Once a fat is transferred to carnitine, it is supposed to be sent into the mitochondria to be burned (oxidized) by the TCA cycle.

Oxidative balance controls the metabolic rate but it DOES NOT define the redox state of the cell.  The level of ROS/RNS does.  Where the ROS comes from also matters deeply in this time ledger.  

WHAT HAPPENS IN MITOCHONDRIA?  

Once inside the mitochondria, the acyl group is transferred from carnitine to another chaperone molecule called Coenzyme A (CoA) to become acyl-CoA.  Fats are broken down in a process called beta-oxidation.  Every round of beta-oxidation produces an acetyl-CoA and a shortened acyl-CoA.  Most fats are 16 or 18 carbons in length and an acetyl group has two carbons so it takes 8 or 9 rounds of beta-oxidation to turn a fat all of the way into acetyl-CoA.  One molecule of fat makes 8 or 9 acetyl-CoA, each of which takes 3 NAD+ to be fully burned.

NAD+ is needed to move the fatty acyl-CoA past the hydroxyacyl-CoA step.

WHERE DOES SUN ALLERGY COME FROM?   CHRONIC LOW NAD+ state due to blue light.

The intrinsic value of vitamin B3-derived NAD+ to human health leads to hyper photosensitivity to sunlight.  This is why so many are solar sensitive or are told they are "allergic" to the sun.  This so-called allergy to the sun is linked to the simultaneous reduction of NAD+ and melatonin due to a lack of sunlight exposure during the day or too much artificial light at night or a combination of both.  They are deficient in NAD+ while having a horrendous redox. Low redox = low energy = low solar exposure state

Most of these people have atrophic skins and downregulated melanin production. Everyone with a melanin issue on their skin gas an altered NAD+ level in their mitochondria.  The reduction of melatonin has direct mitochondrial effects.  Melatonin optimizes autophagy and apoptosis in our colony of mitochondria.  This means melatonin optimizes fat metabolism by controlling heteroplasmy state in mtDNA. (below).  Certain seasons fat metabolism operates better.  Sunlight and temperature controls this "thermostat" in mitochondria.

Melatonin is the chemical in non-hibernating mammals that simulate torpor. Torpor is the metabolic state that mammals use to lower their body temperature to hibernate.

Melatonin acts to lower our thermostat in our hypothalamus at night time after 4 hours of darkness to lower the temperature of CSF around our brain. This allows the passage of leptin into the hypothalamus and removes the need for electrons from food (helps a low NAD+ state).  This is how animals live off their fat stores during sleep of any duration.  

This is why the leptin Rx uses protein early in the day to offset the inability to burn fats well.  Protein satiates animals quickest irrespective of their mitochondrial status.  Eating a lot of protein is not easy to do so.   It also lowers food intake, as a consequence.  

The effect of fasting during hibernation or sleep in mammals causes a rapid rise in PPAR alpha – the master regulator of fat burning because during these times subcutaneous fat is the only source of electrons available for mitochondria.  PPAR alpha upregulates CPT1, which I’m sure you remember is the enzyme that controls the rate at which fat enters the mitochondria.

Sleeping/torpid animals are in reductive stress because they have highly acetylated mitochondrial enzymes.  

The sirtuin proteins perform this task and this is why taking sirtuins during the day makes no quantum mechanical sense.  When animals are sleeping or want to get out of torpor, they surge the production of sirtuin deacetylases to allow mitochondria to operate fully.  

All that you have to do to induce torpor is to flood the mitochondria with fat.  This is why the Leptin Rx does not use a high-fat diet.  Fat is very rich in acetyl groups, providing three times as many, gram per gram, like glucose.  The surge of acetyl-CoA runs down NAD+ levels at cytochrome 1 and floods their little engines = acetylcarnitine rises in the blood.  

There is a catch because not all fat types induce sleep/torpor equally.  Mammals fed saturated fat continued to burn more oxygen compared to the PUFA fed mammals, maintaining a higher metabolic rate.  H+ speeds your metabolic rate up and deuterium tends to slow it down because of its effects on NAD+.  This modulated by your thyroid hormones.   Saturated fats have the highest amount of H+ in them and the lowest amount deuterium in them.  Deuterium does not liberate as many electrons or protons to NAD+ due to its kinetic isotope effect so it becomes an option that mitochondria can use to limit overfilling the engine with protons and electrons as light varies during the seasons.

HOW DOES NAD+/NADH SCALE TO THE CIRCADIAN MECHANISM?

Now for how this scales to your molecular circadian clock and your peripheral clock genes (CCG's). The current model of the mammalian circadian clock includes two interlocking transcription-translation feedback loops comprised of several so-called “clock” genes and their protein products, which ultimately regulate the transcription of “clock-controlled” genes.  Melatonin receptors (MT1,2) are critical in this timing mechanism.

These feedback loops consist of positive and negative components. The positive components include the basic helix-loop-helix-PAS domain transcription factors, CLOCK, and BMAL1. These transcription factors heterodimerize, translocate from the cytosol to the nucleus, and bind to circadian E-box promoter elements that enhance the transcription of genes encoding the negative components PERIOD 1 & 2 and CRYPTOCHROME 1 & 2. The CRYPTOCHROME and PERIOD proteins feedback inhibit the transcription of the Cryptochrome and Period genes by blocking CLOCK/BMAL1-mediated trans-activation. 

The second feedback loop involves the trans-activation of the Rev-Erbα and Rora genes by CLOCK/BMAL1. The protein products of these genes compete for binding to RRE elements in the Bmal1 promoter, driving a daily rhythm of Bmal1 transcription and closing the second feedback loop. Rhythmic expression of these clock gene products produces circadian clock outputs by regulating the transcription of clock-controlled genes (CCGs). 

Remember melatonin is made from tryptophan.  So is NAD+ as I laid out in the Time crystal blog.

Seasonal sources of electrons and protons in foods varies via the sunlight used in the photosynthetic process used to create them in Nature.  NAD+ pays attention to the quality of electrons and protons and we can see this if we understand the seasonal link between acylcarnitine and the isotopes of hydrogen in foods.  Electrons will vary in the power of photons they are excited by.   

In circadian biology, the electrons and protons sent to mitochondria inform the mitochondria what to do with the fuels they get.  

At least some of these CCGs, including aanat, the gene encoding the penultimate enzyme in the melatonin biosynthetic pathway, contain circadian E boxes, which have a core nucleotide sequence of CACGTG and are activated rhythmically by CLOCK/BMAL1. 

Post-translational regulation, including phosphorylation, acetylation (SIRT), ubiquitination, sumoylation, and proteasomal degradation is also important in the regulatory mechanisms generating the circadian oscillation to alter clock periodicity.  Clocks become more accurate the higher periodicity they have.  Seasonal light alters circadian periodicty of clock genes.   

Once your SCN goes haywire in your eye, it is a matter of time before your circadian clock genes in tissues the SCN controls go haywire and malfunction and lead to disease. What will be the ultimate result? EXTINCTION of both sides of the circadian coupling.  

 What gets extinguished?  

NAD+ does.  Now you know what low melatonin really means to longevity.  If you cannot capture electrons and protons optimally in a season, you cannot ideally sculpt your mitochondrion or cells.  This is how disease manifest.

SUMMARY

Your eye can be a clock or a camera. A blind man’s world is bounded by the limits of his touch and he relies on his timing; an ignorant man’s world by the limits of his wisdom; a successful man’s world by the limits of his vision and sense of timing.  

CITES

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