QUANTUM ENGINEERING #37: WHERE DO DIABETES & HYPOTHYROIDISM COME FROM DR. HUBERMAN?

The butterfly effect from my weekend.....with Rick Rubin and Dr. Huberman continues.  Start the video at the 16:00 mark

Huberman wants to come and visit me in my lab and do a podcast mano y mano with me.  In "light" of this I want Andrew to be aware of the butterfly effects of what I said to him so he is ready for the next round of inquiry on light

KEY BLOG POINT: CLIP = Corticotropin-like intermediate lobe peptide and blue light without the protection of IR-A and UV light in the eye cause ACTH release from cells with POMC and as ACTH rises so does CLIP.  HOW?

Implications of this slide above?  In humans, this is how blue light raises blood glucose and insulin.  CLIP cleavage is the major cause of diabetes in modern man.  A big statement backed up by the picture. CLIP raises insulin in response to blue light exposure without any food exposed to the organism. (see below)  I have posted this picture a thousand times and no one asked me the right question.  How in the hell do the papers listed below explain it?  They couldn't.  Read on, because I can.  It is all linked to POMC cleavage and retinal anatomy.

CLIP raises insulin in response to blue light exposure without any food exposed to the organism.  This peptide has massive effects on the exocrine pancreas.  CLIP's physiological role has been investigated in various tissues specifically in the central nervous system.

Big Pharma has been trying to keep a lid on this for a long time.  So beware of where our discussion will go.  What cells specifically make POMC in humans?

Look at the tissues where POMC is located and think about what we teach doctors about the symptoms of diabetes.

Polydipsia

Polyuria

Polyphagia

All are caused by a lack of POMC in the hypothalamus where the central retinal pathways converge before radiating to the rest of the body.  Polydipsia is due to a lack of ADH in the posterior pituitary.  Polyuria is caused at the kidney tubules because there is very little vasopressin in the system to control water balance.  Polyphagia is due to the destruction of the leptin-melanocortin pathways that begin in the retina.

Diabetics carry unusually high risks of retinopathy, nephropathy, and neuropathy.  Do you understand why they do?  The retina anatomy is destroyed by chronic blue light exposure.  The basement membranes of the kidney are destroyed by the chronic elevated blood glucose and insulin related to POMC cleavage due to blue light and neuropathy is caused by a chronic lack of the creation of T3 in peripheral nerves.

THERE ARE MANY MORE IMPLICATIONS ANDREW

Andrew based on our 10 hours of discussion on light/water/magnetism if you look at that list and remember what I told you about in 1923 about mitogenic radiation and NaCl in the CSF you might begin to understand these slides below with new eyes.

^^^^^Please recall Dr. Huberman that the choroid in the eye is where melanin sheets of the RPE and Bruch's membrane are adjacent to POMC in the retina.   We can do an OCT on the retina to see it before the disease begins!!!!  The white arrows below show the choroid vessels and the highly reflective RPE and Bruch's membrane is immediately above them.

The entire substructure of the retina is made of collagen and DHA. Both these biomolecules are wide-band gapped semiconductors because of the quantum chemistry of carbon.

Do you see a new reality developing here in front of your eyes yet Andrew???

Dr. Huberman, do you remember during the podcast when I asked you if you knew what part of the visible spectrum bends the most in the eye and you said you did not know?  Remember when I reminded you that melanopsin and POMC are in very specific locations of the retina and I told you Nature does not make mistakes in where she puts things on our semiconductors?  Ya' know, the AMO physics thing I went on about for ten hours..........

Oh by the way Andrew here is the answer to the visible light bending question I posed to you in the podcast below. Wow.......look at that Violet UV light bends the most.  And since the IpRGCs of melanopsin are located in the middle inner retina they are not affected by peripheral light.  UV light bends the most and this is where the most POMC is located in mammalian eyes.  Your retina has a light map for frequencies built upon it.

Do you know POMC is also located inside of the ring of POMC too......just not as much of it.  Do you know what light bends the next most?  Blue light does.  It is the reason why so many humans today suffer from visual blur because blue light does not fall on the fovea/macula region of the retina.  The macula is normally yellow to acts as the complementary color to blue to absorb stray blue light to preserve central vision sharpness.  It causes another bigger problem in the development of diabetes.  It destroys the blood vessels in this middle region of the retina.  This is why retinopathy is a diabetic problem.  The waste products of this area of the retinal photoreceptors and semiconductors collect just as we see in arterial disease.

The blue light hazard destroys blood vessels in that region around the fovea that I can see as a neurosurgeon with my ophthalmoscope in my clinic when I am looking for it in all the patients I treat (see picture below).  The last two slides show you how the bending of light links to the anatomy of how melanin, ACTH, POMC, RPE, and blood vessels really work in a quantum fashion. (picture below)

Modern ophthalmology is still in the dark on this linkage of light bending to retinal anatomy and this is why they have no idea the blue light hazard really causes diabetes in humans.

They also have no idea that light is activating POMC via molecular resonance to cleave the POMC peptides from the gene.  This can be studied easily today but no one in diabetes research wants a cure when treating the disease fuels a trillion dollars a year profit center for Big Pharma Andrew.  Many of your labs sponsors and your University are kept afloat by these corporations.

Fluorescence resonance energy transfer (FRET) measurements can be done between single pairs of acceptor and donor fluorophore semiconductive proteins to yield information about structural relationships and distance fluctuations between regions of a single biomolecule or between components of an interacting system of biomolecules.  Someone needs to study this in ophthalmologic research after they read this blog.

Blue light causes a machine gun effect of palor in the retina and blood vessels all around the fovea (below).  Diabetics also show an altered response of pupillary response to blue LED vs red LED if they use both.  I have been doing that in my TBI patients for years now because I understand how this system was built to work.  This blue light toxicity is what causes photophobia in brain injuries. Anything that causes acute hypoxia in the retina can cause these effects due to the change in melanin light emission from the RPE in the periphery of the retina.  This is why POMC and the choriocapillaris have the most interesting relationship to oxygen tensions in the human retina.  More on that coming later in the series.

What else does this all imply Andrew?  Most fat diabetics will also have hypothyroidism because of the quantum arrangements in the retina.  This is how we know their diabetes comes from the eye and the leptin-melanocortin destruction at the hypothalamic level at the paraventricular nucleus. Note below the down and up arrows for the paraventricular nucleus which houses most of the thyroid releasing hormone neurons in humans (TRH).

Thyrotropic-releasing hormone (TRH) released from neurons in the paraventricular nucleus of the hypothalamus is stimulated directly by the hormone, leptin and alpha-MSH as the up arrow shows.  This is why American tend to be fat diabetics with hypothyroidism because they are addicted to their tech screens and iPhones.

As the picture above shows multiple factors, either directly or indirectly, regulate TRH neuron activity. Thyroid hormones (T3/T4) are the most potent negative regulators of TRH. T4, efficiently taken up by epithelial cells of the choroid system in the lateral ventricle, binds to transthyretin (T4-binding prealbumin) and is secreted across the blood–brain barrier into the CSF.  Note the top part of the slide below.  Visualize the retina at the left side adjacent to phenylalanine and the basal ganglia and thalamus adjacent to melanin and dopamine next to dopa.  Realize the pituitary and the PVN at the level where T3 & T4 are in the slide.  This defines the distal end of the semiconductive circuits in the central retinal pathways as we enter the brain substance.

In the paraventricular nucleus, type II deiodinase converts T4 to T3, which interacts with thyroid hormone receptors on TRH neurons in the PVN to reduce TRH synthesis and secretion.

Zinc and selenium are two essential mineral dopants required for the conversion of T4 to T3 in this semiconductive pathway.  Both of these atoms lower the bandgap to allow the type two deiodinases to operate.  The numbers in T3/T4 are the numbers of iodine atoms in thyroid hormones.  The Iodine atom has a massive band gap and this is why these two atoms are critical in moving electrons at the PVN/pituitary levels of this neural tract.

Almost 80% of T3 at the paraventricular nucleus originates from the peripheral conversion of T4 in cells outside the brain. Only 20% of hypothalamic T3 crosses the blood–brain barrier directly from the periphery.  This makes T3 much more important in the human brain.  Melanin and DOPA can be used to stimulate T3 production in the brain even when the thyroid is defective or missing.

The more one can tan the better this ability is.  Most hypothyroid/diabetic patients are horrible at tanning because their skin is atrophic due to a lack of alpha, beta, and gamma MSH. Regular exposure to solar UV light via your eyes and skin stimulates your thyroid and brain to make T3, which balances your body's metabolism. Tanning increases your metabolism, which in turn helps you maintain a healthier weight. This is all done via POMC biophysics.  Anything that blocks it fattens you and ruins your thyroid function.  T3 is the biophysical manna of longevity for mammals.  T3 function is the best predictor of longevity for the human myocardium and CNS/PNS.  These are the two tissues that kill humans the most.  You won't hear that from Peter Attia in his new book on longevity.  This completes the lessons I gave you about thyroid function in the cold thermogenesis series of blogs.

The type II deiodinase (Zn/Se), is mainly expressed in third ventricle tanycytes.  You should be asking me what is a tanycyte.  It is an important regulator of TRH neuron activity and plays a major role in T3 availability in the paraventricular nucleus.

Tanycytes are how leptin enters the hypothalamus at night at the median eminence.  They are the most common type of macroglia in the CNS of lower vertebrates. In adult mammals, tanycytes are restricted to certain brain regions where the tissue is rather thin and POMC gene is present. These regions are the wall of the diencephalic third ventricle.  Recall the optic bud and retina are all diencephalic derivatives in the human embryo.

Fasting and infection upregulate tanycyte type II deiodinase expression with Zn/Se atoms, resulting in local increases of hypothalamic T3 which may partially explain the reactive decrease in peripheral TSH observed during fasting or inflammatory diseases. T3 inhibits TRH gene transcription in a classic feedback loop and TSH synthesis. T3 also influences the processing of proTRH neurons adjacent to POMC neurons by altering paraventricular nucleus prohormone convertase (PC) levels. T4 also reduces TRH levels measured in the hypophyseal portal circulation.  This is a very complex dance that few understand because of its optical physics. Understanding biochemistry is not enough.

OUTSIDE THE BRAIN:  TRH has effects

Thyrotropin-releasing hormone (TRH) is expressed throughout the gastrointestinal tract in humans in gastric G cells, in pancreatic islet beta cells, and in neurons constituting the myenteric plexus of the esophagus, stomach, and intestine. In the stomach.  If you are a human and you have a gut problem you have a melanin problem via POMC.  TRH, T3, and T4 are linked back to this story.   TRH modulates pentagastrin-stimulated gastric acid secretion and may attenuate acid secretion in subjects with acid secretory disorders. This is why GERD is fundamentally a nnEMF/blue light story.

In the pancreas, TRH is expressed during perinatal development, and TRH administration in mammals induces pancreatic hyperplasia and inhibits amylase release. TRH also reduces CCK-induced gallbladder smooth muscle contraction and inhibits cholesterol synthesis within the intestinal mucosa but is not trophic to the intestinal mucosa.  Yes, you can get gallbladder pain when you are LACKING SUNLIGHT.  I have a farm member who had this issue and I helped her overcome it using sunlight and the circadian mechanism linked to POMC actions.

Today's diabetes is a result of mammalian innovation that was used to survive the KT event.  How?  Look closely are POMC and what it does.

Light can be transformed when it hits matter like a semiconductive protein.  (see below all the ways light can be changed)  When looking at the POMC rabbit hole you'll notice that the central melanin system is hodologically linked to every sensory pathway in mammals whose neural tracts end in the thalamus.  All 5 senses end in the thalamus and then the thalamus projects to the hemispheric lobes of the brain.

The thalamus is the end station of the diencephalon where the optic bud ends in the embryo.  It is obvious to see the connection when you follow it back embryological (above).

Light frequencies and varies changes in amperage in currents are capable of cleave POMC via molecular resonance into action in the retina.

What if I told you that ACTH is cleaved more from its parent protein POMC based upon the frequency of the light most likely to be there?  Recall in the podcast I asked Huberman did he know which part of visible light bends the most and he was stumped by the question.  Blue light bends second most in the retina's periphery in a circular format.  Would you believe it?  You should.  Might this relationship be present in every mammal retina to bright blue-laden light because blue light was used to stimulate ACTH to create glucocorticoids like cortisol to raise blood glucose when food was sparse and light frequencies changed and the environment got cold?

Well, you should.  Because that is exactly what happened when mammals took over the world and left their holes in the ground and the sun came back. The retina is somatotopically organized to light frequencies.

This exact mechanism was used by ancient mammals and therapod dinosaurs to raise their own blood sugar when photosynthesis was disrupted by an asteroid crash. ACTH was and is upregulated by blue light.  The blue light was present 65 million years ago at the surface level of Earth.  Light created glucose for life to survive.

Today the same effect is causing diabetes in a modern man who has built a world of blue-lit bulbs that has very little UV light to regenerate melanin at the same time this occurs in the retina.  Oh! So you see that now.  Good.  Alpha-MSH and its cousin peptides cannot be liberated or cleaved from POMC unless UV light is present in the anterior chamber of the eye because it is more peripheral to the ipGCRs and melanopsin.

Why is melanopsin the most common opsin in the human brain when blue light cannot pentrate the skull?

Dr. Huberman, do you realize what this also explains?  If explains why modern humans who have the blue light hazard through their eyes are more likely to be obese with diabetes because the leptin-melanocortin pathways from the retina to the hypothalamus are also damaged in this scenario.

Diabetics have melanopsin damage in the peripheral retina (nnEMF/blue light) more in the integument than their eyes will be skinny diabetics.  What else does this imply Andrew?    It means people who have had cataract surgery and get blue light intraocular lenses but have blue light stress on their skin will be skinny diabetics.  Centralized medicine has never been able to explain this difference in the literature.  I gave it to you for 5 bucks.  Do you still think this knowledge is worthless?

MORE NUANCE WITH POMC CLEAVAGE

Do you know that ACTH, cortisol, blood glucose, and insulin all act to decrease melanin's ability to be renovated on our surface because there was no UV light present?  So, Andrew, this means under blue light conditions mitosis would have been stopped on the skin of mammals and feathers of therapod dinosaurs.  They would have lost their colors and tans as they migrated their melanosomes interiorly.

The bending of light should also now fully explain the anatomy of the retinal blood supply in the mammal eye, don't you think Dr. Huberman?  Note how in the center of the retina there are no blood vessels that normally have hemoglobin.  RBCs are also devoid of mitochondria as well.  Hemoglobin is a heme porphyrin that has absorption spectra that spans the entire UV spectrum of terrestrial sunlight but also extend deep into the UVC range = 250nm-600nm light.  Hemoglobin has a sharp cut-off at the IR-A region at 600nm.  Do you see how the pieces fit yet with POMC?  The anatomy of the mammalian eyes is 100% a story of how melanin works in us.

Now let us look at what blue light is doing at the same time in the eye in relation to POMC.  You should recall that from my Vermont 2017 talk we found melanopsin is now in blood vessels.  This means modern lighting destroys photoreceptors just around the fovea when it is mostly blue light.  We can see this effect below.  It looks like a machine gun took out everything around the macula.  In most hypothyroid diabetics the macula also loses its yellow pigment and this tells me the blue light hazard is chronic in their eyes.  Yellow pigments come from lutein and zeaxanthin of the xanthophyll family of carotenoids that are loaded in my survivor soup Patreon post.  They are yellow to preserve the sharp central vision of the macula and absorb any stray blue light as a complementary color.  Blue light causes visual blur when your macula is damaged.  Many diabetics have this before they get diagnosed.

On the left below, you see the control where the red specks are mitochondrial and in the center, the mitochondria vanish under the blue light hazard.  On the right, you can see where IR-A light with blue is protective of some of the photoreceptors.

Hey Andrew do you remember what Rick told us in the podcast when was using my advice to mito-hack himself back to health he told you he noticed when he flew in planes from Costa Rica to California he would always lose his tan quickly and he could not figure out why?  Are you connecting any dots yet Andrew?  You know when you disconnect from the Earth and are not grounded to Earth to close the circuit so this would act to speed up the migration of cells not sensing UV light on the surface.  This would cause melanosomes to migrate inside of you following their embryonic neurulation tract.  This is why people lose their tans.

Remember Gurwitsch's work on mitosis here.  What did Gurwitsch find Andrew about UV light in onion roots in 1923?  The video above shows that at the 16:00 mark.

Now let us have a look back in the eye where POMC and DHA are at the highest level in the human brain.

When you look at this and see "mitosis" and death and you realize those are migrating cells from within that only migrated to the surface skin to deep inside the skull to get to the UV light and when they got there then mitosis showed up on the surface = "neuroectoderm psyops".

Now for the big bow on the present I gave you during the podcast @hubermanlab

LET'S REVIEW THE LESSON:  Thyrotropic-releasing hormone (TRH) released from neurons in the paraventricular nucleus of the hypothalamus is stimulated directly by the hormone, LEPTIN via the leptin-melanocortin pathways.

MASSIVE BLOG POINT: Leptin normally increases melanocortin (α-MSH) and it is required for TRH expression!   This means people with hypothyroidism cannot make POMC or melanin well!!  This means their longevity will be cut.  This is why hypothyroidism is a gateway disease to many others and leads to an earlier demise.  Those with hypothyroidism need massive solar exposure to change this outcomes.  This also implies that hypothyroid patients should have worse outcomes from melanin-related diseases, and they DO!

This makes their skin pale, and these people will also seem to burn more and not know why.  Many will develop autoimmune conditions in the skin and gut and their docs will remain impotent to know why.  Many will tell you they are allergic to the sun.  I just laugh at these comments.  When you know better you do better.

And this makes their tissues atrophic for sunlight = why so many humans have sun hypersensitivity.  Think of lupus, diabetics, fibromyalgia.  Look at the teeth of diabetics/hypothyroidism and you'll notice they are more yellow than translucent white.  This is from POMC defects in dentin.  People using Big pharma drugs like phenothiazine, erythromycin, or tetracycline all mimic this sunsentivity because the drugs alter POMC cleavage.

SUMMARY

The melanocortin system anterior to the braincase in the eye where POMC begins is activated by UV light and by blue light in the sun.  It activates the TRH promoter on DNA through the phosphorylation (dopant atom of the wide band gapped semiconductive melanin protein) of the signal transducer and activator of transcription (Stat3). The Stat response element in the TRH promoter is required for the effects of leptin to occur = Leptin-melanocortin tract wisdom

LOOK AT THE TOP ROW OF THE SLIDE BELOW

TRH is present in virtually all parts of the human brain: cerebral cortex, circumventricular structures, neurohypophysis, pineal gland, and spinal cord.  TRH is also found in pancreatic islet cells and in the gastrointestinal tract. Although it exists in low concentration, the total amount in extra hypothalamic tissues exceeds the amount in the hypothalamus!

The extensive extrahypothalamic distribution of TRH, its localization in nerve endings, and the presence of TRH receptors in brain tissue suggest that TRH serves as a neurotransmitter or neuromodulator outside the hypothalamus.  TRH is a general stimulant and induces hyperthermia on intracerebroventricular injection, suggesting a role in central thermoregulation.

Aromatic amino acids that makeup melanin are all linked to this inside your skull and outside your skull.  The system is ubiquitous in humans.  How do you like me now Andrew?

CITES

1. Neuroendocrinology chapter in

Malcolm J. Low, in Williams Textbook of Endocrinology (Thirteenth Edition), 2016

2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC377492/

3. Ronald M. Lechan, ... Csaba Fekete, in Reference Module in Neuroscience and Biobehavioral Psychology, 2018

4. The Hypothalamic pituitary thyroid axis.  Marco Bonomi, ... Luca Persani, in Encyclopedia of Endocrine Diseases (Second Edition), 2019