QUANTUM ENGINEERING #40: MELANIN, mTOR, MELATONIN, meets TRYPTOPHAN TIME CRYSTALS

The question was good and it is still a POMC story whether you know it or not.  

As melanin degrades so does melatonin and this correlates with low mitochondria redox power and a drop in delta psi. As melatonin breaks down it liberates tryptophan. Tryptophan has two catabolic pathways it can travel. As the time crystal blog on methionine and tryptophan said this AA metabolism is linked to the presence or absence of UV light. Quinolinic acid (QUIN), a neuroactive metabolite of the kynurenine pathway, is normally presented in nanomolar concentrations in the human brain and cerebrospinal fluid (CSF). QUIN is often implicated in the pathogenesis of a variety of human neurological diseases and melanin degradation due to heteroplasmy is one such cause. QA is produced following the metabolic breakdown of the amino acid tryptophan, via the kynurenine pathway. Quinolinate (Quin) is a classic example of a biochemical double-edged sword that needs light programming from our environment, allowing Quin to act as both an essential metabolite and potent neurotoxin. With proper mTOR signaling, Quin is an important metabolite in the kynurenine pathway and tryptophan catabolism leads to the de novo synthesis of nicotinamide adenine dinucleotide (NAD+). When mTOR is screwed up or redox is bad or you use the other pathway for tryptophan catabolism NAD+ is not recycled.  

WHAT IS PROPER mTOR SIGNALING? 

Dr. David Sabatini discovered the mTOR pathway 28 years ago. What is that pathway about?  Look at the picture above.

mTOR = Mammalian target of rapamycin. This semiconductive protein regulates cell proliferation, autophagy, and apoptosis by participating in multiple signaling pathways in tissues in the body. The way it operates in different tissues has confounded Sabatini for 3 decades. There is a reason for that. He has stayed in his centralized biochemical silo and refused to see the light. To understand mTOR fully, you have to understand the physics of organisms first.

Wide-band gapped semiconductors make the light that controls the entire mTOR pathway. This light, stronger than the sun, alters glucose, oxygen, and phosphorous metabolism rostral to mTOR protein.  This changes the light in cells to activate POMC, tryptophan, and methionine biology. Sabatini's eureka came 28 years ago on Easter Island. He doesn't know this info yet, but after my podcast with Rick and Andrew, you should. That endogenous light cells created from the mass in the wide-band gapped semiconductors is how mTOR protein does the things it can do. Alterations in light emission are controlled by dopants on these semiconductors. I have found light around 380 nm changes HUMAN metabolism from anabolic to catabolic. Summer is the time for anabolic living and winter time is the time for catabolic living.  This is why human muscle anabolism and catabolism are more active during the day and at night, respectively.  Light is transformed from atoms everywhere inside of us, but we cannot see it because of our atomic arrangement in cells (AMO physics).

380 nm light (UV-A) is the photonic switch between catabolism and anabolism in the mTOR pathway. That selection tells us something deep about what happened at the KT event.  Living in nature's visible light spectra induces POMC translation on our surfaces. This, in turn, stimulates the semiconductive circuits deep inside cells to create VUV-IR-A endogenously where our colonies of mitochondria reside. The frequencies of light created endogenously below 380 nm is where mammalian longevity occurs in humans.  This reality exists because of what happens at small scales via the translation of the POMC gene.  This gene has been amplified and  is buried in the pathways of tissues inside of us. This explains why the human brain is littered with light chromophore proteins. That is where Noether's theorem comes into the story of life. Centralized science does not know, much less accept, what I just told you about Noether's theorem but they will soon.. That is fine. With time, you'll remember this post and the picture below. Dr's Sabatini and Attia have been staring at the answer for a long time in the literature but ignoring it at your peril.  Light alters metabolism in a big way.

Now how it happens is a bit mind boggling.  UV-A light stimulate both alpha MSH and ACTH but the translation of ACTH is frequency related.  Blue light is a more powerful stimulus to ACTH cleavage than UV-A light.  Ultraviolet B radiation stimulates increased expression of the proopiomelanocortin (POMC) gene which is accompanied by production and release of alpha melanocyte stimulating hormone (a-MSH) by both normal and malignant human melanocytes and keratinocytes.  This alone should have told centralized scientists the sun could not be the cause of melanoma.  It was not.  What differentiated the cleavage in mammals who survived the KT event? The production and release of both peptides are also stimulated by cyclic adenosine monophosphate (cAMP) the breakdown product of ATP and interleukin (IL-1) but not by endothelin-1 (ET-1) or tumor necrosis factor-a (TNF-a).  

N-acetyl-cysteine (NAC), a precursor of glutathione (GSH), an intracellular free radical scavenger created , abolishes the UVB-stimulated POMC peptide production and secretion.  

Glutathione is a tripeptide (cysteine, glycine, and glutamic acid) found in surprisingly high levels—5 millimolar—concentrations in most cells. As can be seen in Figure 1, this is the same concentration in cells as glucose, potassium, and cholesterol! Considering the high level of metabolic activity required to produce glutathione, such a high level underlines its importance.

Did you know glutathione absorbs strongly from VUV light to 290nm with a strong peak at 280 nm.  That means endogenously created light raise glutathione levels which in turn, quenches melanin action, and acts to limit surface level melanin production from UV light we get from the sun.  This always keeps the balance of melanin creation on our insides compared to our exteriors as humans. 

Chalk one up for negative entropy again.  Now you know why I am no fan of exogenous use of NAC or glutathione.  I also hate acetaminophen use because it blocks the endogenous production of glutathione in humans.  I actually think people who use this drug maybe at higher risk of melanoma in the skin.  

Glutathione exists in cells in 2 states: reduced (GSH) and oxidized (GSSG). As can be seen in Figure 2, oxidized glutathione is actually 2 reduced glutathiones bound together at the sulfur atoms. 

GSH biosynthesis is also regulated post-translationally by changes in cellular oxidation.  This is important in understanding how light operates with GSH and POMC cleavage.  POMC has to have UV light to be translated first and then GSH can operate inside the cell if a lack of electrons develop. If electrons are deficient so will light in the system.  This is what a low redox state and is the MAIN pillar of morbity and mortality in the longevity of mammals. This is what oxidation is.  The redox homeostasis of a cell ensures that endogenous and exogenous stimuli are modulated by the redox homeostasis of a cell. However, altered mitochondrial redox homeostasis leads to cellular oxidative stress, which in turn may lead to aberrant cell death and contribute to disease development.  Glutathione synthesis is stimulated when UV light and IR-A light are scarce for mammals. 

The GSH tripeptide is derived from Cys, Glu, and Gly and is synthesized exclusively in the cytosol in a cell.

GSH is critical for maintaining redox balance in cells at the mitochondrial level, so GSH biosynthesis is upregulated in response to oxidizing conditions that mtDNA sense. Animal tissues generally have a fairly high concentration of GSH (0.5–10 mM) in comparison to cysteine (10–100 µM).  This is another clue that mammals are designed to be in the sun to raise GSH and explains why POMC has beta endorphin in it from an evolutionary perspective (below).  Mammals get high by being the in the sun.  This keeps their motivation high to seek it.  There is also another reason this is important.  Mammals eye clock is directly wired to the retina in all species.  This became important in humans when they lost Vitamin C, expanded glutathione and melanin inside their heads with encephalization.  This system is highly attuned to light via the eye since mammals get most of their light sense via their pupil and the retinohypothalamic tract.  I think when humans began to encephalize and wear clothes this one thing alone kept the unbalance between surface melanin to melanin that was absorbed into the body over our 4 million years ago. 

The ratio of GSH to GSSG determines cell redox status of cells. Healthy cells at rest have a GSH/GSSG ratio >100 while the ratio drops to 1 to 10 in cells exposed to oxidant stress. Glutathione is also recognized as a thiol buffer maintaining sulfhydryl groups of many proteins in their reduced form. 

Glutathione is produced exclusively in the cytosol and actively pumped into mitochondria. GSH is made available in cells in 3 ways:

1. De novo synthesis via a 2-step process catalyzed by the enzymes glutamate cysteine ligase (GCL) and glutathione synthetase (requires ATP).
2. Regeneration of oxidized GSSG to reduced GSH by glutathione reductase (requires NADPH).
3. Recycling of cysteine from conjugated glutathione via GGTP (requires NADPH).

Notice that all 3 require energy. The rate of synthesis, regeneration, and recycling is determined primarily by 3 factors:

1. De novo glutathione synthesis is primarily controlled by the cellular level of the amino acid cysteine, the availability of which is the rate-limiting step.
2. GCL activity is in part regulated by GSH feedback inhibition.
3. If GSH is depleted due to oxidative stress, inflammation, or exposure to xenobiotics, de novo synthesis of GSH is upregulated primarily by increasing availability of cysteine through recycling of GSSG.

These 3 methods for producing glutathione can be seen in Figure 3. 

Many people currently believe it is hard to overstate the importance of glutathione.  For me glutathione is Robin and melanin is Batman for mammals.  These systems co-evolved while we deleted Vitamin C genes from use.  Glutathione plays a role in shielding cellular macromolecules from endogenous and exogenous reactive oxygen and nitrogen species. Melanin's role is far more important.  While GSH directly quenches some free radicals, it power pales in comparison to the capabilities of melanin in how free radicals and heavy metals are handled in mammals. Glutathione has a greater importance closer to the surfaces of mammals where light comes into the system because it deals directly with the causes of topological oxidative stress.  Melanin does the same deeper inside of our tissues with absolute power (Noether's theorem) and this is critical in setting the stage for quantum coherence in a warm wet environment.  Glutathione limits quantum processes at our surfaces.  This is why GSH is synthesized exclusively in the cytosol of the cell.  This is why deuterium is so common in blood.  

BACK TO THE KT EVENT that linked mTOR to tryptophan

Neuropsin is an opsin family member known to function as a solar UV-A light detector.   responsive to wavelengths in the near-UV (λ max = 380 nm). After my podcast with Mr. Rubin, you'll know that neuropsin was linked to the KT event and the ascent of mammals because of an interruption of photosynthesis and UV light. Neuropsin is the afferent reflex arc and mTOR is the efferent reflex arc for metabolism of all mammals. All mammalian metabolism, like photosynthesis is controlled by solar frequencies. I've been saying it for a long time, but everyone else wanted to focus on Dr. Sabatini's work and not photosynthesis.

I have thought for 25 years light had to be the major controller of metabolism in us. It makes too much sense, but the mechanism was difficult to explain for biology. Once you exit the biochemistry silo and enter the silo of physics the mechanism was not difficult to figure out in those 18 months.  Even the microbiome releases massive light in response to feeding. The melanin sheets of the enterochromaffin cells are their target in our gut.

How does mTOR link to the light story?   Tryptophan is the key.

Tryptophan metabolism occurs via the kynurenine pathway or the serotonin pathway to produce bioactive metabolites. The kynurenine pathway is responsible for metabolizing most of the free tryptophan in mammals. It is activated by infectious agents, inflammatory mediators, and stress (ACTH from POMC).  A small fraction of free L-tryptophan (Trp) is used for protein synthesis and the production of neurotransmitters such as serotonin and neuromodulators such as tryptamine (below middle panel) which is important for. Tryptamines act predominantly as hallucinogens (mental illness). Classic hallucinogens (psychedelics) mediate specific serotonin-receptor activities and produce hallucinations. Substances in these groups mimic the effects of traditional drugs such as 2C-B, LSD, and DMT but may also possess residual stimulant activity in non-mental illness states where the circadian mechanism is intact. 90% of kynurenine pathway degradation occurs in the liver via TDO conversion of TPH to kynurenine. The remaining kynurenine degradation occurs by IDO in the brain, GI tract, and liver. 

There is a blog that tells you the rest of the linkage.........read it sometime

When we can’t make water in the mitochondrial matrix our metabolic pathways (mTOR) are not surrounded by the water they need to operate like a wide band gapped semiconductive diode. This alters the VUV-IR-A light show around mTOR and it does not work like Sabatini's papers say it should. Blue light antenna in our skin control melatonin levels. Those antennas are called melanopsin. The light antenna in us is blue and it is linked to Vitamin A in neuroectodermal tissues where POMC also resides. Vitamin A is linked to Vitamin D at the RXR receptor in the brain where both of them are linked back to the DHA receptor that controls the retinohypothalamic tract which is step one in the pathway. This is how the peripheral clock genes in tissues are linked to melatonin levels locally in tissues. They are also linked to tryptophan metabolism.  

L-Tryptophan is an essential amino acid for mammals (all of them) that is obtained exclusively from diet. Trp and its metabolites have key roles in diverse physiological processes, ranging from cell growth and maintenance, in which Trp serves as a building block of proteins, to the coordination of organismal responses to environmental and dietary cues via photosynthetic signals (light), in which Trp metabolites serve as neurotransmitters and signaling molecules. Together, these functions suggest that, during evolution, Trp metabolism has become linked to the revolution of Earth around the sun and electromagnetic signals became programmed into the cellular pathways (mTOR & NAD+). This energy & information footprint has been codified in our AMO organization at a subcellular level. The cellular electronic and vibrational state is affected by this process. This is why tryptophan and methionine are time crystals. This is how cells know about the environment. No brain is necessary. This is the basis of the brain-gut axis too. Waking up yet? Told ya' this POMC is a big deal. This is why tryptophan and methionine organismal communication strategies align food availability with physiology and behavior.  

As Vitamin A drops in the plasma so does melatonin levels. Melatonin repairs the peripheral clock gene mechanism in humans at the local tissue level when things go awry. Tryptophan has to be metabolized when this happens. Our cells pay attention to this. How? Remember ubiquitin marking and all those blogs I wrote about them?  

Maybe you're beginning to see where they all fit. 

 

As a result, our proteins become dehydrated and lose their topologic charge, this causes size and shape changes in many small signaling proteins in mitochondria that control apoptosis and autophagy. It also alters the light frequencies your endogenous semiconductive proteins make. This alters mTOR signaling. The defective protein in these self-regulatory programs then gets marked for a turnover by ubiquitin. The protein that does this is ubiquitin. I have written an entire series on this protein.  This protein is also controlled by the peripheral circadian mechanism hardwired from the retina to the SCN.

The circle of life is controlled by life below your ability to see it much less understand it.

CITES

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699458/

2. https://pdf.sciencedirectassets.com/271024/1-s2.0-S0167488900X00213/1-s2.0-0167488996000638/main.pdf