QUANTUM ENGINEERING #46: DIABETIC RETINOPATHY & A LOT MORE

Diabetic retinopathy (DR) is a well-recognized microvascular complication of diabetes. What is not well recognized is that light stress release of ACTH from POMc and CLIP is the main driver of the disease.  Blue light is a nnEMF that causes diabetic neuropathy.  It causes many other diseases as well.  

Growing evidence suggests that, in addition to retinal vascular damage, there is significant damage to retinal neural tissue in diabetic retinopathy. This is especially true in the RPE melanin sheets which have many functions in the eye.

OCT IS USED TO VISUALIZE THE RPE IN RETINAL SCANS: VIDEO

Studies have revealed neuronal damage before clinically evident vascular lesions and this alone should have gotten researchers to realize that light into the eye and not food is the key driver of these diseases. Centralized medicine now classifies DR as a neurovascular complication. ACTH release drives blood sugar and insulin higher. Hyperglycemia from ACTH actually turns off the cleavage of alpha-MSH, Beta-MSH, and gamma-MSH. This lowers the dopamine level in the eye via hypoxia and elongates the globe to cause myopia.  What else might it cause?  The blog has many new diseases linked to this mechanism.  The last blog showed you how autism was linked to it.  

Here is a video map of the RPE:  VIDEO

In contrast to skin melanin, which is constantly synthesized by the epidermal melanocytes, it is currently believed that melanin in the RPE does not regenerate I no longer believe this is true.   Melanin is known to function as a potential radical scavenger and photoprotective agent.  It also scavengers metal ions when photoreceptors are destroyed by the action of seeing using sunlight.  The retina had to be built a certain way to compensate for this ability.  What are the implications of Nature's design in the retina with respect to modern disease creation?

The neural retina and retinal pigment epithelium (RPE) diverge from the optic vesicle during early embryonic development. The optic vesicle forms as an evagination from the diencephalon.  They originate from different portions of the optic vesicle, the more distal part developing as the neural retina and the proximal part as RPE.

I believe they retain their neuroplasticity and today's textbooks are wrong.   So when the RPE is damaged their connection will be in the diencephalon before there is radiation into the cerebral hemispheres.  I believe this is where the defect begins in autism during neurulation.  I also think this is where blood disorders like Hemophilia, von Willebrand's disease, and Von Hippau Lindau's disease arise as well.

Wait, what?

So when retinal changes are present during my exam I am always interested in an MRI of the brain in the diencephalon as the next step in my own work-up because I am looking for things no one else looks for.  The diencephalon is the region of the embryonic vertebrate neural tube that gives rise to anterior forebrain structures including the thalamus, hypothalamus, posterior portion of the pituitary gland, and pineal gland. The diencephalon also encloses the third ventricle. Below in the center picture, you will see a massively enlarged 3rd ventricle in someone with non-visual photoreceptor problem that began in their retina.  It came to my office as a case of normal pressure hydrocephalus and brain atrophy.  A look in the eye made the link for me easy.  

Ventricular size measurement is necessary for the determination and follow-up of many neurological illnesses, and pathologies. Ventricular enlargement is an indicator of brain parenchyma loss (Karakas et al, 2011). Furthermore, ventricular size measurements are used in studies of hydrocephalus, schizophrenia, tumors, trauma, Alzheimer’s disease, Parkinson’s disease, gender, aging, and atrophy which is associated with many neurological diseases such as stroke and dementia, Huntington’s disease (Karakas et al.; Gameraddin et al.; Honnegowda et al.) and provides useful indices of cerebral asymmetry and atrophy. The knowledge of ventricular system anatomy is essential for clinicians, neurosurgeons, and radiologists (Kanakaraj et al., 2016; Farheen & Sukre, 2017). Due to literature findings, ventricular size is considered a potential indicator in the determination of many diseases related to the brain. I think it is the key to understanding where melanopsin and melanin damage are located in the human brain.  It is a treasure trove of non-visual photoreceptor damage that we can use to predict future diseases.  Additionally, the normal reference values of ventricles obtained by MRI are necessary to form the baseline data for interpreting pathological changes, planning neurosurgical operations, and determining the presence and progress of some neurological diseases. Below you see the 3rd ventricle is almost nonexistent in a healthy brain compared to the picture above.  

Fig. 1 above is an Axial T2-weighted Turbo Spin Echo MRI (TR:3600, TE:87 ms) of measurement areas of healthy subjects. (FH) Frontal horn width. (TIDS) The maximum transverse inner diameter of the skull.  Note how the 3rd ventricle is small here in the pic.

Today's facts are the boundary of human knowledge. These facts are set for it, but should not bind us to what the central paradigm believes.  We must look past that edge to explain things they cannot. If our mind is open, we can spot new data and formulate ideas to test. Our mind requires nature's connection to provide the software to run the hardware inside the skull.  To build this natural quality, a "natural mind" is also a necessary requirement for this process.  These facts allow our species to travel hopefully throughout life, and this appears to be why the journey of discovery supersedes the arrival.

Below is the location in the periphery of the retina where most of the melanopsin IPGRCs are located in the periphery of the retina and not in the macula/fovea.  AMD, cataracts, and many neurodegenerative disorders show defects in this same area on OCT scans.  Central vision is not affected early in these diseases.  This paradox needs an explanation.  Today, you'll get my explanation from my 30 years of careful observation in a decentralized fashion.

Damage in this peripheral area outside the fovea correlates with cognitive decline in neurodegenerative diseases.  Most ophthalmologists are not taught the reason why this area of the retina has the highest amount of O2 utilization in the entire human body.  These photoreceptors use high O2 because this increases the band gap of the semiconductive proteins in the RPE to regenerate melanin in the RPE.  Most eye professionals are told that RPE has no regenerative potential.  I'm not so sure I believe this any longer.  The cells may not divide but the melanin inside of them needs constant renovation via POMC activation and/or migration from Bruch's membrane of the choroid where melanocytes are closest to RPE in adult humans for some reason.  Moreover, this is where most retinal bleeds occur in diabetic retinas and this is where most retinal surgeons use laser coagulation to stop diabetic retinal changes and bleeding from proceeding.  I doubt many of them realize this puts their patients at higher risk of many neurodegenerative conditions due to the disruption of the VUV creation at the WBG semiconductors of the eye. Please note the last line in the slide below. It will be critical in your understanding later in this blog.

KEY POINT: A recent systematic review and meta-analysis reported that vision impairment is associated with 2.4-fold greater odds of cognitive impairment in existing cross-sectional studies and 1.7-fold greater odds in longitudinal studies.

------> https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2781965

Do you still think laser treatment for retinal bleeds has few risks with 800-1200 burn holes from retinal surgeons' lasers?

What is the link?  The key feature for most neurodegenerative disorders is the accumulation of misfolded protein aggregates, framing them within the classification concept of proteinopathies or “protein conformational disorders”. The key change is alpha helices are changed to the beta format by changes in the pH of the surrounding fluids.  People forget that pH is a log function of the H+/D ratio of the tissue.  Here we are back to seeing the impact of the Kruse for Dummies lecture yet again.  The H+/D ratio is key to understanding chiral effects in tissues and how certain diseases manifest.  Diabetic retinopathy is one of those diseases.

If you want to listen to it------> https://optimalklubs.com/kruse-for-dummies-general/

However, it is important to underscore that not all neurodegenerative diseases can & should be considered protein-conformational disorders.  Proteins are semiconductive materials in cells that need constant care and rejuvenation (redox management).  Protein conformational changes can happen from the protein or water side of the biological semiconductor.  If the redox power in the cell is suboptimal those semiconductive proteins will misfold and accumulate with their associated components.  We see these changes in the retina all the time in the RPE before diseases in the brain or other tissue manifest.  This mimics what we see in the choroid of children who will become fat because their choroid has thickened.  This was the key lesson I taught you in the Vermont 2017 lecture.

I just never told you it explains a whole lot more.  And none of you bothered to ask me either.

Although the molecular underpinnings of neurodegeneration are still not completely understood by centralized medicine, if you are following my thesis over the last 20 years, it should be obvious where the problem lies.  It begins with altered light frequencies at surfaces to cause unusual diseases.  Melanin's charge separates water to make H+, oxygen, and electrons.  Therefore it is the most powerful redox semiconductor in a cell.  It explains why most melanin tends to be adjacent to the perikaryon in cells where mitochondria also reside.  There are no coincidences in Nature.  Recall that mitochondria make 95% of melatonin in a cell and that melatonin acts as the change programmer of the matrix and a major antioxidant to control ROS/RNS generation along with melanin that is adjacent to it.

As melanin is degraded or lost in the eye photoreceptor complex we see the loss of the RPE microvilli on the basal side of the RPE.  This causes infolding by the microvilli and increases the surface area of the RPE over a millionfold.  The loss of microvilli is the first clinical sign of a POMC problem in the retina.  This is the clinical sign one can see on OCT retinal scans that melanin needs renovation.  As melanin is lost so is the redox power of the cristae in mitochondria.  As a result, melatonin levels drop locally in those mitochondria and they all make less water and consume less oxygen.  As a result, the tissue becomes hypoxic.  This changes the free radical stream in mitochondria which changes the biochemical pathways used by the photoreceptors to regenerate in the retina.  When this occurs, simultaneously DHA is consumed locally in photoreceptor damage. Normally most people think the consumption and oxidation of DHA are pathologic (Ray Peat) but that is wrong.  It is wrong because DHA is the only PUFA in evolutionary history found to be transformed into highly anti-inflammatory chemicals called docasanoids and elovanoids to protect the RPE from ROS generation.  This is an optical switch used in photo repair that requires UV-A light to be present when hypoxia exists in the retina.  This is the basis of the Bazan short loop in the eye.  This is pictured below in detail.  This is direct evidence that redox power in the retina is lost because melatonin and melanin are both redox proteins that respond to this signal in retinal cells.  Note that the liberated Vitamin A from the non-visual photoreceptor damage in the eye is what destroys the redox power of melanin and melatonin in tissues.  Normally this process is tightly controlled by the physiology of the retina and terrestrial sunlight frequencies with DHA in the retina.  If any of these thermodynamic givens are disrupted disease manifests.

Recall that dopamine can be made from L-DOPA from melanin in hypoxia but this ability is lost as well.  As a result, the ROS made in the eye cannot be absorbed by melanin.  This increases the oxidative stress associated with the eye and into the brain via tracts that are topographically linked to the RPE and the rest of the human cortex.

As we age heteroplasmy rises and so does melanin degradation.  Thus, aging is associated with increasing levels of pro-oxidant factors (reactive oxygen species, ROS) and the dysfunction of the antioxidant systems in the brain, leading to protein and cellular damage and ultimately to neurodegeneration.  That is the real cause of most cases of neurodegeneration.  This is why Alzheimer's disease is now referred to as Type 3 Diabetes.

Hyperglycemia causes retinal damage through complex metabolic pathways leading to oxidative stress, inflammation, vascular damage, capillary ischemia, and retinal tissue hypoxia. Melanin scavenges ROS/RNS/metal ions to clear them to prevent protein misfolding of the semiconductor complexes in retinal tissues that connect to deeper optical tracts in the brain.  This mimics how prions spread disease.

This preserves non-linear optical processes in tissues to maintain tissue function. When melanin is absent or degraded the production of reactive oxygen species (ROS/RNS) leads to the generation of oxidative stress (lowered melatonin/melanin), which will result in the excessive production and accumulation of catabolism of these semiconductive proteins in these areas of the body.  Melanin normally cleans up this debris when the eye is healthy.  Without UV light exposure, the creation and accumulation of these complexes will occur and disease follows.

In ophthalmology textbooks, they repeat this statement all the time.  Melanin granules in the retinal pigment epithelium (RPE) have many important functions which are not yet completely understood by centralized science.

One thing they do get right is that melanin in the RPE protects the cell from damage caused by oxidative stress. It also turns off vascularization of the fovea of the macula.  This pigment acts as a free radical sink and diminishes cytotoxic lipid peroxidation that occurs in most eye diseases when melanin is not present in the RPE.  Melanin in the retinal pigment epithelium is mostly eumelanin. There are two types of eumelanin, which are brown and black, synthesized from levodopa or tyrosine. The melanin amount in the RPE reduces importantly in aged eyes.  When this occurs we know by definition melanin and Vitamin A are a problem in the eye.  This is what destroys the Bazan loops in the eye and what also increases the need for DHA in the central retinal pathways.

Retinal hypoxia is further worsened by high oxygen consumption in the rods in the periphery. This seems like a problem to centralized researchers who do not seem to realize this is how dopamine is made from melanin to regenerate all the photoreceptors in the visual and nonvisual systems.  The rods use a Warburg metabolism by design because of this arrangement.  Melanopsin synthesis needs a massive blood supply in the periphery of the retina to create astronomical amounts of this opsin in the retina.   I believe the reason for this is to increase the band gap because the rods and iPGRCs of melanopsin use so much oxygen to regenerate. The collateral effect of this arrangement creates more VUV light and ROS that stimulates melanin renovation on the RPE.  This is why the RPE is so close to it in the retina.

The RPE cells are the workhorse of the retina and have a large job to do as the slide shows above, yet the RPE is a thin layer of cells that textbooks say does not UNDERGO mitosis.  If it does not undergo mitosis it means its nucleus has to be protected from any stray VUV light created endogenously.  This is the job of melanin in this layer in the RPE.  It absorbs all frequencies of light to keep the nucleus of the RPE cells from dividing.  This is why the RPE has dark neuromelanin.  Persistent hypoxia in this area results in the destruction of pericytes around the retinal vascular arcades that first create A-V shunts in the retina.  I believe this is exactly how AVMs of the brain form in maldevelopment in embryos and in adult forms of humans.  This is also the first step in diabetic neuropathy.  I believe it is also a step we see to varying degrees in TBI cases.  Centralized medicine has missed this in TBI because they are not doing OCTs as part of the workup.  

This increases vascular endothelial growth factor (VEGF) and other pro-angiogenic factors )lack of melanin) always lead to vascular proliferative diabetic retinopathy/macular edema and progressive visual impairment when melanin is absent or not renovated by adjacent melanopsin damage.

BAZAN SHORT LOOP LOSS OF DHA DUE TO LACK OF MELANIN/MELATONIN

Optimal glucose control has favorable effects on diabetic retinopathy primarily because this allows for melanin renovation. POMC is such a unique mammalian intervention because the cleavage products work in opposition to one another, yet mammals figured out a way to make food directly from light without an intermediary WBG like chlorophyll. Melanin utilization was truly an innovation of evolutionary design using the colors of sunlight that bend the most inside the globe.

This blog is showing you how Nature hides her recipes in plain sight.  What is most obvious is also often most concealed in Nature by her design. This is why you need curiosity to see what she is really doing and understand why she is doing it.

Melatonin controls mitochondrial DNA biology but dopamine creation from melanin controls how we decipher and sense time between the inside and the outside world. This creates the illusion Nature needs and wants. Nature never wanted us to see that 380 nm light is her favorite spectral density to run her photo repair process using the NON-VISUAL PHOTORECEPTOR SYSTEM.  This system is far more critical to life than sight because it controls the eye clock pathways that are designed to simulate the physics of your environment from your brain to make the best metabolic choices of biochemical pathways in cells linked to the leptin-melanocortin pathways of humans.  This is the best prediction machine evolution has ever built.

Implications of this idea?  You can live well blind unless your eye clock mechanism is involved in your blindness.  You will never thrive when your non-visual photoreceptor system is damaged whether you are sighted or not.  This is the critical piece that modern centralized ophthalmology is missing today  Creating melatonin in the mitochondria of tissues like the eye is the most critical surface for humans.  The cristae are where the magic really happens.  Melatonin initially controls all regeneration of the photoreceptors, visual and nonvisual in humans except the Muller cells in the retina. This is also by Nature's design. Melatonin needs help from the non-visual photoreceptors to finish the job of photo repair in the CNS.  Both of these chemical molecules are made by sunlight early in the day when a certain spectral frequency falls to Earth as it collides with aromatic amino acids in our eye to slow light down and create the quantum magic we call life. RNA and DNA have a homochirality to them.  <-------Do not miss this hyperlink.

Below are two of the slides from that Vermont 2018 talk that put forth this idea for the first time in public.

^^^^The exact same thing goes on in your retina where melanin is located in the RPE.

This implies that your eye is off and on the switch of the human brain's non-visual photoreceptive system.  Now I am showing the wiring diagram of how this optical switch was built by nature.

Aromatic amino acids have to have an opposite chirality to fit this design quantum mechanically.  You might remember my lecture from Vermont in 2018 introduced the idea of chirality to my thesis.  The chiral heat effect of UV light is critical in this process.  If this process is disturbed the entire system becomes off-kilter and disease will result.  That is how and what melatonin, dopamine, DHA, and melanin, surrounded by matrix water are doing and what Nature is hiding from the observers of centralized science in the retinohypothalamic tract.

I wonder when centralized science will realize that the mitochondria also generate a magnetic field that is far stronger than the Earth or the sun's magnetic effect because its scale shrinks.  They seem to forget the lesson in physics as scale shrinks the electromagnetic force gains in strength.  Might Mother Nature be using these forces in her quantum design to do things that are impossible at the macroscopic level that centralized science observes cells?

YEP.

Modern centralized treatments never focus on the intricate photo-regeneration of the retina.  This process is critical in TBI and many brain diseases as well.  This is just not a retina story developing before your eyes Patrons.  The closest we came to this comprehension and realization of these ideas was in Becker's work on regeneration.  Another place we came close to in centralized science was in the work of neurosurgeon Robert Spetzler in the 1980s.

We still have not appreciated what either man really found (pic above and below).  No one in neurosurgery today realizes that AVMs and aneurysms are due to a defect in melanin and melanopsin in the arterial beds of the brain that mimic what happens in the embryogenesis of the human retina.  Instead, the focus of centralized scientists has been on the anatomic realignment of what appears in tissue in post-natal life.  Big mistake.

AVMs anywhere in the post-natal human is a sign of melanopsin damage and a melanin problem passed down transgenerationally.  AVMs of the dura and skin are big-time signs we still do not understand.

Aneursyms of the brain are also markers for melanopsin and melanin issues within.

Aneurysms of the aorta are also markers of melanopsin and melanin renovation problems postnatally.  An aortic aneurysm is the type of aneurysm rupture that Albert Einstein died from.  It is also the type of aneurysm that Rick Rubin almost died from.

LESSONS FROM  DIABETIC NEUROPATHY

Diabetic retinopathy stoichiometry defines most traumatic brain injuries.  Every diabetic provides a lesson for a decentralized clinician.  Centralized clinicians remain in the dark because they are bad at understanding opsin math.  

What goes bad in diabetes in the eye?  The photorepair regeneration system goes awry and this gives the decentralized MD something to understand the optical physiology of the human brain.  In the Rod Outer Segment melanin renovation is astounding.  It goes bad in diabetic retinopathy.  Humans have  125,000, 000 rods in the retina.,  1 RPE cell attends to > 200 photoreceptors.  Each rod sheds approximately 3 mm a day.  Thus, the human retina must shed 375 meters each day.  This means > 10,000,000 meters of the disk have been shed by the age of 75.  The most astounding ability of the human retina is that it must synthesize 9 billion opsin molecules per second in order to maintain its function.  If it cannot regenerate the rhodopsin, melanopsin, or neuropsin you are guaranteed to get get some neurodegenerative condition linked to some degree of diencephalic breakdown in a topological map.  Where the opsin is destroyed is a marker for where the disease will manifest as time elapses.

Other treatments for diabetic retinopathy include laser photocoagulation, which improves retinal oxygenation by destroying the high oxygen-consuming rods by their replacement of low oxygen-consuming glial tissue. No one has thought to use melanin renovation of the RPE to solve this problem because no one in ophthalmology realizes that melanin is a wonderful creation of condensed matter physics and atomic molecular orbital engineering. It is truly the most amazing protein anywhere in the human brain. No wonder humans put it in every organ system compared to other primates.  In places it is absent or missing destruction lies in its wake.  Remember alpha MSH is stimulated by UV-A light.  380nm light is UV-A light.  It shares this common tie for its love of UV-A light with melatonin.

Hypoxia is a potent stimulator of VEGF, and HIF-1 alpha and intravitreal anti-VEGF antibodies have been somewhat effective in regressing macular edema according to some studies done in retinal neovascularization. The problem is using natural light to renovate the photoreceptors that should have hit somebody's mind in 125 years still astounds me. We know that dopamine and melatonin regenerate the photoreceptors and we also know melanin creation improves the regeneration of dopamine from melanin by way of L-DOPA. We also know as melanin returns to the RPE the amount of melatonin made in the mitochondria of the retina also improves. When the RPE is loaded with melanin sleep improves tremendously because Vitamin A goes down and the visual cycle of photoreceptor regeneration is CONTROLLED locally in the eye by DHA, dopamine, melatonin, and melanin working in concert. This is why sunny days at the beach always lead to great sleep.

Very few people have linked the complex pathophysiology of diabetic retinopathy with an altered spectrum of sunlight because they do not seem to understand the biology of POMC even today in 2023. They continue a biochemical focus with their lens pointed to retinal oxygen/fuel consumption with resultant hypoxic damage to retinal neurons. Blue light destroys melanin because it raises blood glucose and insulin. UV light and IR-A light is what are critical in the melanin renovation of the RPE. The biochemical focus wants to continue to discuss potential mechanisms through which sodium-glucose cotransporter 2 (SGLT2) inhibitors improve retinal hypoxia—through ketone bodies. This is incredibly myopic because no one seems to understand mammals make glucose and insulin from blue light.

Melatonin plays a key role in the coordination of the diurnal and seasonal circadian system, which underlies how the biological clock works everywhere in humans.

Mitochondrial DNA is more vulnerable to alteration than nuclear DNA, mainly for two reasons. As such mtDNA damage LOWERS local melatonin levels.  So circadian disruption alters melatonin levels locally in many tissues. That lead to diseases.

Melatonin controls mitochondrial DNA and dopamine controls how we experience, decipher, and sense time between the inside and the outside world. Nature hid that she made this dopamine in the eye when parts of the retina were forced to be hypoxic to degrade melanin to create dopamine.  In this way, Nature never wanted us to know how important melanin was.  Creating melatonin also occurs first in the eye and is the most critical surface creation for humans. Melatonin is made by the aromatic amino acid tryptophan which absorbs a very unusual amount of full-spectrum UV light according to its absorption spectra. This is light that never reaches the surface of the Earth in most places. So the curious would ask themselves how does this happen?  Deuterium in the circulatory system of the retina, when sunlight entered the eye and hemoglobin's unique optical window of 250-600nm, was the key to solving that mystery in the eye.  This explained why the choriocapillaris exists as it does in the adult human retina.

The choriocapillaris is the innermost structure of the choroid in humans that directly nourishes the retinal pigment epithelium and photoreceptors.

The embryology of this layer of the retina shows the power of melanin.  The initial human choriocapillaris form by hemo-vasculogenesis. This is how hemoglobin if formed in the human embryo.  This area of the retina forms just like red blood cells do in our marrow and liver. This means the same cells in this region of the retina express special fetal hemoglobin called Hb-ε as well as CD31, CD34, VEGFR-2, or vWf (where hemophilia and von Willebrand's disease comes from), further suggesting the same precursors were capable of erythropoiesis, hematopoiesis, and vasculogenesis, the definition of hemo-vasculogenesis, as occurs in blood islands in cells. In the fetal period, hemo-vasculogenesis is completed the same way for blood cells and new blood vessels. They appear to form by angiogenesis since endothelial cells were proliferating in the same way at the same time.  So is melanopsin. 9 billion opsin molecules are synthesized per second in the retina's outer photoreceptor region.  This requires massive amounts of oxygen to synthesize this amount of melanopsin.  All these unique pieces fit now and make sense.   Porphyrins are another non-visual photoreceptor in humans.

What was the key to this entire process occurring?  Melanin had to be absent in the embryo at a specific time in morphogenesis when the choriocapillaris is forming.  Just the presence of melanin in this area of the retina appears to stop hemo-vasculogenesis in the embryo's retina creating the picture above in the adult retina.  This is why the retinal angiogram of the adult human retina shows no blood vessels in the adult macula.  Diabetic retinopathy is like autism.  It is an atavistic effect of the embryo of previous stages of evolution of the eye that allowed for blood vessel growth in the fovea.

It is also why diabetic retinopathy is associated with neovascularization or angiogenesis with excessive blue light exposure.  When melanin/melanopsin is disrupted or destroyed, blood vessels can grow and neurulation is changed in the optical pathways.  You saw the same thing in the last blog on autism.  Blue light also changes the retinoid cycle of the retina.  Melanin's presence or absence is critical in both the embryo and in the adult form of humans.  Blood vessels bring RBC and RBC brings oxygen and oxygen is key to melanin biology.  When hypoxia develops dopamine shows up from melanin degradation.  Have I told you yet that the choriocapillaris creates the highest blood flow of any human tissue and it has the outer rod photoreceptors adjacent to it that consume the most oxygen of any tissue in humans?  Do you want to guess why this arrangement exists?  The picture below gives the answer.

If you have a high demand for oxygen you keep melanin in its optimal state and any photooxidation in the visual system of the photoreceptors needs dopamine.  It also is needed to make 9 billion opsins per second.  If the non-visual photoreceptor system fails, you'll wind up with some diseases mentioned in this blog.

Dopamine is made from tyrosine, another aromatic amino acid that also absorbs short-wave UV light. This is why both molecules are tied to the physiology in the sys and skin and are linked to melanopsin. Melatonin controls all regeneration of the photoreceptors in man except the Muller cells in the eye. Both of these chemical molecules are made by sunlight as it collides with aromatic amino acids in our eye to slow sunlight down so it can become matter. That is how they link to one another. The Reality #12 blog told you long ago how they work in a cell but no one asked me in the comments the right question.

Most people with Parkinson's disease know that they are deficient in dopamine in the midbrain, but most people do not know that that defect in that area spreads to the region from the eye first in a very similar fashion to how a prion disease works.  The Vitamin A deficit in the eye is how the blood disorder von Willenbrands disease or hemophilia A happens due to the changes in the retinoid cycle of the embryo.  These can be transgenerational diseases but few people see what I see in the embryology of the retina.  This is why PD patients have misfolded proteins associated with their disease that mimics how prions operate in disease states.  It is a story laid out in the OSF #3 blog post in detail.  I've been telling you this story for a long time but now you have new eyes to perceive it. What has always been the clinical take home from Uncle Jack?

My Rx was not hard.  Most of you refused to believe it was this simply because you were all ignorant of the optics of the non-visual photoreceptive system built into us by Nature.  Stop complaining and just do what Nature requires you to do. I am giving you my life's work for the cost of a cup of coffee.  SHARE IT.  You owe me that much.

MORE SCIENCE TO MOTIVATE YOU INTO NATURE

First, mitochondria are a major source of intracellular reactive oxygen species (ROS) via cytochrome C oxidase's ability to hold oxygen between Fe and Cu ions.  The electrostatic grip is linked to the free radical made.  The light in the environment controls the electrostatic power via the effect of D shell electrons in these metal atoms. Therefore mitochondrial DNA is under much stronger oxidative stress than nuclear DNA. Second, mitochondria have a matrix-side negative membrane potential for oxidative phosphorylation. This membrane potential concentrates lipophilic cations inside the mitochondrial matrix up to approximately 1,000-fold. Deuterium and H+ are positive cations.    Deuterium and H+ are both positive cations that varying lipophilic attributes FYI. Too bad some of the deuterium critics don't know these basics.  This is why the matrix favors H+ over deuterium and why the ECF and non-lipophilic tissues will naturally contain more deuterium (plasma).  This deuterium in the blood is how cells make their own UVC light used to make neurohormones from aromatic amino acids that control local mitochondrial biogenesis.

^^^^Both slides were from Vermont in 2018.  Please stop telling me I have not been telling you this story for years when the reality is you refused to sink to my level and LEVER up your knowledge.  If you do not lever up your knowledge you are never going to stop believing the dermatologists and ophthalmologists who are being paid by Big Pharma to keep you from the most simple things to keep you healthy.  The slide below was used in 2017 in Cancun by a group of optometrists/ophthalmologists who refused to see where diabetes came from.........blue light toxicity.  I hope you get the lesson today they still cannot fathom.

SUMMARY

Diabetes has been and will always be a chronic mammalian disease when the purple and red light is removed from our environmental light. The focus on a ketogenic diet is misplaced when you consider the quantum effects of manufactured light on the photoreceptors mentioned above.

The biochemical ideas continue to dominate the literature because they believe ketones are energetically as efficient as glucose and yield more ATP per molecule of oxygen consumed than fat, with less oxidative stress. While this is true, no ketogenic diet has ever been able to reverse DR primarily because diabetes is not a disease of diet. It is a disease of blue light. Instead, we need a paradigm shift where eye physicians begin to realize full spectrum sunlight leads to direct retinal benefits which occur quickly when UV light and IR-A light are reintroduced to improved fuel energetics. these two frequencies of light induce less hypoxia and reduce inflammation through the recycling of DHA and the neuroprotective metabolites of the short loop of Bazan in the eye. Modern eye care is in the dark ages in treating this disease of blue light overexposure.

GAME SET MATCH.

CITES
https://pubs.rsc.org/en/content/articlelanding/2022/an/d2an00588c

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7829956/