QUANTUM ENGINEERING #47: BIPOLAR DISORDER AND POMC

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Today is the summer solstice and that is why this blog is being released today. More people with bipolar disorder will be admitted to ER’s in the Northern hemisphere today than any other day.  Now you are going to learn why this is the case.

Bipolar disorder (BD) is a chronic and common psychiatric pathology, which can be particularly disabling. The disease has a global prevalence rate of 1–4%, begins at an early age, i.e. predominantly between 15 and 25 years old, and persists throughout the life of patients. BD is characterized by a recurrence of mood depressive episodes (pathological decrease in mood and energy), hypomanic or manic episodes (pathological increase in mood and energy), or even mixed episodes (simultaneous presence of depressive and manic symptoms).

Bipolar disorder is a common mental condition in our modern world with a seasonal pattern of onset. In the spring, there is a higher incidence rate of mania or mixed onset and suicide associated with equinox and solstice.  The reason for this is a defective pruning mechanism related to the cortisol melatonin cycle in cells.  The question is then what controls this pruning in us?

LINK

The pruning method of control in the brain is normally controlled by the cortisol melatonin cycle.  Cortisol usually creates new pathways and melatonin trims or prunes them to suit the environment the person is in.

In bipolar disorder this system has gone awry.  Remember cortisol is controlled by light via ACTH and melatonin levels are made by the mitochondrial matrix.

Explain this me like I am a 3rd grader Uncle Jack?

What if I told it was because the FM radio station evolution built into your head went awry because the manner in which it works was usurped by your light choices. Would you believe that?

The FM receiver used by Mother Nature in our brain includes a clock that measures light and cavities filled with water. It turns out that the shape of things in our head is prognostic on how good time our clocks tells. Imagine that. These two antenna use a phase locked loop system that is also used in modern FM radio receivers in our car. Can you believe that? Because of its usefulness, the phase locked loop is found in many wireless, radio, and general electronic items from mobile phones to broadcast radios, televisions to Wi-Fi routers, walkie talkie radios to professional communications systems and very much more.

Mother Nature built this FM radio station in the nervous system over 3 billion years ago. This is why brain’s first became important. Their original purpose was to inform cells of the seasonal connection between the sun and Earth. In turn, this data could be made useful to direct biological changes. This is how light changes biochemistry inside of us. This is how we know it is summer time. In bipolar disorder this system is awry when it is encumbered by too much mass in the antennae of the system.

What bends space/time in the universe? The masses associated with the matter in the universe does. Anything that has more mass than the smallest atomused inside of our molecular clocks changes how we experience time. Mass bends space/time!  Now ask yourself what do magnetic fields do to space-time?

Magnetic fields tend to flatten and stiffen the fabric of space-time when masses are added to them and this alters our perception of seasons.

The circadian activity generated in the SCN clock of the eye needs to be transmitted to the rest of the brain in some way. It seems like the clock timing tract splits into two wires and informs the brain of what season it is. In Bipolar Disorder this is impossible because the in the eye clock is usually where the defect lies.  That defect in the antenna ruins the fidelity of the system and our brain cannot tell where the Earth and sun are in relation to one another. Pretty remarkable gadget Nature built in our head. It appears the excess mass in the antenna screws up the connection of the FM radio station. Without a proper connection, the fidelity of the music coming from system fails. That is what bipolar disease is to a metronome. Can you believe that? My friend the metronome says it’s all true because of the physics of clock timing. It is apparently thrown off when we have too much weight (mass) in our clocks. Does something to the fabric of space time to deform magnetic fields. Wild decentralized stuff I tell you.

3rd grade bipolar lesson is over.

BACK TO THE SCIENTIFIC EXPLANATION OF BIPOLAR DISEASE

These thymic episodes the bipolar patient experiences are interspersed with phases of clinical remission, known as “euthymic” episodes. The disease is associated with a high morbidity and mortality rate and due to the significant functional impact it induces, including during euthymic periods, BD is the cause of poor quality of life and is one of the ten most disabling diseases according to the World Health Organization. The diagnosis of BD is mainly clinical and can be supported using scales or questionnaires. The diagnostic delay is estimated at around 10 years. This delay is clearly related to the heterogeneity of the clinical expression of the disease. The phenotype of the disease is relative because how patients experience time is relative to the environment they inhabit.

The study of the literature shows that this delay in treatment seriously affects the prognosis, particularly on the functional level, and constitutes a major public health problem. In addition, there are no good biomarkers, easily usable in current practice, to help the clinical decision for the diagnosis or for predicting the course or prognosis of the disease.  One thing is known about bipolar people.  Many of them have the same changes in their eye as diabetics.  They also tend to get metabolic syndrome in the guts more frequently than any other mental illness as is documented in the cites below. They tend to have pale skin in their thoracic and lumbar regions as well.

WHY ARE SLEEP DISORDERS ALWAYS LINKED TO THIS DISEASE?  

Sleep disturbances and sleep/wake rhythms are major in BD. These disturbances are observed during the different phases of the disease and are major symptoms of mood episodes and belong to the diagnostic criteria for depression, hypomania, and mania. In addition, these anomalies are also found during the euthymic phases of this disease. Indeed, patients suffering from BD would be more likely to present a more evening chronotype and a more languid and rigid circadian type than healthy subjects as well as a decrease in the efficiency of their sleep, an increase in sleep duration, an increased sleep latency and a prolongation of the duration of awakenings after the onset of sleep. These disturbances in sleep and wake/sleep rhythms are associated, among other things, with more frequent relapses, an alteration in the quality of life, and cognitive disorders.

Additionally, neurocognitive deficits are frequently associated with BD. Most typical deteriorations found are impairment of episodic verbal memory, executive functions, processing speed, and sustained attention. These troubles can be present during mood episodes but also in around 30% of patients during euthymic phases. Cognitive deficits of patients with BD have a direct impact on their psychosocial functioning, on the risk of relapse, on treatment adherence, or even on their ability to insight. Their early detection associated with the identification of prognostic and predictive biomarkers of the response to cognitive and functional remediation tools is essential in order to be able to offer early and appropriate treatment.

Due to its embryological origin, the retina is an integral part of the central nervous system. The retina is a complex neural tissue (above in a BD patient), consisting of several layers of retinal neurons. They have structural and functional properties similar to cerebral neurons.  You’ve seen this laid out in detail in this series.  In addition, molecules involved in brain neurotransmission such as dopamine, serotonin, glutamate, or GABA, are also involved in retinal neurotransmission. The retina is now considered a relevant candidate for the study of neurotransmission abnormalities in neuropsychiatric pathologies. The function of retinal neurons can be measured using the OCT (below) or the electroretinogram (ERG).

ERG is a simple, fast, inexpensive, and non-invasive process that aims to measure the electrical activity of retinal neurons in response to light stimulation and provides indicators of synaptic transmission. This technique can represent an important electrophysiological measurement in biomarker research within psychiatric diseases. However, studies evaluating retinal function with ERG in BD are very few today.  I think in the future  In addition to the electrophysiological anomalies mentioned above, structural anomalies at the retinal level have been described. Indeed, several studies carried out in optical coherence tomography (OCT) have shown that subjects with BD present a thinning of the layers of retinal neurons. Additionally, results also seem to suggest that retinal thinning in the periphery of the retina where melanopsin is located may be related to disease progression.  People with bipolar disease are equisitely sensitive to light it appears.  This is what makes them different.

As previously described elsewhere on Patreon, retinal neurons and cortical neurons have similar properties. It should be noted that measurements of retinal function with ERG and measurements of cortical function with visual evoked potentials (VEP) share the same characteristics. Indeed, both can be performed using light flash stimulation and using luminous black-and white reversing checkerboard (pattern stimulation). In addition, they are complementary measures for the analysis of dysfunctions of the central visual pathways. Thus, the combined study of VEP using EEG could be relevant and complementary to ERG for a study of all visual neural pathways in neuropsychiatric pathologies in the future.  I think OCT shows these changes when clinicians think to order them in bipolar patients.  This is going to be how centralized medicine slowly decentralizes in my opinion as these tests reveal the quantum mechanical changes that occur in the antennae of the phased loop signaling you are about to learn about in this blog.

BIPOLAR DISEASES AND LITHIUM & METABOLIC SYNDROME

Lithium is the most common drug used to treat bipolar disorder.  Overall, compared to placebo, lithium appears to decrease the risk of suicide by more than 60% in bipolar disorder.

Blue light increases blood glucose and insulin from POMC cleavage of ACTH and CLIP.  Did you know that people with newly diagnosed bipolar disorder are 3.5 times more likely to have metabolic syndrome? What is the connection?  Abnormal light in their environment is the link.  Metabolic syndrome changes how the gut works with the brain because of changes in the SCN and the CSF that surrounds the thalamus.  It is most often seen in those who live an indoor existence while bathing themselves in blue light and nnEMF.  The best way to avoid all mental illness is to remain in the sun and remain in the dark when the sun sets.   It is not that hard when you understand how light changes the topology of the eye, skin, and gut.  When you bathe in light at night or day mental illness and a sleep disorder will find you eventually in some way.

ISOTOPIC LESSON ON LITHIUM:  DEEP PHYSICS

Lithium drugs are widely used for treating bipolar disorder. They work, but nobody really knows how they work in cells. I think I might. How might a mitochondriac attack this problem? How about by mito-hacking the periodic table of elements yet again?

Consider the link between size discrepancy and the proton spin crisis between B-meson and protons. B-mesons are approximately 2/3 the size of protons and each of the quarks that make them up have a spin of 1/2. Protons do not follow the expected spin predictions that mesons have given us. Why would lithium be linked to this proton story? Remember that mitochondria in neurons deal with protons and B-mesons in the mitochondrial matrix as I laid out in my April 2016 webinar on this topic.  Those details are not important here but the size difference of the atoms is.

Might lithium’s effects somehow be due to the quantum effects of the size variation of isotopes found in the matrix in the SCN and the leptin melanocortin pathways in some areas as it travels through the brain?

You do know that different isotopes of elements have different nuclear spins, right?  People who listened to my Kruse for Dummies lecture should now fully understand why lithium works in bipolar disorder and why it can help reverse some of their Metabolic syndrome effects. Lithium alters the binary code of life because it has spin number that mimics one fo the atoms used in the binary code.

Guess why a mitochondrion favors protium (H+) over deuterium (D)?  Atomic mass is the answer.

Might isotopic effects cause some quantum change in a material or a receiver built into our system? Might the size variation of isotopes found in the blood be linked by Nature to make circulating blood act differently than water in other parts of our body?   LINK TO THE LECTURE

IS BIPOLAR DISEASE REALLY AN ALTERED SIMULATION OF REALITY DUE TO ISOTOPE VARIATION IN NEURONS?

Deuterium is an isotope with spin = 1, unlike hydrogen-1, which has spin = 1/2.

Photons (particles of light) can have a spin of –1 or +1.

Why can’t photons have 0 spins?

The definition of the spin as the angular momentum of a particle at rest is also inapplicable to the photon since there is no rest frame for the photon, which moves at the speed of light. Light never rests or stands still once it is liberated from matter.

What bends space/time? Mass does. Since Deuterium has more mass than H+ it bends space/time more than protium. Now ask yourself what do magnetic fields do to space-time?

By reanalyzing the basic equations of general relativity, a researcher has discovered that magnetic fields tend to flatten and stiffen the fabric of space-time when masses are added to them.

How does this affect the circuit between the sun, earth, and the human brain?

It should immediately raise a question about this solar circuit in bipolar patients.  Daytime has strong electric fields associated with sunlight.  Nighttime has little.

Does a strong electric field cause time dilation in the SCN and the tracts linked to it in the mammalian brain to cause bipolar disorder?

The spacetime curvature for a charged static spherical body is given by the Reissner–Nordström metric:

With these mathematics, you can feed in the value of whatever charge you want and calculate the time dilation as a function of distance from the charged body. If you do this you’ll discover something rather odd in Einstein’s field equations, namely, the charge reverses the effect of the mass.

Do you remember how many times I have told you in podcasts that redox potential is the net negative charge in a cell?  Do you see now how that charge can offset the bad isotopic variation in some of your tissues to make your clocks work better in the circuit that tells the brain what season it is?  Remember sunlight deuterium depletes us.  Light at night adds deuterium to our tissues.  This ruins our clock function.

Is this why mammals conserve charge using their POMC biology in their cells Uncle Jack to offset this deuterium problem?  Yep.  The excess mass of heavier isotopes in cells and mitochondria causes time to slow (relative to the observer at infinity) but adding charges back to proteins/water (of either sign) can make the time speed up again.

Wait a minute Dr. Kruse, explain that again.

The sun creates massive electric fields during daylight. Implications for Bipolar Disorder?

Does a strong electric field cause time dilation in the universe?  Yes, it does  because a strong electric field generated by the sun adds a massive net negative charge to cells that absorb this radiation.  POMC makes sure this happens in the human brain via Noether’s thereom.

This is true because the mathematics of physics says it operates this way.

It appears this is what really causes Bipolar disorder at its fundamental core.

TYING IT BACK TO MY THESIS OF THIS SERIES

The adrenal medulla of mammals was born under the light stress of the KT event. This is why I wrote the adrenal fatigue blog years ago but no one saw things back then like they do now. I told the implications of that Huberman/Rubin podcast were VAST.  Bipolar disorder is one of the effects.

Man’s five senses can capture the vastness and the immensity of our cosmos and POMC is the paintbrush that allows it. POMC is the paint that goes on the canvas, your brain. POMC is a color palate that humans use to paint their mind. In some ways, that palate confines us to the limited real estate of the sensory organs in our brains to understand all the complexity of the universe. All 5 senses tract directly to the thalamus of humans that surrounds the 3rd ventricle of their brains.  But there is a wisdom in being connected to nature in this fashion. Yet, few see the artistic symmetry of confinement. I am trying to explain this art to you now every day, in every word I write in everyone of these blogs.  It is time for you to LEVER UP your knowledge.

THE LEVER UP LESSON:  The adrenal cortex synthesizes three main groups of hormones (glucocorticoids, mineralocorticoids, and adrenal androgens) (Auchus and Miller, 2001). The homeostasis of glucocorticoids is regulated by a feedback mechanism CONTROLLED BY POMC gene translation via solar light and temperature sensors (non-visual photoreceptors) in the skin, eye, and autonomic nervous systems that are relayed to and through the hypothalamic POMC center and the circumventricular organs (water networks in the ventricular system of the brain) by means of corticotropin-releasing hormone (CRH), the pituitary gland by ACTH, and the adrenal cortex by cortisol (Koch, 2004).

The mammalian cell responds to all stress, including light stress, by increasing cholesterol production. 

Cholesterol is the MAIN non visual photoreceptor of the brain.  If you go into an ICU with a patient with an acute infection and draw their lipids (not often done except by a tool like me) you will find sky-high LDL cholesterol. 

And that is both LDL and HDL, but the LDL fraction is much higher. Is that a problem? No. But Big Pharma has trained centralized MDs to reflexively reach for the Rx pad to write for a statin. This is why so many people with Bipolar disorder also have metabolic syndrome as a comorbidity as well.  Their LDL is high because they are all solar deficient.  Remember LDL cholesterol lacks electrons realtive to HDL cholesterol.  

The other non visual photoreceptor in the brain that is common is melanopsin and it is found in the blood vessels.  With blue light at night it increases blood flow and increases blood pressure excessively.  High blood pressure is part of metabolic syndrome.  

Few MDs & psychiatrists today are trained to even know full spectrum sunlight lowers cholesterol naturally.  Even fewer realize sunlight is the best treatment option for Bipolar disorder.  Blue light at night makes this disease deadly.

In fact, in metabolic syndrome, higher LDL cholesterol stabilizes the inner mitochondrial membrane function during heavy oxidative phosphorylation (cellular energy production). So a raised LDL actually helps mitochondria retain its electric charge to condense H+ inside the mitochondrial matrix to make energy using the light hydrogen isotope. 

This is how the cell controls space time and magnetic fields inside of their tissues to ACCURATELY SIMULATE THE PHYSICS OF YOUR ENVIRONMENT.

In bipolar disorder, this is a broken mechanism at the level of the SCN because there are atoms in it with higher masses than their should be.  (D>H+)

Do you know what sits really close to the outer mitochondrial membrane in most mammalian cells?

POMC waiting to create melanin from the biophotons released from the mitochondria right next to it. Making CO2 and DDW is the reason our cells stole bacteria 600 million years ago. And since the cell is trying to recover from a light stressor, it needs a good inner mitochondrial membrane in which to transfer its electrons to oxygen and use the H+ liberated by melanin buried in water to make ATP by the spinning ATPase Fo head.

When the deuterium isotopic variation mechanism is broken in the SCN, lithium can be used to help offset that loss in the CSF networks in the ventricular system of the brain.  Effectively, lithium is adding mass to the water of CSF to offset the deuterium in the SCN to allow it act as a better FM radio antenna to tell the season for the brain.

That is why lithium can help some of these people.

The problem with lithium is that it can never reverse the disease.  Only strict sun exposure and darkness at night can repair the broken mechanism at the SCN level to help eradicate this disease in humans.  When the SCN is loaded with too much deuterium, as such, it cannot accurately tell time.

The isotopic variation changes as their choices in light vary leading to mania and depression cycles in things the ipRGCs link directly to.  Note the positioning of the habenular nucleus in the next two pictures and you’ll see the circuit manifest before your eyes.

What controls the autonomic nervous system in the gut of mammals that get metabolic syndrome?

NEUROANATOMY LESSON TIME:  POMC does because it is found in high concentration normally in the outflow tracts of the neurons from the hypothalamus that connect to the gut.  This connection is made via the dorsal longitudinal fasciculus.  That tract targets the thoracic nerves that connect to somites where other melanin stores are located from the neural crest.  Remember before when I told you bipolar people tend to have pale trunks and abdomenal skin?  Now you know why this link is important.  These dermatomal layers need melanin renovation in BD.

When I see a patient with BD I always examine their skin in these areas before I order an MRI (above).  Why?  Pale skin in these areas always corelate to white matter lesions in their brain (shown above).  Centralized science is still clueless why this is the case.  You no longer will be.  This is decentralized medicine 101.  White matter hyperintensities (WMH) are much more common in subjects with bipolar disorder (BP) than in healthy subjects.  The more prominent that lesion or the larger their ventricles tells me how severe their disease is.  LINK   I have also observed that paleness of the skin in these areas also corelates with thicken of the choroid on OCT images of the retina and with changes in the inferior nasal retina on my eye exams.

The hypothalamus is the key brain site for central control of the autonomic nervous system, and the paraventricular nucleus is the key hypothalamic site for this control. Much of the medial surface of the thalamus and hypothalamus form the wall of the third ventricle pictured above.Part of the hypothalamus forms its floor. Its thin, membranous roof contains the choroid plexus that makes cerebrospinal fluid which is 99.8% water. The third ventricle narrows quickly at the posterior end of the mammillary bodies.  These bodies are the key to memory formation and important in dreaming.  Anatomically, the PVN is adjacent to the third ventricle and many of its neurons project to the posterior pituitary. These projecting neurons secrete oxytocin and a smaller amount of vasopressin, otherwise the nucleus also secretes corticotropin-releasing hormone (CRH) and thyrotropin-releasing hormone (TRH).

Recall my Brain Gut #16 blog told you that the PVN is where adrenal fatigue began.  It is a light disease that turns off POMC in the hypothalamus and not a real adrenal disease.

The PVM neurons massively express POMC but without UV light this switch never gets turned on. Bipolar patients are all lacking that critical UV light switch.  The major pathway from the hypothalamus for autonomic control is the dorsal longitudinal fasciculus in the human brain.  Below is another picture of the third ventricle (red box) that is adjacent to the hypothalamus and thalamus in humans.

The dorsal longitudinal fasciculus (fasciculus of Schutz) is a periaqueductal (area around ventricular system Aq above) ascending and descending fiber system arising from the hypothalamus and terminating to the autonomic nuclei of the pons and the medulla, conveying autonomic fibers from the brain to the gut in humans.  It also conveys pain and is important in sleep pathways of humans.  These are usually altered in bipolar patients as well because of a lack of melanin in these areas.

The dorsal longitudinal fasciculus is found within the dorsal brainstem tegmentum. It passes through the periaqueductal gray matter and contains both ascending and descending fibers. The ascending fibers pass from the reticular formation (sleep region/insomnia) passing to the hypothalamus thus transmitting information related to the viscera.

People who travel a lot across time zones or people who use a lot of blue light or nnEMF in their cities are going to have massive sleep disturbances like people with mental disorders because they have broken the same rules of Nature.  I view insomnia as a mental disorder in decentralized medicine.

This surface is acritical in barrier in the brain health of humans.  This is the pathway where metabolic syndrome, poor sleep, and fatty liver all come from.  Many of these same findings are found in diabetics, bipolar disorder, and those with sleep disorders like insomnia.  Patients with bipolar disorder tend to have all these symptoms at times that vary based on how defective their FM antennae are.

This explains how a lack of sunlight leads to most gut and sleep issues modern humans face. Without proper DLF input to the gut via the brainstem, ferroelectric currents are lost and circadian control of the gut lumen is awry. This opens the gut barrier to many potential problems.

Pro-opiomelanocortin co-localizes with corticotropin-releasing factor in axon terminals of the noradrenergic nucleus locus coeruleus.  It is not just a PVN sotry folks. Where the problems lies will determine aspects of the disease you get.
This nucleus is filled with neuromelanin. The locus coeruleus (LC), a small brainstem nucleus, is the primary source of the neuromodulator norepinephrine (NE) in the brain. The LC receives input from widespread brain regions, especially the hypothalamus and projects throughout the forebrain, brainstem, cerebellum, and spinal cord.

What is the main function of locus coeruleus?

It is the brain’s main source of the neurotransmitter noradrenaline (norepinephrine). This chemical is excitatory and is released in response to pain or stress, stimulating what is referred to as the ‘fight-or-flight’ mechanism. This means that it activates the sympathetic nervous system via those thoracic nerves I mentioned above.  Those are the same nerves that innervate your brown fat and also give input to the superior cervical ganglia that I mentioned in Time 12.  Without UV light exposure in the eye and skin in these dermatomes melanin is degraded and noradrenaline is diminished.  You remember that nor adrenalin can be made from melanin right?  See the slide below far right top line.

Neuropsin is a 380 nm light sensor that the locus coeruleus needs to function well.

Without this system operational, this opens the BBB and the gut barriers. We see this in most psychiatric cases and in TBI cases due to the stress response.  Now you can see why really the brain-gut barrier is linked. Usually, there is a lack of melanin in the DLF and/or the locus coeruleus to create the aura of brain-gut barrier when in reality what links the two is a lack of UV light to stimulate POMC in both hypothalamic pathways and melanin is degraded leading to many disease phenotypes.  Each somite in the spinal cord also has POMC in it derived from the neural crest in this part of the body.  For the gut this is linked to the celiac ganglion which comes from T5 -T11 thoracic nerves.  So thoracic level solar exposure is key to renovating gut level melanin.  It is counterintuitive until you see it all laid out in front of you.  A lot of this deep science would have been the Vermont 2019 video I was going to give 4 years ago.  I think I still might do it for the Kruse for Dummies folks.

SUMMARY

Neil Cherry PhD from New Zealand  showed in 2002 that there is strong and robust scientific evidence of the human brain detects and responds to the Schumann Resonance signal based on the work of many researchers Robert O. Becker worked with in the 1970s.  People with bipolar disorder cannot connect well with the Schumann resonance because of excess mass contained within the receivers of the signal which comes from the sun and Earth.  As a result this leads to behavioral and neurologic dysfunction.  Since increased mass of isotopes used in this system affects coherence times that are possible in cells, they lose their ability to maintain quantum coherence and the system becomes dysfunctional.  How long a system can maintain coherence is a function of the atomic mass in that system.  You can see now why any additional masses in the SCN or habenular nucleus destroy this realtionship.  The pictures below shows the specific details of the pathogy laid out for you.

The brain uses a range of frequency patterns monitored by the EEG system in our neurosurgical clinics. The frequency range of the EEG rhythms coincide with the frequency range of Schumann Resonance signal (0–45Hz). The alpha wave is identical to the frequency most commonly linked with Schumann resonace on Earth.  The normal brain has developed an ELF oscillating ion system, primarily using calcium ions (above), to control neurotransmitter release.  The release is awry in BD.  Dr. Russ Adey at UCLA established this in the 1970s.  Adey work is cited below. The human brain and its optical clock lattice in the SCN is now well established in the literature.  Blackman’s work on calcium ion resonace frequencies was cited multiple times in Becker’s books and my early blogs on the non ionizing effects of nnEMF and neurological compromise. Blackman’s research also cited below, has taught decentralized MDs that external electromagnetic ELF signals induce altered neuron calcium ion effluxes in mitochondria of brain tissue.

These ELF signals between the sun and Earth are weak, yet they match the ultraweak UV biophotons that cells create in response to the Schumann extraterrestrial signal.  This allows the brain to know the season.  The stable synchronization of the brain’s electromagnetic systems using a system that mimicks an FM radio has actually led to humans becoming thinking, emotional, memory machines of biology that are capable of quite a bit of intelligence in the human central nervous system. In order to carry out these functions the brain has developed electromagnetic transmitters and receivers in the neurons to accomplish this task in the SCN, leptin melanocortin pathway that extends into the thalamus of man and into his spinal cord.  The thalamus is where the alpha wave finds its genesis in humans. This connection is pictured below.

The receivers used by Mother Nature in the human brain included a phase locked loop system, described by Ahissar et al.  This paper is cited below. The phase locked loop system is also used in modern FM radio receivers in your car.  In the human brain it provides an FM radio receiver that non-linearly resonantly interacts with the Schumann Resonance signal.  The phase locked loop or PLL is a particularly useful circuit block that is widely used in radio frequency or wireless applications in tech gear.  In view of its usefulness, the phase locked loop or PLL is found in many wireless, radio, and general electronic items from mobile phones to broadcast radios, televisions to Wi-Fi routers, walkie talkie radios to professional communications systems and very much more.

Mother Nature built this system over 3 billion years ago in the brain’s of living systems to inform cells of the seasonal connection between the sun and Earth so this data could be useful for biological changes.  In bipolar disorder this system is awry when it is encumbered by too much mass in the recievers.

The circadian activity generated in the SCN needs to be transmitted to the rest of the brain and henceforth to the rest of the body via non-optical signaling to stay well. In Bipolar Disorder this is impossible because the SCN is where the defect lies.  That receiver is not receptive to the Schumann’s information.  Coherent connection ruins the fidelity of the system.  Most of the centralized science right now believes it is through direct wiring tracts. I do not. I think it is via the hydrogen bonding network in water through the areas where there is no blood-brain barrier in the brain that provides the fidelity of the phased locked loop. This allows electron and proton tunneling and quantum coherence to allow for rapid communication in the system. I believe all biological processes in any living organism are due to the creation of biological biophotons in the ultraweak VUV-IR-A range. Light can dictate highly selective and specific electromagnetic interactions between particular biomolecules because of changes in mass or the magnetic moments of the component boxcars of biochemistry. In most cases, these interactions involve and are driven by semiconductive proteins surrounded by water, which act as logic gates do in the system of organization seen in solid-state physics.

The human brain SCN contains the key mechanism to having a strong diurnal pattern that assists the sun to maintain the circadian rhythm.   The Schumann Resonance signal continuously synchronizes the brain wave ELF patterns in a set range of grouped frequencies that begin in the thalamus that surrounds the 3rd ventricle of the brain.  The ventricular system also acts a resonant cavity on Earth to receive the signals.  The hydrogen bonding network in CSF is another receiver in the phased locked loop communication system mentioned above.  This stabilizes the brain’s electromagnetic system of communication and its fidelity has enabled intelligence and stable thinking to evolve to the point where this complex understanding of the biophysical environment interacting with the human brain can be reasoned, understood, and appreciated.

DNA only codes for the key backbone proteins that will become the main conductors of any life process within the organism. The mitochondrial matrix created the other part (water hydrogen bonding network) of this semiconductive backbone in cells to surround the protein.  Both parts of the semiconductor have to be operational to simulate time from your environment at the level of the SCN.  Everyone focuses on refraction errors in the eyes.  Few spend time understanding how the eye clock really operates at a quantum mechanical level with the Schumann frequency.  This is why psychiatry remains impotent to help reverse this disease.

Let’s review the lessons from 100’s of my blogs now in relation to this disease.

A. Hydrogen bonds form between water molecules, giving rise to supramolecular aggregates/clusters/coherent domains. Some call this EZ water.  The clustering of water is a cooperative phenomenon, which means that forming one hydrogen immediately favors the formation of several other hydrogen bonds, and vice versa, breaking one bond leads to breaking up a whole cluster. Thus clusters are dynamic flickering networks with lifetimes of 10^- 11 to 10^-10 seconds. Light changes those hydrogen bonding networks by moving charges around.
https://phys.org/news/2022-10-revolutionary-technique-hydrogen-efficiently.html

B. Hydrogen bonds are the key to coherence in cells. Hydrogen bonds act like a spec of dust in the formation of snow, ice, or crystals.

How do coherent excitations make the system sensitive to specific, weak signals? Such a weak signal will be received by the system only when the system is ‘in tune’ — rather like a very sensitive FM radio receiver, which can resonate to the signal. Furthermore, a small signal will be greatly amplified for it will not only affect one molecule, but because many other molecules are in the same state of readiness, they too, will be affected in the same way, and the signal is correspondingly multiplied as many times as there are molecules responding to it.

The shape of your ventricular system which is filled with H+/D is another clue for me that the receiver system is broken.

The hydrogen bonds in water have a critical point at which they change and act like dust. When enough energy is pumped in bond angles change and this makes water liquid crystalline and a better antenna to receive signals of what season it really is.  People bipolar disorder have bad antennas.

More lessons from old blogs you need to recall now to understand Bipolar:

C. Sunlight creates electric fields in our atmosphere every day and that sunlight creates a Coulomb force in our body. Coulomb force is an electrostatic force. Electrostatic phenomena arise from the forces that electric charges exert on each other. Such forces are described by Coulomb’s law. Even though electrostatically induced forces seem to be rather weak because of how we experience them in life, when the scale shrinks, as it does in a cell, the electrostatic force increases tremendously in strength as the scale drops. Scale drops = less mass present

D. For example, some electrostatic forces such as the one between an electron and a proton, that together make up a hydrogen atom, are about 36 orders of magnitude stronger than the gravitational force acting between them. The electrostatic force generated in your skin is another example of a strong electrostatic force because the skin, as an insulator can hold large amounts of charge from the sun if it is normal.  It is not in bipolar disorder.

E. Modern physics now has proven that energy and information are equivalent in physics. Landauer’s Principle of 1961 & Shannon’s 1948 work was critical in making this linkage. Modern quantum biology has experimentally proven that energy is trapped directly at the electronic level in cells. Energy is stored not only as vibrational and electronic bond energies in biochemicals, but also in the structure of the system: its membranes, and in gradients, fields and flow patterns, compartments, organelles, cell water, and tissues. All this in turn enables organisms to mobilize their energies coherently at any time it is needed and hence make available the entire spectrum of stored energies for physiological work. It is energy on demand by atomic design.

F. What is the bandwidth of the entire electromagnetic spectrum of light? The electromagnetic spectrum starts from wavelengths of 10^-14 m at one extreme to 10^8 m at the other, spanning a range of 10^22. In terms of doublings, 10^22 ≈ 273, or 73 octaves. Visible light is a small fraction of this bandwidth but that bandwidth does very specific things that cells take full advantage of.

Light is an EMF. Sunlight (visible light) is a very specific EMF that interacts with specificity for atoms in cells. That specificity is created because the EMF selects the type of water created by the dissipative system. This DDW water surrounds the atomic lattice inside cells whose integrity is maintained by the nuclear genome blueprint. The atomic arrangement in cells also allows for light absorption and light emission. The light that cells emit is also quite specific. It is an ultraweak extreme low-frequency biophoton that spans the visible spectrum frequencies. This is the light that is used for optical signaling and it drives the molecular resonances that drive the internal motions of biochemicals in cells. Light drives biochemistry. Biochemistry does not drive light.  

Conventional centralized biochemists do not understand these nuances of what biophotons are and how they are created by EMFs, water, and oxygen in cells. So You should not expect centralized physicians (psychiatrist) to get this nuance either.

G. Claude Shannon taught the world that information flows via entropy. All clocks should be thought of as flowmeters for entry. This includes the biological circadian clocks in cells. Wheeler taught physics that information and energy are one and the same thing. Shannon’s mathematics from his 1948 paper advanced the linkage of entropy and information. Shannon’s paper also told us anything can be a message.  (Kruse for Dummies lecture)  H+ and electrons are fermions.  Deuterium is a boson and this small difference can ruin how an FM antenna works.

I believe sunlight messages for mitochondrial DNA and nuclear are controlled by “fermion messaging” (pic above from old blogs). DNA is informed about what to do with optical information from the sun via mtDNA signaling (optical and free radical) and this message is transmitted over water’s hydrogen bonds adjacent to proteins in a cell. DNA is a very complex topologic insulator that is an antenna for our star’s information.

H. Water makes up 99% of molecules in every cell and it fills the ventricles of our brain. Water is a very small molecule that has more hydrogen bonds in it than any other compound. Liquid water contains the densest hydrogen bonding of any solvent, with almost as many hydrogen bonds as there are covalent bonds and hydrogen bonds in its structure found anywhere on Earth. These two bonding networks are the binary code in water. Just as a computer can use a 1 and 0 to create digital information on the internet, hydrogen bonds create the internet in your cells. Shannon taught us the information content of any kind of message could be measured in binary digits or just bits. This was the basis of the Kruse for Dummies talk. 

I. Water’s hydrogen bond network changes at a pico and femtosecond level in any environment. Inside a cell, its atomic arrangement is controlled by electrostatic forces in a cell created by the redox power of the mitochondria in that cell. These hydrogen bonds can rapidly rearrange in response to, light frequencies, charge density, and changing conditions and environments (for example, solutes like K+ in a cell).  This is how our ventricles tell seasons in us.  When the FM system is bad you cannot tell seasons and bipolar disorder is the result.  

J. Shannon demonstrated, contrary to what was commonly believed in the 1940s, that engineers could beat their worst enemy ever: transmission errors-or in their technical jargon, “noise.” Noise is anything that disturbs communication. Your FM radio antenna does not work when there is noise in the system.  It can be an electric signal in a telephone wire that causes crosstalk in an adjacent wire, a thunderstorm static that perturbs TV signals distorting the image on the screen, or a failure in network noise to increase the energy of the transmission signals or send the same message repeatedly-much as when, in a crowded pub, you have to shout for a beer several times. Shannon showed a better way to avoid errors without wasting so much energy and time: coding. Nature does the same thing.

She takes the message in the hydrogen bonding network of water that surrounds every protein and encodes that information in fermionic code in mRNA, mtDNA, RNA, tRNA, and DNA. Deuterium is a BOSON.  It ruins the fermionic signal and that CAUSES bipolar disorder.  

DO YOU GET IT YET?

K. Coding is at the heart of information theory. All communication processes need some sort of coding to limit the noise and create a high-fidelity signal that doesn’t degrade. Bipolar disorder is due to tissues in our FM radio station in our head having too much mass in them.  Water preserves the information and transfers it to nucleic acids via hydrogen bonds. Just as the telephone system transforms the spoken voice into electrical signals. In Morse code, letters are transmitted with combinations of dots and dashes. The DNA molecule specifies a protein’s structure with four types of genetic bases. Digital communication systems use bits to represent or encoded information. Each letter of the alphabet, for example, can be represented with a group of bits, a sequence of zeroes, and ones. You can assign any number of bits to each letter and arrange the bits in any way you want. In other words, you can create as many codes as desired. Cells have done this to run life’s program.  The more mass a tissue has the less time it can remain quantum coherent to transfer information in any system.  

All of these lettered lessons above ^^^^^ have been published in my blogs or forum for years.  Please ASSIMILATE THEM NOW.

If you do not believe me review this thread:  https://forum.jackkruse.com/threads/mitochondrial-thermodynamics-diy-lesson-thread.27408/

This blog was easy to write because piece and parts of it are in hundreds of other blogs.

The emission and absorption spectra of proteins can be used to make predictions of what light frequencies will couple with proteins and the matrix to create DDW water. The logic in the system of operation can only be comprehended when you understand how the subatomic parts of nature are able to be used and manipulated by quantum mechanical abilities. I told you a long time ago, in the Cold Thermogenesis series, that the default state of life was sleep.  Then as evolution progressed with evolved wakefulness.  This idea was counterintuitive to many at the time.  The reason for my prediction was simple.  I read Feynman’s 1982 paper on a computer simulating the physics of the environment and thought to myself what organ in humans fit his description of an ability to simulate the physics of Nature?  The SCN fit perfectly.

The SCN filled with deuterium and your CSF overhwelmed by deuterium is where bipolar disease comes from.  Patients with Bipolar Disorder also have a higher risk associated with retinal detachment, primary retinopathy, diabetes retinopathy, hypertensive retinopathy, and retinal vascular complications than the controls.  Now you all know why this blog came after the last one.

Please re-read QE # 44-47 again.  The concepts are there to explain this disease and all sleep disorders.  The last blog was on diabetic retinopathy.  Those patients also always have features of metabolic syndrome.  So do most mental disorders and sleep disorders.  Now you can see why they are all linked.  You have effectively broken the FM antenna station nature put inside your skull.  If you have insomnia, (yes, Sam this is for you)  part of your system in the periaqueductal grey area is broken in your brain because you loaded this area up with deuterium by using Netflix too often while travelling outside your time zone to omuch for your brain, and you decided to live in Chicago with all its associated nnEMF and population density.  It should be obvious why you cannot sleep with these circumstances, no?

What I am explaining to you now is where in the topological map of the human brain the POMC deficit is located leads to the phenotype of the disease we see in our clinics.  Patients with this disorder intuitively know they need more sun.  How they go about it is often incorrect as you see in cite 4 below.

Understanding the human eye and retina and linking it to entropy in a cell was the only quantum leap I made to understand this concept.  The flow of entropy is why I made this prediction back in 2010.  All molecular clocks are flow meters for entropy.  I knew the SCN had to be doing something unusual with the retina and the brain during sleep.  The SCN appears to be a perpetual motion machine built into the brain.  Feynman wrote a paper in 1982 stating he believed a quantum computer could simulate physics if it used a time crystal.

The SCN is a small computer in your eye that is simulating the physics of the environment between the sun and Earth to make the best predictions for cells in tissues.  In bipolar disease that time crystal is not working well because the mass inside of it put there by the light you allow ruins it.  Adding mass back to the water networks, using lithium is how lithium operates.  

The problem is the system fidelity operates at quantum mechanical precision with respect to mass and this is why results are so uneven in patients with this disease.  

CITES

https://www.psychiatryadvisor.com/home/topics/mood-disorders/bipolar-disorder/increased-metabolic-syndrome-prevalence-rates-linked-to-newly-diagnosed-bipolar-disorder/

https://www.patreon.com/posts/quantum-44-your-83629619

https://pubmed.ncbi.nlm.nih.gov/34994991/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1860187/

Adey W. R. Electromagnetic fields and the essence of living systems. In: J. Bach Anderson (ed). Modern Radio Science. Oxford University Press; 1990. p. 1–37.

Ahissar, E., Haidarliu, S., Zacksenhouse, M., 1997. Decoding temporally encoded sensory input by cortical oscillations and thalamic phase comparators. Proc. Nat. Acad. Sci. USA 94, 11633–11638.

Blackman C. F. ELF effects on calcium homeostasis. In: B. W. Wilson, R. G. Stevens, L. E. Anderson (eds). Extremely low frequency electromagnetic fields: The question of cancer. Columbus: Publ. Battelle Press, 1990: 187–208.

Cherry N. J. Schumann Resonances, a plausible biophysical mechanism for the human health effects of Solar/ Geomagnetic Activity. Nat Hazards 2002; 26: 279–331.

QUANTUM ENGINEERING #46: DIABETIC RETINOPATHY & A LOT MORE

video
play-sharp-fill

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-εas 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.

QUANTUM ENGINEERING #45: AUTISM & MELANIN/MELANOPSIN: A MIGRATION PROBLEM

MORE ON THE ipRGCs of the retina and SCN.  Someday if someone funds my research, autism might be the first topic I’d suggest we study.  Why?

Melanin seems to be important for migration of neurons in all mammals. I told you that in the recent blogs around melanin and metastasis.  And this idea clued me long ago in that I might be able to explain autism because of my unique perspective on melanocyte migration and how it links to melanopsin regeneration.

Implications of a lack melanin pigment in mothers and fathers and what this might mean to their germ lines that become a child?  Here is one of my kids above.

Today’s lesson is going to come from kitty.  Most of you know I love cats.  My favorite cat has always been the Siamese cat.  My first cat was one and my current cat (above) is a Siamese.  You might not know why I am fond of Siamese cats but you will soon.  They taught me a lot about melanin when I was a boy in New York City.

CATS & HUMANS WHO ARE ALBINOS HAVE A MELANOPSIN LESSON TO TEACH

Most albino human beings and albino cats lacking retinal pigment in the RPE have observable nystagmus and many exhibit strabismus. The optic chiasm (pic above) of albino mammals including human beings and cats shows that almost all their retinal ganglion cells cross at the optic chiasm with few uncrossed optic fibers. This shows you there is a problem with morphology in mammals neurulation patterns.  Something has to be behind this misrouting behavior.  My bet is a lack of melanin allows the stickier deuterium isotope to affect cell migration during neurulation of the mammalin brain due to the kinetic isotope effect of deuterium on hydrogen in cells.  One D controls 96 atoms of H+ (pic below).  I think the massive increase of atomic weight and the kinetic isotope effect are critical in the misrouting behavior of neurons and this has dramatic effects on organization of the visual system of mammals.  There are details about mammalian embryology that have lead me to this conclusion.  I think it might be behind what causes autism, as well.  A lack of melanin in the parents and their germ line cells maybe the precipatating event that begins this cascade of events on. I believe this idea is tied to autism because the effect is quite heterogenous in presentation, hence why they call autism a spectrum of disorders.

In 1965, C.L. Sheridan noticed that retinal ganglion cells originating in temporal retina of albino rats did not function well, hypothesizing that albino rats have fewer uncrossed, non-decussating optic fibers. R.D. Lund anatomically verified that albino rats have fewer non-decussating optic fibers compared to pigmented rats. For several years the abnormality of reduced non-decussating optic fibers at the optic chiasm in albinos was thought to be limited to rats and rabbits. Guillery reported atypical visual system organization in Siamese cats, but the association with albinism was not identified.

CIRCADIAN BIOLOGY ENTERS THE FRAY OF MY KITTY STORY

The mammalian SCN is controlled by light and temperature and by the ipRGC of melanopsin.  I told you that a long time ago in the Cold Thermogenesis #6 blog.  What else didn’t I mention back then?

In 1971, Creel initially published the connection between Siamese cats and albinism, and hypothesis that reduced non-decussating optic fibers likely is a “highly general transspecies phenomenon in albino mammals”.  Siamese cats all have blue eyes and blue eyes = less melanin in the iris.  Siamese cats, Himalayan mice, rats, and rabbits all express a mutation that is a temperature-sensitive pigmentation defect, that is, allowing pigment to show up only on the cold parts of the body.

This is why their coats are so grey and white (my kitty above).  Moreover, their retinae lack pigment too.  Many human infants are born with blue eyes because their brains are devoid of melanin because humans brains are born into life in an immature state.  That is the case for human blue eyes, but what about the cats?  Why do Siamese cats have blue eyes almost all time? It is not just their iris that has reduced melanin.  Here we see the interplay of UV light and cold and begin to understand why this link is present from an evolutionary standpoint.  Wide band gapped semiconductors can make the same light endogenously from atoms doped to proteins or via cooling environmental temperatures.  I believe this is the basis of where the mammalian dive reflex comes from.  Most humans who live at high latitudes where it is colder also tend to have blue eyes and blonde hair. The link is unmistakable when you realize it.

Cooling is usually occurs at surfaces in mammals (eccrine sweat glands) and most of their surface has arterioles loaded with higher levels of deuterium that act a Bose Einstein condensate because of deuterium unique nuclear spin.  This makes their surface something important.  It is called a topological insulator.  Mammals interiors are filled with fermions = electrons and H+ ions.  They follow Dirac fermion statistics.  Here we see a physical difference manifesting in mammals for some reason.

Is there a trade off for mammals who live in colder environments?  Yes there is.  what is it?

They have less visual and non visual photoreceptors in their sensory organs.

Is this true in human mammals too, Uncle Jack?  YEP.

Note when humans have normal pigmentation in the eye (RPE) tend to have optimized neuro-opthalmological migration in their visual system as well.  It appears melanin is a beacon for proper migration of neurons in the eye to deeper brain structures in humans.  This is critical in the eye because of the location of the SCN to the RPE.  The SCN controls the eye clock, circadian rhythms, and the pupillary response in mammals to bright light.  It also affects their behavior.  This is markedly changed in autistic kids.

In humans with pigmented retinae, retinal blood vessels spare the foveal area. In albino human retinae, blood vessels intrude into foveal area.  Pigmented human retina exhibit an avascular zone surrounding the fovea. Albinos do not exhibit this arrangement.  They have blood vessel encroach into their fovea.  Humans with destroyed RPE from diseases like diabetes get the very same neovascularization of the fovea.  This ruins their central vision over time.

This is a big clue for what decentralized clinicians should be looking for in human’s with autism.  If a lack of melanin is part of the pathophysiology of this disorder than we should see some subtle changes in OCT and their arteriole beds in the diencephalic derivative of the brain if we look for it, if I am correct.  I think a lack of melanin pigment initiates atavistic expression in autistic kids of the central and peripheral nervous system.  This lack of POMC or POMC translation leads to alterations in the melanopsin system that ruins normal neural migration.

The phenomenon is called atavism—this is the reappearance of a trait that had been lost during evolution before in the same species. In autism many of these kids cannot talk or interact with their species.  We know our nearest cousins cannot speak either.  We also know that early primates were loners and that social networking became a big trait later on in evolutionary history of the primate.  This is another throw back behavior seen in autism that would have been seen in transitional chimps on their way to us.  This change would not be found in our DNA either.  Our genes do not determine who we are, but with atavism, they can sometimes serve as reminders of our evolutionary past.  Functionally this is what autism in humans looks like to me from my current perspective.  Another big clue for my hypothesis is found in the embryology of the visual and auditory systems of mammals.

MELANIN IS ALSO A TIME CRYSTAL FOR EMBRYOGENESIS IN MAMMALS

Embryonic progression in albino mammals’ visual and auditory systems seem to also take a step back in evolutionary time and it seems this program is initiated by lack of melanin pigment.  Non albino animals do not exhibit this altered migratory pattern.  Abnormalities of optic chiasmic misrouting in albino mammals is a developmental field defect that is seen normally in preceding phylogeny. Complete crossing of optic neurons at the chiasm is a normal developmental event in vertebrates prior to mammals. This reinforces my beliefs that atavism is a central problem in understanding modern autism.

The presence of melanin pigment in the embryonic retina is the signal that initiates retinal ganglion cell pathway routing from the eye to the SCN and from the SCN deep into the brain. Insufficient coding for retinal pigment launches an earlier, more stable genetic package directing a different targeting of optic neurons and this results in autism.

Genetic makeup includes preserved earlier evolutionary features. Charles Darwin popularized atavism in the 1860s as the term for reappearance of ancestral characteristics in future generations.

Today we know that vision and hearing evolved together dating back to the PaxB gene, which is a single gene controlling eye and precursors to hearing (mechanoreceptors) in box jellyfish.  This occurred before independent Pax 2 and Pax 6 genes showed up in primates much later. There are evolutionary connections between eyes and mechanoreceptors of the inner ear to the extent that during evolution are linked to melanin generation in those sense organs.  I told you earlier in the series melanin was the favored semiconductor of all mammals post KT event.  This story fits this narrative as well.  If POMC/melanin is absent for any reason, it appears human neuroplastiticty allows sensory cells to shift their sensory modalities to an older phylogeny experienced in evolutionary history.  Why is this a big deal?  The melanopsin phylogeny predates even primate evolution in time.

I think this happens in modern humans because of a loss of information and energy transformation in the embryo due to a lack of POMC or POMC translation in the parents cells and their germ lines that create their child.  I think this is what autism is at its core.  It is lack of POMC that has huge implications for the neurulation of the diencephalon in humans and its really old relationship to melanopsin biology.

BACK TO THE CATS

What happens when cats lack melanin in their eyes?  Do they exhibit traits that mimic human autism?  They exhibit fewer photoreceptors, they have foveal/area centralis hypoplasia, & exhibit misrouting of the temporal retinal ganglion cells, while having a variation of geniculate terminations, and most importantly they develop vascular intrusion into foveal area.  They also exhibit abnormal cortical projections, and fewer cones in macular area.  Lacking pigment in the cat leads to some major migration problems in the adult form.  It seems albino kitties and Siamese cats have a lot in common with autism.

The animal model closest to organization of primate visual system studied the most is the albino cat. Albino cats have observable nystagmus, and many have strabismus. Figure 1 above pictures the optic chiasm of an OCA1 albino cat shows almost all retinal ganglion cells (RGCs) cross at the chiasm.

Not all of them do and the ones that do not cross tend to innervate areas they should not be in.  The non visual photoreceptor associated with these RGCs is melanopsin.  The number of binocular cells was found to be reduced in visual cortical areas of Brodman numbered 17, 18, and 19 in Siamese cats and albino cats.  This impairs their stereovision.  So these cats do not have great vision, but this is because they are adapted to colder environments with more blue light and less UV light.  Their SCN periodicity can be retuned by cold weather.  The trade off for their lack of melanin is altered neural migration in their brains.

This surface temperature thing is a big deal in mammals because our SCN changes its periodicity to temperature and light.  I believe this explains why autistic kids do not like temperature changes or being touched. (another sensory processing delay).  I have a sense why this happens in autistic kids because these changes are seen in cats as well who lack pigment.  Autistic kids have a broken topological insulator in their skin, eyes, and circulatory system.  I think they are exquisitely sensitive to the chiral pinch of deuterium in their blood and this creates a lot of endogenous light that overwhelms their system because they have poor melanin sheets within the basal levels of their skin.  This allows too much deuterium to leach out of the circulatory system and into the substance of their subcutaneous tissues.  These leaching of deuterium than alters non visual photoreceptors in that location.

There is some rather unique things to know about this situation.  Evolution seems very fond of the SCN melanopsin connections I mentioned in QE #44.  Why?  Melanopsin retinal ganglion cells are always completely crossed or bilaterally projected into suprachiasmatic nuclei above the optic chiasm and these projections are not affected by albinism in any mammals.  Interesting don’t you think?

I think this goes back to where melanopsin came from phylogenetically.  It came from our fish amphibian origins 380 million years ago.  Phylogenetically older connections are less abnormal in albino mammals by exhibiting a bilateral suprachiasmatic projection pathway to the SCN.  These tracts appear to be unaffected in albinos. This tells me this system is highly protected by evolution because of how important it is to be able to simulate the physics of your environment to be highly adaptable.  This also explains another peculiarity about the melanopsin system.

Melanopsin regeneratiion acts largely independently of the visual cycle. This tells me the melanopsin system has old roots in evolution and evolution has specifically made sure it did not co evolve similar mechanisms with the rod and cone system of the eye.  Melanopsin neurons also control pupillary size with the autonomic nervous fibers of the third cranial nerve.

When this system is disrupted we get mammals that are not adaptable at all.  This defines modern humans who are on the autism spectrum.  Most children with autism have trouble sleeping, which may exacerbate other challenges associated with the condition. Sleep problems hint at disruptions in the circadian clock, a cellular timer that keeps cells in sync with the day-night cycle. Vitamin A disruption causes sleep disorders.

I have a sense that we will find out in the future that autistic children have wiring defects in their chiasms and in their sensory relay pathways because of a broken Vitamin A cycle in the melanopsin system along with a lack of melanin and POMC activity in the germ cells. This Vitamin A problem will lead to science realizing these kids all have altered melanopsin regeneration pathways compared to humans that do not have this deficit.  I believe the melanopsin system has its own regeneration system because it is VITAL to accurate time crystal managment of the circadian mechanism you saw in the last blog.  The SCN simulates the physics of our environment to program our metabolism from these light signals.  This is broken in autism.

LACK OF POMC/MELANIN = ALTER MELANOPSIN REGENERATION = VITAMIN A PROBLEM

Vitamin A is necessary for normal embryonic development in humans, but its role in the adult brain is poorly understood by centralized science in 2023. Vitamin A derivatives, called retinoids, are involved in a complex signaling pathway that regulates gene expression and, in the central nervous system, controls neuronal differentiation and neural tube patterning.

There is another reason why I think this Vitamin A, melanin, melanopsin story is linked to autism.  Most people know that the majority of melanin in the eye is in the RPE.  What many however do not know is that the photosensitivity melanopsin requires a steady supply of cis-retinaldehyde, a type of retinoid. The primary source of this vitamin chromophore (328nm) in the vertebrate eye comes from a complex multistep enzymatic pathway, known as the retinoid or visual cycle (above).  In this cycle by 11-cis retinaldehyde is regenerated from bleached alltrans originating in photoreceptor outer segments of rods. The critical elements of this pathway occur in the retinal pigment epithelium (RPE). Here is the problem.  Since melanopsin is found in the more superficial layers of the retina, quite distant from the RPE, it would seem poorly placed to obtain cis-retinaldehyde from this RPE source. So how does melanopsin do it?  Why does it have its own regeneration pathway separate from rods and cones?

Chromophore regeneration in rod photoreceptors relies solely on a tissue adjacent to the rod and cone layer of the retinal pigment epithelium. Cone photoreceptors rely both on the RPE and Müller glia, which traverse the entire depth of the retina to regenerate.  Melanopsin doesn’t use either system.

In the mammalian photoptic retina light activates melanopsin to trigger a G protein cascade that causes membrane depolarization.  The ipRGCs/melanopsin  response is opposite to that seen in our rods and cones, which hyperpolarize, but resembles the actions of photoreceptors found in invertebrates like fruit flies and horseshoe crabs. This system exhibits atavism mentioned above.  In humans, ipRGCs fire spikes. They are understood to use glutamate as their primary neurotransmitter; uniquely among RGCs, they also express a peptide neurotransmitter called PACAP (pituitary adenylate cyclase activating peptide).

Known influences of ipRGCs extend well beyond their direct targets. Examples are regulation of melatonin synthesis in the pineal gland and the development of synaptic plasticity in the hippocampus.  I believe they drive synaptic plasticity in all of our brain’s circuits and this is why melanopsin is the most numerous opsin in humans.

Why do I mention this detail?  Most people forgot human embryology of the brain and skin. They have forgotten that Vitamin A/retinoic acid have massive effects in the morphogenesis and growth of the neural tube.  Not only will deuterium affect neural migration from the notochord, but the chemical signal governing it is likely also awry.  Most of which can be explained by defective notochord signalling.  This would cause neurulation defects from the thalamus to the adult hemispheres.  This process is how humans create their hemispheres in the last trimester and postnatally.  This set of circumstances fits the modern phenotype of autism based upon my knowledge of human brain embryology.  I think the key problem in the autistic embryo is a problem of Vitamin A signaling being comingled in the eye, optic chiasm, hypothalamus, thalamus and eventually the neocortex in humans.  This would create a wide spectrum phenotype in the adult human.

Modern humans are new phylogenetic creatures in evolution and we know that optic projections near chiasm projecting into hypothalamus antecede vertebrates evolution because they occurred in early chordates.  Chordates first appeared on Earth 590 million years ago. Those are the animals that innovated melanopsin originally.

It appears that fact surprised Dr. Huberman and Dr. Berson based on what Huberman said in the Rubin podcast.  It did not shock me because I knew mammals came from early chordates because of my time in the Museum of Natural History in New York.  This is why it made sense to me why we had melanopsin in our brains.  I was shocked to learn in 2014-2017 that we also have it all our blood vessels, skin, fat, and our outer inferior retina.  Nature does not make mistakes.

This is my kitty today as I write this blog.  She likes IR-A and UV-A light now.  I have a sense all parents with autism need to learn a lot more about full spectrum sunlight and the key frequencies of IR-A light and the 380 nm light that controls the photorepair mechanisms in mammals.  When they do, they will realize how to help fix the problem they created by their abuse of blue light and tech screens.

SUMMARY

When I was 8 was the first time I got a Siamese cat.  I asked the lady at the museum why my cats eyes were different colors than other cats and she did not know the answer.  She told me she’d find out and few weeks later I found out about melanin as an 8 year old kid.  She told me all chordates had retinal pigments matching vertebrates.  Humans were the latest version of vertebrates.  That lesson would come in big later in my life.  I never forgot about my kitty’s eyes.  And that is why it never surprised me that the melanopsin chromophore showed up in human brain.  My childhood was prepping me for a later discovery around this amazing protein.  People with autism one day may thank Siamese cats for solving this enigma disorder for centralized science.

CITES

1. Sheridan CL. Interocular transfer of brightness and pattern discriminations in normal and corpus callosum sectioned rats. Journal of Comparative and Physiological Psychology. 1965;59:292-294

2. Lund RC. Uncrossed visual pathways of hooded and albino rats. Science. 1965;149:1505-1507

3. Giolli RA, Guthrie MD. The primary optic projections in the rabbit: An experimental degeneration study. The Journal of Comparative Neurology. 1969;136:99-126

4. Guillery RW. An abnormal retinogeniculate projection in Siamese cats. Brain Research. 1969;14:739-741

5. Creel DJ. Visual system anomaly associated with albinism in the cat. Nature. 1971;231:465-466

6. Creel DJ. Differences of ipsilateral and contralateral visually evoked responses in cats: Strains compared. Journal of Comparative and Physiological Psychology. 1971;77:161-165

7. Creel D, Witkop CJ Jr, King RA. Asymmetric visually evoked potentials in human albinos: Evidence for visual system anomalies. Investigative Ophthalmology & Visual Science. 1974;13(6):430-440

8. Sanderson KJ. Retinogeniculate projections in the rabbits of the albino allelomorphic series1. The Journal of Comparative Neurology. 1975;159:15-27

9. Creel DJ, Giolli RA. Retinogeniculate projections in albino and ocularly hypopigmented rats. The Journal of Comparative Neurology. 1976;166:445-455

10. Guillery RW, Oberdorfer MD, Murphy EH. Abnormal retino-geniculate and geniculo-cortical pathways in several genetically distinct color phases of the mink (Mustela vison). The Journal of Comparative Neurology. 1979;185:623-655

11. Piatigorsky J, Kozmik Z. Cubozoan jellyfish: An Evo/Devo model for eyes and other sensory systems. The International Journal of Developmental Biology. 2004;48(8-9):719-729

12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1571178/

13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6601915/

14. https://www.cell.com/cell-reports/pdf/S2211-1247(18)31754-6.pdf

QUANTUM ENGINEERING # 44: YOUR SCN IS A LONGEVITY TIME CRYSTAL

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The SCN is an optical lattice clock that pays attention to all the zip codes in a cell and functions as a true time crystal.  It mitochondria imprint the time signal into the water & melatonin that the SCN’s mitochondrial create.  This amazing part of the brain and a direct target of the ipRGC’s of melanopsin from the inferior nasal portions of the retina. (slide below from my Vermont 2018 talk)

I discussed time crystals in my 2018 Vermont talk briefly and told my members they were first thought about in 1982, rediscovered in 2012, and physically discovered in 2014.  Today, in 2023, the time crystal is a new category of phases of matter, expanding the definition of what a phase is. All other known phases, like water or ice, are in thermal equilibrium: time crystals are dissipative far from equillibrium structures.  Their constituent atoms have settled into the state with the lowest energy permitted by the ambient temperature in the environment, and their properties don’t change with time. This makes them a perfect metronome to keep time for multiple zip codes that exist in cells.  The time crystal is the first “out-of-equilibrium” phase: It has order and perfect stability despite being in an excited and evolving state.  This makes it highly responsive to light photons to create the tick-tock of periodicity that exists in circadian controlled mechanisms.

Essentially a time crystal is an object whose parts move in a regular, repeating cycle, sustaining this constant change without burning any energy. they are harvesting information in the system to create order from chaos.

The consequence is amazing: You appear to evade the second law of thermodynamics, which states that disorder always increases over time.  We know from Maxwell’s work in “demon’s” and the work of Lindauer, that there is an infantessimal requirement of energy and information loss, so that this state of matter still has to obey all of physics laws.  Kruse for Dummies attendees heard this in my presentation.  Because of this, this explains why all living things must sleep.  In sleep this debt is paid back to the system to remain highly ordered time crystal.  I told you a long time ago, in the Cold Thermogenesis series, that the default state of life was sleep.  Then as evolution progressed with evolved wakefulness.  This idea was counterintuiitve to many at the time.  The reason for my prediction was simple.  I read Feynman;’s 1982 paper and thought to myself what organ in humans fit his description of an ability to simulate the physics of Nature?  The SCN fit perfectly.

When I read the paper in my residency I immediately thought to myself is this what the SCN is doing for the body?  It is an organ that can simulate the physics of the environment to inform the rest of the body of that information to create some semblance of order.  Everybody knows that perpetual motion machines are impossible. However, in quantum physics perpetual motion is okay as long as we keep our eyes closed and do not observe it. By sneaking through this crack we can make time crystals operate.  This mimics sleep.

My intuition was rewarded in 2012, when Physics Nobel Laureate Frank Wilczek theorized that time crystals had to exist and they were finally identified in 2014- 2016.  Time crystals exhibit the bizarre property of being in constant, repeating motion in time despite no external input. Their atoms are constantly oscillating, spinning, or moving first in one direction, and then the other.  The recipe for a time crystal is below.

Note the bottom part of the picture above.  This appears to be exactly what is happening when sunlight hits the RPE in the eye and send photonic information to the SCN with no synapsing in between.  The information stream is UNINTERRUPTED.  This is unusual in the mammalian retina.  Almost every tract in the eye synapses before it gets into the brain.  This one does not.  Interestingly the same tract sends uniterrupted information of light to the habenular nucleus that controls mood and behavior in mammals.  It also makes sense why the same intrinsic photoreceptor retinal ganglion cells of this melanopsin tract send its information to the habenular nucleus of the thalamus.

The eye is the off and on switch for time for the entire diencephalon of mammals.  This turns on and off the brain.  It made sense to me finally why the thalamus created alpha waves of 7.83 Hz prior to sleep cycling.  The thalamus has to be able to record the asymetry of light and day accurately to awaken the rest fo the brain from the default state.  It turns out few people have realized the Schumann resonance on Earth varies day to night.  This helps attune the periodicity of our time crystals in the SCN.  They become more accurate clocks as periodicity increases.

A coupling between geomagnetic activity and the human nervous system’s function has now been fully identified by virtue of continuous monitoring of heart rate variability (HRV) and the time-varying geomagnetic field over a 31-day period in a group of 10 individuals who went about their normal day-to-day lives. (paper above)

It was found that the participants’ HRV rhythms synchronized across the 31-day period at a period of approximately 2.5 days, even though all participants were in separate locations on Earth.  This tells us the ability is built into all mammals. Overall, this suggests that daily autonomic nervous system activity not only responds to changes in solar and geomagnetic activity, but is synchronized with the time-varying magnetic fields associated with geomagnetic field-line resonances and Schumann resonances.  Biology is amazing when you observe its abilities.

The Schuman resonance is a charging opportunity for the human brain’s time crystals:  How do cells charge?

Charging by friction – this is useful for charging insulators/semiconductors. If you rub one material with another (say, a plastic ruler with a piece of paper towel), electrons have a tendency to be transferred from one material to the other. For example, rubbing glass with silk or saran wrap generally leaves the glass with a positive charge; rubbing PVC rod with fur generally gives the rod a negative charge.  Vortexing liquid crystals semiconductors also creates friction which can generate a charge that is quantized.  This is how water gains charge in the circulatory system via turbulent flow around the cells in blood plasma.

Charging by conduction – useful for charging metals and other conductors. If a charged object touches a conductor, some charge will be transferred between the object and the conductor, charging the conductor with the same sign as the charge on the object. RBC’s are conductors and can transfer their charge to water in blood plasma.  This is why coherent domains in water develops a net negative charge when it forms.  This is how you build redox power in sunlight because charge is being transferred.

Charging by induction – also useful for charging metals (dopants on our semiconductors) and other conductors. Again, a charged object is used, but this time it is only brought close to the conductor, and does not touch it.  This mimics how sunlight interacts with melanin, hemoglobin and chloroplasts in living systems in trapping light energy before it changes to an electric charge in the coherent domains water.  To gain the charge best from sunlight you need to be grounded to Earth.   If the conductor is connected to ground (ground is basically anything neutral that can give up electrons to, or take electrons from, an object), electrons will either flow on to it or away from it. When the ground connection is removed , the conductor will have a charge opposite in sign to that of the charged object.  This is why being disconnected from Earth chronically leads to things like rouleux formation and clotting.  Since water molecules, are naturally polarized (magnetic dipole), they can quickly remove charge from a charged object.  This is why blood is 93% water by volume.  Mother Nature uses every last bit of physics the universe gives her to work with.

On sunny clear days with low humidity are associated with ionospheres with high electric fields, low magnetic fields and diminished energy transfer from the sun to us if we do not have a connection to Earth.  Why?  Electrostatic charges are not transferred well when water is not present in the ionosphere.  This is why dehydration from a lack or water production in mitochondria favors illness. It is also why deuterium is not favored by living systems in nature.  It cannot transfer charge as well as light hydrogen can, because its extra mass affects bonding strengths in all molecules it is used in.  This is why life tries to exclude it. (kinetic isotope effect = one D controls 96 H+ atoms)  This restricts semiconductive flow from eye, skin, and gut to internal structures.

Dry air is a relatively good electrical insulator, so if something is charged, like clouds on a sunny day,  the charge tends to stay in th cloud where the water is. In more humid conditions, such as you find on a typical summer day in New Orleans, water molecules, become polarized because water is a magnetic dipole, as such, theycan quickly remove “a charge” from a charged object.  This is why the southeast has massive electrical storms.  Electrical storms are how the Schumann resonance on Earth is formed.  It is also why humans can get massive benefits even in cloudy weather in the southeast but the same is not true in Seattle.  Seattle has the clouds but not the humidity or the electric storms of the Southeast.  The humidity of the ionosphere does not allow charge transfer from the solar plasma to the ionosphere to out wide band gapped wetware carbon based semiconductors.

LINK TO THE KRUSE FOR DUMMIES LECTURE

Your brain is filled with water (CSF) next to your thalamus.  CSF is deuterium depleted water.  You probably understand why it is this way now if you listened to the Kruse for Dummies lecture.  H+ transfers charge better in the brain than deuterium can.  It is designed to sense this daily diurnal change of the Schumann resonance created by these electrical storms. This is why living further south where these storms are more common is longevity building 101 behavior for mammals who want high fidelity information.

The NC State research findings on water raises some interesting questions about the behavior of liquids when confined at a small scale in a cell or inside a mitochondria.  It appear life took big advantage of this”sheet effect”  3.8 billion years ago when bacteria first showed up on Earth because it held promise for shaping future energy-storage technologies for cells who could take advantage of it.

When water is depleted of its atomic mass it improves its magnetic moment while restricting the heavy deuterium in our blood and out of our tissues.  This creates a unique surface on mitochondria.  I talked about that unique surface here.  Surface changes are a change in topology. This helps to preserve stability of hydrogen bond networks in the coherent domains inside of cells, protecting against aneuploidy in chromosomes and resisting strand breaks in nucleic acids.  This also lengthens our telomeres and gives us longevity.  It also allows for optimized non linear optical signaling within the cell to preserve the liquid crystaline structure inside the cell in water.  That water sits adjacent to your protein semiconductors who work by Fermion statistics in the topology.  This can affect a persons ability to handle a stressed environment who is exposed to nnEMF radiation, blue light, or food eaten out of season or from the wrong latitude. It likely is the reasonn autism exists.

Blood is designed to carry this charge information like a Jacquard card from the sun.  Moroever, the information is in quantized format (H+/D ratio in the spectrum of light) to mitochondria for processing.  It does this for sunlight and it does it for food as well.  Food is broken down in the gut and carried to cells in lipid rafts in our cell membranes that act as electric field sensors for our environment. Our food grown locally in our environment has its hydrogen stripped off and are broken down to electrons.  Allopathic medicine and functional medicine remain ignorant of how charge is quantized and how that effect is brought to bear massive effects in tissue to our mitochondrial colonies.  We have ten to the 14th mitochondrion in our cells.  This far outstrips the bacterial colonies we have in our gut.

Anyone who tells you the microbiome control our health is some expert you need to avoid.  The math of quantum biology says otherwise.

What is the special ability “time crystals” afford cells?

Time crystals could be used to build quantum devices that work at room temperatures in a wet environment.  The wet environment would provide the quibits in the form of H+ and deuterium as its binary code.

Time crystals are also the first objects to spontaneously break “time-translation symmetry,” the usual rule that a stable object will remain the same throughout time. A time crystal is an engima because it is both stable and ever-changing, with special moments that come at periodic intervals in time.  Its periodicity links to its accuracy as a time piece.  In this way all time crystals should be thought of as flow meters to measure entropy.  This is what time functionally is.

In Feynman’s 1982 paper proposing time crystals in quantum computers/devices, the physicist argued that they could be used to simulate the particles of any imaginable quantum system.  A time crystal exemplifies that vision. It’s a quantum object that nature has created in your eye in the middle of your retina-hypothalamic tract, and given its complex combination of delicate ingredients it is capable of imagining and conjuring up the recipe provide to it by the local environment to create a solution for those conditions of existence that allow for the lowest entropy state.  These neurons in the SCN filled with melanopsin and POMC are stirred to action to decipher the best code for cells by using nature’s most baffling laws as their substrate.  The basis of their action is H+ and deuterium levels at the atomic level.  My members who listened to the Kruse for Dummies lecture are probably smiling now because this blog really makes sense to them now.

SUMMARY

There have always been certain “Rules of the Road” when it comes to our Universe, and one of them is the Second Law of Thermodynamics.

This law states that when energy changes from one form to another, or when matter moves freely, entropy (disorder) in a closed system always increases. Entropy is a measure of the spread of matter and energy to everywhere in the Universe to which it has access.

The best way to understand entropy is to consider my kitchen: Every day there are dirty dishes in the sink and the countertops are covered with various substances. Every day, I wash the dishes and clean the countertops, thus decreasing their entropy, but the very next day, the sink is again full of dirty dishes and the counters are covered.

How can something move, and keep moving forever, without expending energy? At the outset, this seemed an absurd idea — a major break from the accepted laws of physics. But Wilczek’s papers on quantum and classical time crystals (the latter co-authored by Alfred Shapere of the University of Kentucky) survived a panel of expert reviewers and were published in Physical Review Letters in October 2012. Wilczek didn’t claim to know whether objects that break the symmetry of time exist in nature, but he wanted experimentalists to try to make one.

“It’s like you draw targets and wait for arrows to hit them,” he said. “If there’s no logical barrier to this behavior being realized, then I expect it will be realized.”

The experimentalist found his idea in Nature.

My axiom:  What Nature does not forbid eventually occurs. This is a true evolutionary axiom.  And “time crystals” seem to be one of the first states of matter cells innovated billions of years ago on Earth when life was simple in its bacterial and Archean formats.

“Time crystals” — are physical structures that move in a repeating pattern, like minute hands rounding clocks, without expending energy or ever winding down. Unlike clocks or any other known objects, time crystals derive their movement not from stored energy but from a break in the symmetry of time, enabling a special form of perpetual motion to exist.  Once this idea was thought to be crazy, it is now been proven to exist in Nature.

The SCN is the most special state of matter in you because it is where your time crystal story begins and orders everything important in your cells.  Something that’s this stable makes it so unusual, and because of this, special things become useful to the organism.  Now it makes total sense to me why the retina wires directly to the SCN and the habenular nucleus in the thalamus.

This is how our time crystals in our eye clock tell the rest of the body to simulate the physics inside of cells.  This choses what biochemical pathways are best to create the best chance of survival on that day.  EVOLUTION IS HAPPENING EVERY SECOND YOU ARE ALIVE.  Most have no idea this is true.  When you interupt the pathway from the environment to your time crystals disease is the result.

WHEN YOU KNOW BETTER YOU DO BETTER

Time for you to level up you knowledge.  

Next blog in this series on Autism will floor you.  It links directly to this blog.

CITES

1. https://link.springer.com/article/10.1007/BF02650179

2. “Nonlinear two-level dynamics of quantum time crystals” by S. Autti, P. J. Heikkinen, J. Nissinen, J. T. Mäkinen, G. E. Volovik, V. V. Zavyalov and V. B. Eltsov, 2 June 2022, Nature Communications.

DOI: 10.1038/s41467-022-30783-w

3. https://ai.googleblog.com/2021/06/achieving-precision-in-quantum-material.html

4. https://www.quantamagazine.org/perpetual-motion-test-could-amend-theory-of-time-20130425/

5. https://journals.aps.org/prl/abstract/10.1103/PhysRevLett.118.030401

6. https://physicsworld.com/a/time-crystals-the-search-for-a-new-phase-of-matter/

7. https://agupubs.onlinelibrary.wiley.com/doi/full/10.1029/2006RS003456

8. https://news.ncsu.edu/2017/04/water-pseudocapacitors-2017/

9. https://optimalklubs.com/kruse-for-dummies-general/

10. https://www.patreon.com/posts/14768134

QUANTUM ENGINEERING #43: POMC’s SCULPTING OF MAN

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The first primate-like mammals, or proto-primates, evolved in the early Paleocene Epoch (65.5-55.8 million years ago) at the beginning of the Cenozoic Era. They were roughly similar to squirrels and tree shrews in size and appearance. The existing, very fragmentary fossil evidence (from Asia, Europe, North Africa, and especially Western North America) suggests that they were adapted to an arboreal way of life in warm, moist climates.

They probably were equipped with relatively good eyesight as well as hands and feet adapted for climbing in trees. These primate-like mammals (Plesiadapiformes) would remain rather shadowy creatures for us until more fossil data become available. These animals bodies were rapidly changed by POMC, specifically ACTH, and the appearance of flowering plants bearing fruit loaded with deuterium. This raised their blood sugar and insulin levels to stimulate the rapid sexual development we see today in humans called precocious puberty. This is why they changed so rapidly and why they radiated so quickly once the sun returned to Earth. Slowly over time, both parts of the POMC gene sculpted early mammals to become primates in the ten million years after KT.

The primate-like mammals do not seem to have played an important role in the general transformation of terrestrial animal life immediately following the massive KT global extinction of plants and animals that occurred about 65,500,000 years ago. The most dramatic changes were brought about by the emergence of grazing and browsing mammals with tough hoofs, grinding teeth, and digestive tracts specialized for the processing of grass, leaves, and other fibrous plant materials. The evolution of these herbivorous mammals provided the opportunity for the evolution of the carnivorous mammals that specialized to eat them. Sorry, PETA but Nature does not care about ideology. These new hunters and scavengers included the evolutionary lines that would later produce the dogs, cats, and bears of our time.  Adaptive radiation was resulting in the rapid evolution of new species to fill expanding ecological niches, or food-getting opportunities. Most of these new animals were placental mammals and their interiors were being filled with melanin. With the exception of bats, none of them reached Australia and New Guinea. This explains why they did not exist there until people brought them in recent times. South America had also drifted away from Africa and was no longer connected to North America after 80,000,000 years ago. However, around 20,000,000 years ago, South America reconnected with North America and placental mammals streamed in for the first time, resulting in the extinction of most of the existing marsupials there.

The beginning of the Eocene Epoch (55.8-33.9 million years ago) coincides with the emergence of early forms of most of the placental mammal orders that are present today. In addition, placental mammals with larger bodies and bigger brains began to appear in the fossil record at this time. Paul Falkowski has suggested that this is due to the fact that the amount of oxygen in the earth’s atmosphere more or less doubled around 50 million years ago. Larger mammals have relatively fewer capillaries for the distribution of oxygen to the cells of their bodies. Subsequently, they must breathe air that is more oxygenated. Brains have especially high oxygen requirements. In addition, pregnant placental mammals must transmit a substantial portion of the oxygen in their blood to their fetuses. Coinciding with the increase in atmospheric oxygen at the beginning of the Eocene Epoch was a relatively abrupt global warming of 9-16 F. (5-9 C.) lasting at least 200,000 years. This also would have been a major factor in the rapid evolution of animals and plants at the time. Overall, climates were significantly warmer during the Eocene than now. There were crocodiles in the Arctic, pine forests in the Antarctic, and palm trees in Wyoming. There was no polar ice. As a consequence, sea levels were close to 330 feet higher than today. Sea rise is likely critical in the primate clade for future encephalization.

The first true primates evolved 55 million years ago or a bit earlier, near the beginning of the Eocene Epoch. Their fossils have been found in North America, Europe, and Asia. They looked different from the primates today. They were still somewhat squirrel-like in size and appearance, but apparently, they had grasping hands and feet that were increasingly more efficient in manipulating objects and climbing trees. The position of their eyes indicates that they were developing more effective stereoscopic vision as well.

Major evolutionary changes were beginning in some of the Eocene prosimians that foreshadow species yet to come. Their brains and eyes were becoming larger, while their snouts were getting smaller. At the base of a skull, there is a hole through which the spinal cord passes. This opening is the foramen magnum (literally the “large hole or opening” in Latin). The position of the foramen magnum is a strong indicator of the angle of the spinal column to the head and subsequently, whether the body is habitually horizontal (like a horse) or vertical (like a monkey). During the Eocene, the foramen magnum in some primate species was beginning to move from the back of the skull toward the center. This suggests that they were beginning to hold their bodies erect while hopping and sitting, like modern lemurs, galagos, and tarsiers. By the end of the Eocene Epoch, many of the prosimian species had become extinct. This may be connected with cooler temperatures which helped drive the evolution of wide-band gapped semiconductors in cells because they work better to create more VUV light to sculpt the mammalian body plan and the appearance of the first monkeys during the transition to the next geologic epoch, the Oligocene period happens about 34 million years ago.

Early Monkeys and Apes
The body size of mammals in many species lines progressively increased after the end of the age of dinosaurs as they took advantage of the vast expanses of land and plant food made available by the extinction of the giant reptiles. The biggest land mammals ever to live evolved around 39-40 million years ago (near the end of the Eocene Epoch) and flourished during the subsequent Oligocene Epoch (33.9-23 million years ago). The largest of them was a hornless rhinoceros (Indricotherium transouralicum) living in Eurasia that weighed 16.5 tons (15,000 kg.) and stood 18 feet (5.5 m.) at the shoulders. By comparison, the biggest African elephants today weigh 6.7 tons (6,046 kg.) and stand 13 feet (4 m.) at the shoulders.

Unfortunately, the Oligocene Epoch was largely a gap in the primate fossil record in most parts of the world. This is especially true for prosimian fossils. Most of what we know about them came from the Fayum deposits in Western Egypt. While this area is a desert today, 36-31 million years ago it was a tropical rainforest on the edge of a large lake or sea. The marine chain was always close to these animals.

Monkeys evolved during the early Oligocene or possibly near the end of the Eocene. Their ancestors were most likely prosimians. These monkeys were the first species of our infra order–the Anthropoidea. Several genera of early monkeys have been identified.  Apidium and Aegyptopithecus are the most well-known. The former was about the size of a fat squirrel (2-3 pounds or .9-1.4 kg.), while the latter was the size of a small dog (13-20 pounds or 5.9-9.1 kg.). Compared to the prosimians, they had fewer teeth, less fox-like snouts, larger brains, and increasingly more forward-looking eyes. These and other anatomical features suggest that the early monkeys were becoming mostly diurnal fruit and seed-eating forest tree-dwellers.

New World monkeys appeared for the first time about 30 million years ago. It is generally thought that they began as isolated groups of Old World monkeys that somehow drifted to South America either from North America or Africa on large clumps of vegetation and soil. The evidence suggests that Africa is the most likely continent of origin. Such “floating islands” produced as a result of powerful storms tearing at the land still occur in tropical regions of the world today. It is likely that other kinds of small animals were transported to South America in this way as well.

Due to the comparative scarcity of Oligocene Epoch prosimians in the fossil record, it is generally believed that the monkeys out-competed and replaced them in most environments at that time. Supporting this hypothesis is the fact that modern prosimians either live in locations where monkeys and apes are absent or they are normally active only at nighttime when most of the larger, more intelligent primates are sleeping.

The Oligocene was an epoch of major geological change with resulting regional climate shifts that likely affected the direction of evolution and altered fossil preservation conditions. By the beginning of the Oligocene, North America, and Europe drifted apart and became distinct continents. The Great Rift Valley system of East Africa also was formed during the Oligocene along a 1200-mile-long volcanically active fault zone between tectonic plates that are moving away from each other. We believe this is the cradle of man.

^^^^AVAGADRO’S NUMBER ON DISPLAY IN METABOLIC WATER

This created an easy north-south regional migration route for animals. Around 120 million years ago, the tectonic plate that forms the Indian subcontinent began to rapidly drift north across the Indian Ocean from Antarctica. By 50.5 million years ago, India began crashing into Asia at a rate of 10-12 inches (25-30 cm.) a year and continues to do so today forming the Sahara desert. The crashing of India turned a rainforest and ocean in Africa into a desert. This has progressively forced up the Himalayan chain of mountains and the high Tibetan Plateau beyond. During the Oligocene, the continuing growth of this immense barrier altered continental weather patterns significantly by redirecting the summer monsoonal rains to the east. This created a vast arid rain shadow region in Central Asia and very likely triggered global climate changes. The cooling and drying trend with the associated expansion of grasslands that had begun in the late Eocene Epoch accelerated, especially in the northern hemisphere. A result was the general disappearance of primates from these northern areas. However, climates in most regions were still warmer than today.

By 16-14 million years ago, in the middle of the Miocene Epoch (23-5.3 million years ago), the ongoing movement of tectonic plates in the Great Rift Valley system created new volcanic mountain chains in east Central Africa. These in turn altered local weather patterns. Some areas became wetter while others more arid due to local rain shadows. In addition, the progressive global cooling trend continued. Growing polar ice caps reduced the amount of water in the oceans, causing sea levels to drop. This exposed previously submerged coastal lands. As a result of this and continental drift, a land connection was reestablished between Africa and Eurasia along the eastern Mediterranean Sea coast that provided a migration route for primates and other animals between these continents. Much of the East African and South Asian tropical forests began to be replaced by sparse woodlands and dry grasslands because of climate changes. As a result, there were new selective pressures affecting primate evolution.

Primate fossils are common from the Miocene. However, not all primates are equally represented in the fossil record. Apes apparently evolved from monkeys early in this epoch. Fossil monkeys and prosimians are comparatively rare from most of the Miocene, but apes are common. It appears that apes at that time occupied some ecological niches that would later be filled by monkeys. One of the earliest of the monkey-to-ape transitional primates was Proconsul. It lived in African forests 21-14 million years ago.

Among the numerous Miocene primate species were the ancestors of all modern apes and humans. By 14 million years ago, the group of apes that included our ancestors were apparently in the process of adapting to life on the edges of the expanding savannas in Southern Europe. They were very likely members of the genus Dryopithecus, which were generally similar in appearance to modern African apes. These apes evolved mostly during a relatively short global heat wave that began around 15 million years ago. This caused enough polar ice to melt so that sea levels once again rose 80-130 feet.

Toward the end of the Miocene, less hospitable cooler conditions in the northern hemisphere once again caused many primate species to become extinct while some survived by migrating south into Africa and South Asia where it remained relatively warm. About 8-9 million years ago, the descendants of the dryopithecines. in Africa diverged into two lines–one that led to gorillas and another to humans, chimpanzees, and bonobos. Around 7 million years ago, a further divergence occurred which separated the ancestors of modern chimpanzees and bonobos from the early hominins (human-like primates) that were our direct ancestors.

Who Are We, Really?

The more clearly we can focus our attention on the wonders and realities of the universe about us the less taste we shall have for the destruction of our species. Wonder and humility are wholesome emotions, and they do not exist side by side with a lust for destruction.  Where we invest our time and attention is MORE important than how we invest our money.  Time is the most valuable asset most waste.  Do things in life, be clenched, and curious. Do not wait for inspiration’s shove or society’s kiss on your forehead. Pay attention.  In fact, pay deep attention.   It’s all about paying attention. Attention is vital to your humanity. It connects you with others. It makes you eager, to learn and be curious.

If you are a paleoanthropologist or archeologist you think fossils are the Rosetta Stone for discovering the path that human evolution took. If you are a proteomic evolutionary biochemist you think molecular arrays are the best way to decipher the tea leaves of Mother Nature ways. If you are a geneticist you think RNA/DNA is the Holy Grail of human evolution. If you are a dental specialist, like University of Arkansas professor, Dr. Peter Ungar you think it’s all about the mammalian teeth.

Today’s bro scientists on the internet like to define evolutionary thinking by thinking about the Paleolithic epoch and how it might have shaped the hominid tree. The Paleolithic shaped the tree to be sure, but had nothing to do with planting the acorn.  What we came from was alien to who we are now.

Our complexity came from a binary code that became more able to bend and expand the neural tube of primates.  Bringing melanin into our interiors was the key to creating those bends and encephalizing primates.

We are silly talking monkeys whose body plan was sculpted by light captured by melanin that charge separated water to augment the power plant buried in biochemistry and mitochondria.

Clock genes were used to coordinate all zip codes inside the Jacquard cards of biochemistry to measure the overall flow of energy to extract information about where the Earth is in relation to the sun. The sun created the most powerful protein in Earth’s history because it can harvest the power of the entire electromagnetic spectrum.  Water was the plasma for most of Earth’s history, but nature created melanin to work with water something unique occurred.  The binary code of life that builds order from chaos begins by deciphering the code that exists between H+ and deuterium separated from water and plugged into ancient biochemical pathways to sculpt something new.

Metabolic pathways called the PPP and TCA cycle control the fractionation of hydrogen isotopes in mammals, and as such, determine morphogenesis in the neural tube because it places with precision where the isotopes have to be located to create the bends needed in the notochord to build a human brain from a primate’s brain.

Metabolism is 100% controlled by the SCN optical lattice clock in your eye.  Melatonin acts here.  Without that precision, there would be an improper mix of lipids at the lipid rafts that control the morphogenetic plan of humans.  That precision of lipid (DHA/cholesterol) content allowed for maximum absorption of sunlight to create an electric current that could control deuterium with its large magnetic moment.

Melatonin controls the 2 change programs in mitochondria and mitochondrial create melatonin and water.  In the above 4 slides, you see how hydrogen is being moved in these boxcars.  Changing the isotope of hydrogen changes everything in the mammal body and brain plan.  This is how primates changed.

Melatonin is made from a time crystal that controls the timing mechanism in all zip codes of the cells as it changes.  This means when hydrogen or deuterium is added to its back it changes its timing mechanism.  This leads to more bending of the neural plate in locations it occurs in the brain.

Cells of the mammalian grow and divide at different rates because of the amount of deuterium and hydrogen in them. This created NEW neural folds that allowed for a new plan to develop from the primate brain. These quantum processes are regulated by a complex interplay between the underlying notochord and overlying ectoderm, by putting hydrogen isotopes in specific places on signaling molecules used in brain growth.  These semiconductive proteins are called Sonic Hedgehog (Shh), bone morphogenic protein-2 (BMP2), and noggin.  They operate via the Jacquard card of the Wnt signaling pathway that has been used in life all the way bad to the first form of life on Earth.  The differential growth of the neurons between those bends is wholly linked to deuterium content as its different magnetic moment interacts with electric currents from the lipid rafts in the embryo to cause the issue. The sun is the source of that information current.

The seasonal light stress that primates faced was sensed by the non-visual photoreceptive proteins and POMC.  This non-visual system was designed by Nature to allow mammals to alter the fat content in their lipid rafts to better handle UV light.  This is why cholesterol also has an absorption spectra of 220nm light.  Most do not know this.  When UV light returns to the mammalian environment membranes sense the change non-visually and this information is sent to their colony of mitochondria where a redox shift occurred involving mTOR.

380 nm UV light captured by neuropsin sends an anabolic electrical signal onward in mammal embryos.  This was connected to 290-320nm light captured by cholesterol to create Vitamin D.   Cholesterol and neuropsin are non-visual photoreceptors.  Cholesterol and Vitamin D3 are nearly identical in chemical structure. Full-spectrum sunlight naturally sulfates both of these photoreceptors.  The only difference in both bio-molecules is a single double bond in the second ring of the cholesterol backbone. This gives Vitamin D3 one less hydrogen atom than the closed ring of cholesterol.  Hydrogen is the chameleon sculptor.

Sulfation makes chemicals more water-soluble.  Now we can see why water pathways in the brain became so important in humans and the way their brains were used.

This electrical information from the non-visual system acted like Morse code to the hypothalamus in the embryos of primates which were gaining more melanocytes as primates lost their hair. That internalization of melanin created more POMC neurons inside the skull which created more beta lipotropin peptide from POMC cleavage. This created more HDL cholesterol in the skin of these transitioning primates.  Sunlight also sulfates this HDL version of cholesterol  Why?  Sulfated HDL cholesterol has more electron density at its electronic level and this makes it another ideal nonvisual skin photoreceptor.  It also changes how the other non-visual photoreceptor in the skin which is more famous operates.  That is the vitamin D machinery in the skin.  Vitamin D is linked up to the non-visual photoreceptor system Vitamin, namely Vitamin A at the RXR receptor.

This signal is also picked up in the eye at the RPE of the retina.  This information was sent to the hypothalamus to also assist in the mammals changing the surfaces and bending of the notochord.  This was all done by fractionation of the isotopic mix of hydrogen which affected the translation of the POMC gene.  The bending of the notochord in primates lead to movements of the foramen magnum of primates from the immediate back of the head to the center of the head to help bipedalism.  In favt bipedalism was the first thing to change in humans from chimps.

At term, the human fetus has about 13 % of body weight as fat, a key form of energy insurance supporting brain development that is not found in other primates.  The location of neonatal fat is mostly subcutaneous while the brain is still underdeveloped.  What does fat become in human metabolism?  CO2 and metabolic water.  That water is the fuel source to build our brains.  As we lost hair we expanded the eccrine sweat glands on our skin to eliminate deuterium from sweating and this also cooled our surfaces to allow melanin’s ability to charge separate water to become more efficient.

A human child at birth cannot walk or talk.  This makes them unique in the primate tree.  They also lost most of their hair exposing their skin to the sun.  Most of their melanin was imported to their interiors while their brains developed.  As the brain matured, the child lost much of its subcutaneous fat.   It almost seems that the survival of the fattest (primate infant) was the key to human brain evolution.  It should be no surprise that the leptin-melanocortin pathway controls that biology by way of POMC.

The proopiomelanocortin (POMC) gene was most likely derived from an ancestral opioid-coding gene following the 1R chordate genome duplication event. During the radiation of the jawless fish, the POMC organization plan emerged multiple melanocortin sequences (α-MSH/ACTH and β-MSH) and a C-terminally extended opioid sequence (β-endorphin).

Following the 2R genome duplication event, the γ-MSH sequence was gained. Among the jawed vertebrates, three distinct trends in the evolution of the POMC gene are apparent: the gain of the δ-MSH sequence (cartilaginous fish), the loss of the γ-MSH sequence (ray-finned fish), and the retention of the post 2R POMC organization plan (lobe-finned fish/tetrapods). POMC is synthesized in the pituitary gland and in neurons of the hypothalamus, where an array of posttranslational processing mechanisms, such as endoproteolytic cleavage and N-acetylation, generate distinct sets of end-products in these tissues.

The most striking feature of the melanocortin end-products is the rigorous conservation of the primary sequence of α-MSH and the first 25 amino acids of ACTH throughout the family of mammals.  That stronghold has lasted for the entire evolutionary history of mammals on Earth.

Does Nature make mistakes?

Melanin, our wide-band semiconductor made from alpha MSH, and ACTH sculpted our morphologic and physiological change without any major changes to our genomes. They used the binary code of hydrogen and deuterium with sunlight to do the job. That story was covered in my first Kruse for Dummies lecture.

The binary code of life is the isotopic variation of hydrogen and deuterium parsed through the human Jacquard loom.  That loom was the POMC gene of mammals.  The result of the code interacting with the loom was a gorgeous wide band gapped semiconductor that sculpted the subatomic world inside of cells to create the most intricate fabric the universe has to date.  Humans.

https://twitter.com/DrJackKruse/status/1659238658933653515

“The task is … not so much to see what no one has yet seen; but to think what nobody has yet thought, about that which everybody sees.”

― Erwin Schrodinger

CITES

https://doi.org/10.1073/pnas.2209139119

Huang PL. Nitric oxide and cerebral ischemic preconditioning. Cell Calcium. 2004;36(3–4):323–329.

https://onlinelibrary.wiley.com/doi/full/10.1111/j.1600-079X.2004.00181.x

 

QUANTUM ENGINEERING #42: PERIODIC TABLE HACK PART DEUX

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Part one ended by asking you a provocative question…………

Part two begins with the answer.  All life is built around atoms.  Atoms were unknown at the time of Darwin.  Not even the math equations of Maxwell on light were complete.  But Faraday’s work was done in Darwin’s time.  It seems Darwin never thought about the sun on his trip in the Beagle on his way to Equador’s Galapagos Islands.

Darwin’s theory on evolution stated in his book stated: “As natural selection acts solely by accumulating slight, successive, favorable variations, it can produce no great or sudden modifications; it can act only by short and slow steps” (Darwin 1859).

Darwin cannot explain 3 things we know are true today

1. Cambrian explosion

2. The transition from a chimp to human

3. Why do primates have the same number of genes as humans yet are so different?

A longstanding debate in evolutionary biology concerns whether species diverge gradually through time or by rapid punctuational bursts at the time of speciation. The theory of punctuated equilibrium states that evolutionary change is characterized by short periods of rapid evolution followed by longer periods of stasis in which no change occurs. Despite years of work seeking evidence for punctuational change in the fossil record, the theory remains contentious. This changed in September 2022 when genomic arrays of the clade of mammals were completed. What did it show?

The reason evolutionary biologists were impotent to find these answers in the fossil record was that melanin from the POMC gene explained these paradoxes and was highly conserved in DNA that was stable in the mammalian tree.

See that September 2022 paper here.

https://doi.org/10.1073/pnas.2209139119

Mammalian superpowers were not only having the ability to create sugar from light but they all had the intrinsic property of using melanin to transform light energy into chemical energy (H+) to create ATP. This meant that they did not need a ton of food or oxygen to live. This explains why they were so successful during the age of dinosaurs living underground in poorly lit environments.

Today, we now realize this mammalian superpower was underutilized 65 million years ago by these animals because most of their melanin was external to their body plans. After the KT event, oxygen creation by photosynthetic plants was disrupted for some time. This played right into mammalian survival and dinosaur demise. The lack of UV light in the terrestrial environment allowed for melanin neuroplasticity (metastatic motion) of internalizing melanin from their exteriors into their body plans.

This UV quantum effect allows for future melanin superpowers seen in mammals post-KT event to interact with water in their bodies to create ATP without total reliance on oxygen. When melanin is hydrated and in the presence of full-spectrum light, there is water molecule dissociation and ongoing transforming energy.  This meant ATP could be created almost completely from the energy that emanates from the melanin by the charge separation of water inside of cells.

IF SO WHERE IS MELANIN LOCATED IN MAMMALS?

Melanin granules in mammals are strategically placed in cells being placed mainly in the perinuclear space (perikaryon), and completely surround the cell nucleus; which fully explains the operation of this protein.  The RPE concentrates its melansomes at its apical end where the rod outer segment is engulfed by the RPE cell.  This area doesn’t have the mitochondrial capacity that the basal end does that abuts Bruch’s membrane and the chriocapillaris of the choroid.  This border mimic what we see in the gut.

Melanin can augment mitochondrial energy production in mammals.  This energy source was critical in changing the body plans in mammals over the last 65 million years.  This tells you melanin renovation is a critical piece of all mammal biology. This largely has been ignored by centralized science.

The perinuclear space and its melanosomes are surrounded by the rough endoplasmic reticulum (RER); which allows this organelle to capture molecules of hydrogen as they emanate from melanin sheets via charge separation.  As long as there is a light source inside mammals water is continuously split into H+ oxygen and a massive pile of electrons that can be powered up and used in semiconductive circuits.  They can be used to form another source of endogenous energy to meet the energy requirements of the cell.  It is not solely the job of ATP as centralized science believes.  This would have made Gilbert Ling very happy. This explained why Mitchell’s chemiosmosis model never could account for the ATP deficit a cell would run if Mitchell was right.

Why does this make sense? The RER in mammals doesn’t have mitochondria or ATP inside of it either.  Many have forgotten this.   Mitochondria touch the RER but they are not inside of it.  Why is this odd?  The RER in mammals is a semiconductor factory.  In general, its function is to produce proteins for the rest of the cell to function. The rough endoplasmic reticulum has on it ribosomes, which are small, round organelles whose function is to make those proteins.  It makes no sense to have no energy organelle in your semiconductor fabrication plant, does it?

Does nature make mistakes?

It makes sense when you realize cells are creating endogenous light to translate the POMC gene inside of their cells to make melanin sheets next to the semiconductive fabrication plant. This is the arrangement of the rods to RPE in the eye. The creation of the peptide bond is one of the most costly things in energy to make.  Melanin had to be charge separating a ton of water to make a ton of H+ to create a lot of chemical energy. Ling’s stoichiometry told me to look for an energy-producing molecule other than ATP to satisfy Ling’s shortfall.  Leptin was the accountant and it turned out POMC was the Source that filled the energy deficit in the eye.

HUMANS WERE NEVER MEANT TO EAT THIS MUCH

IR-A light increases energy production within the mitochondria. In fact, Infrared light from the Sun makes ATP within the cell through CCO (Cytochrome C Oxidase) without ANY FOOD ELECTRONS.

Fact: 42% of sunlight is composed of IR-A light to spin the ATPase.

Also Fact: a 70kg man has to make 85kg of ATP per day.  This sounds nuts!

His body must produce his entire mass worth +30lbs of ATP every single day. The same is true of your body in the same proportions.

1/3rd of these excited electrons for ATP come from food.

2/3rds come from sunlight IR-A to spin the ATPase and the rest from melanin induced by UV light to create H+ to spin the ATPase and electrons to add to ECT.

Nature also put the Vitamin D receptor on the inner mitochondrial membrane to slow electron flow and get help from UV-A light to reduce ATP production via Nitric oxide creation…….

Or at least…they’re supposed to be in the sun………..

But how many of you are reading this while being buck naked outside in the direct sunlight?

I’ll guess 0.

Remind me again why it’s all about food…….?

You are a repository for sunlight. In the absence of star fuel, we have to eat copious amounts of food to maintain energy levels to live.

The more sunlight you get when you’re grounded to Earth the less food you need.

Go get that sunlight, because let’s be honest, we’re basically houseplants with complicated emotions.

This meme was created by Nick Stumphauzer and inspired by my work

This ability must be associated with a specific molecule capable of breaking symmetry.  Melanin is a symmetry breaker too.  This meant Noether’s theorem had to be in play, in my mind.  H20 can “unfold” or ‘charge separate’ into H+ and -OH with the addition of infrared heat from a cell or the sun or when it lies adjacent to hydrophilic substances.  Collagen and melanin are both hydrophilic.

I kept my focus on where hydrogen was and how it moved in the boxcars of biochemical pathways and realized the ionized form H+ would be affected by another universal law of nature = Noether’s thereom.  Einstein’s relativity required Noether’s theorem to be accepted by physics long ago. Why?

So how does Einstein’s relativity directly tie to this short narrative on hydrogen?

Einstein’s relativity theory allows for space and time-bending (Noether’s theorem). It also bends the mind of many people who look deep enough to see how far-reaching this idea really goes in cells. It turns out relativity has a major effect on the elements of the periodic table. When electrons slow down, this actually increases their small mass because of the mass equivalence equation. For those of you who don’t know magnetism from the adjacent mitochondria acts to slow electrons down as a nuclear effect.  I began to see a new perspective that allowed me to see another world I’d been missing in biochemistry textbooks.

Here we see a thermodynamic problem that must be solved. This small change causes the innermost electrons to get closer to the nucleus than usual. The longer-range effect of this shields the outermost electrons from the pull of the nucleus. This causes the outer shells of electrons to expand outward into space. Here again, when this happens, electrons’ energies decrease, and because of the E-mc^2 law,  mass must increase.  This explained obesity to me.  As thing got larger we lost energy.  I immediately thought of hydrogen and realized because it had double the atomic mass it would require more energy to move it in the boxcars of biochemistry.

FOOD IS NOT WHAT YOU THINK IT IS.  THE LAWS OF THE UNIVERSE SAY IT’S NOT UNCLE JACK

This idea based in the theory of relativity of elements raised new questions in my head.  For example, what happens to hydrogen when a single neutron is added to its sole proton and electron? This is what happens in deuterium.  Does something unique occur atomically that I am missing? If an electron slowing down invoked relativity, and it made that big a deal, what the hell was the effect of adding a neutron to H+?  In the subatomic world, a neutron is a giant compared to an electron.  That question opened a new door in my mind.  A door most of you won’t believe until you see it laid out.

A single neutron addition explained to me the food was not the key issue for health or longevity in mammals. Because of relativity, I realized an axiom in medicine that food is medicine is false.  Why?  Food can be medicine in certain environments and deadly in others because of Einstein’s relativity. It sounded nuts to me when I first thought about it, but I remember Feynman saying Nature is absurd in how she operates.  So I held onto the idea to give it due diligence.

So I held this paradox in my head and thought it through.

I thought about wild animals in Nature and the fact the food web is built 100% by photosynthesis using all forms of water on Earth at every latitude. Then I thought about the water a mitochondria was making around melanin,  and what melanin was doing to this water. It was creating massive amounts of hydrogen but no deuterium because of the proton channel size in the ATPase.  I knew something did not add up. Photosynthesis allows deuterium to be in foods, so this meant animals had to have all these fancy enzymes to isolate deuterium from the mitochondrial matrix. In fact, at this moment, I realized this is how ruminant mammals could tell the seasons and know when to migrate.  Their brains weren’t developed enough to allow for this behavior so how did they do it?

Since wild animals cannot think to know when to migrate to seek new food, and they don’t have the ability to read a clock, I knew some other mechanism of telling time was operational.  I realized they gained the ability to tell time from the amount of deuterium in their diets. Deuterium weight double H+ and it also had a radically different nuclear spin.  Protons spin is also sensed by the mitochondria because all the channels in the mitochondrial matrix & ATPase are quantum nanomachines that are built exclusively for the atomic radius of H+ and not for the larger atom of deuterium = which is H+ plus one neutron.

This small change in mass in the animal enterocyte also invoked Einstein’s relativity if the electron did in atoms.  Einstein’s relativity theory is why gold is yellow. In fact, this is the same thing used in an iPhone’s GPS system. The level of deuterium in the matrix of wild animals informs animals of this small change & therefore also simulates the season inside the matrix of the mitochondria. When I was a little boy, I went on a tour in the museum of natural history and I learned that all mammals membranes change their lipid rafts seasonally by altering their cholesterol levels.  This is how their coats changed as light and temperature levels changed.  Who knew that lesson as a kid would solve a mystery.

The amount of deuterium entering the matrix via UCP-2 alters the metabolic rate of the spin cycle in the TCA and urea cycles of mammalian mitochondria.  These changes also changed the melanin coats on their surfaces.

This entire system is 100% programmed by the power density of sunlight in that season and this is how the ZIP CODE of seasons could be coded for the inside of all mammals. The more deuterium that is present, the more swelling would show up in the colony of mitochondria of their guts. This information could be sent to the brain via the peripheral nervous system and the autonomic system to adjust behavior and feeding.  It could morphologically change its melanin coats externally just as a cephalopod or chameleon does because a TINY change in mass = a change in energy and when energy varies color and shapes have to vary too.

This shows you why thermodynamics and size and shape changes within the colony of mitochondria in tissues can be sensed macroscopically by our sensory systems in our thalamus which is filled with CSF made mostly from water. As you heard in the podcast linked above, the thalamus is the end target of the POMC neurons in the eye’s semiconductive pathway where light enters the system of timing. All the pieces fit in this quantum design. This alters the tensegrity of the mitochondrial system and the cell and changes water made in the mitochondria which surrounds every semiconductive protein in life. This changes the VUV-IR-A light a cell can transform.

I realized at the foot of David in Florence we’re being instructed by waves.  We’re sentient beings made from atoms hiding behind a facade of box car biochemicals designed to hide the “magics” of the cosmos from our reason so we act/do/follow what the recipe requires.  This allows the cosmic wand, the Source, to continue to direct our syncytium of atoms across space-time. From above and from below, the heavens instruct our cells how to properly behave to conduct the tissues in our bodies as the instruments which play the melodies capable of soothing our souls.

HOW DOES THE MAMMALIAN BRAIN LINK TO EARTH TO TELL US ABOUT OUR GROCERY LIST?

The mammalian thalamus also has normal resonant frequencies it absorbs and emits. It creates the 7.83 Hz alpha wave on EEGs which links all mammals to the heartbeat of the Earth. This thalamic frequency is tuned by molecular resonance to the Earth’s ionosphere as it revolves around the sun. The ionosphere resonant frequency varies seasonally and mammals can sense this too deep inside their heads.  This allows them to alter their coats and semiconductors in cells to a changing light environment. Think of this system of signaling as the electric and magnetic GPS compass to monitor the position of the Earth as it revolves around the sun and it is communicating that quantum data to your thalamus. Anything in the thalamus linked to the thalamus in mammals also happens to be loaded with the POMC gene. This is the gene that codes for MELANIN. These electromagnetic signals are essentially informing POMC and alpha, beta, and gamma MSH to control feeding and link it with the photosynthetic food growth cycles. All the pieces fit perfectly.  Now, many of you will now understand why Uncle Jack thinks most people do not understand food as they should.

DO YOU REALLY UNDERSTAND WHAT I JUST SAID ABOUT FOOD?

It means a banana eaten in Boston on December 31st is a MITOCHONDRIAL TOXIN, not a medicine as your doctor or bro scientist tells you.  This is especially true if you are getting 12/31 sunlight at the 44th latitude via your skin and eyes.  This creates a ton of inflammation in your colony of mitochondria.  I said this as the keynote speaker at the first annual Paleo Fx conference and was mocked by their leaders.

When you eat out of seasons or in the wrong light for the food in question, you are making a MASSIVE quantum mechanical error for your mitochondria and central retinal pathways.  Why?  George Mourou & Donna Strickland got a Nobel for their development of Chirped Pulse Amplification (CPA) at the University of Rochester. In his speech, he referred to his “passion for extreme light.”  What else did Mourou say in his acceptance of the Nobel Prize speech?

Read it.

Mourou said, “Take the nucleus of an atom. It is made up of protons and neutrons. If we add or take away a neutron, it changes absolutely everything. It is no longer the same atom, and its properties will completely change. The lifespan of nuclear waste is fundamentally changed, and we could cut this from a million years to 30 minutes!

HYPERLINK

Hard STOP for the disbelievers.

What did Uncle Jack say 4 years after Paleo Fx in Austin, in 2016 when I was in Vermont on this very topic?  Could deuterium turn healthy food into a toxin?

I showed a picture slide and asked the room why no one stuck at the biochemical level of understanding of food ever ask themselves this question.  Remember they were all Weston A. Price folks………….nobody said a word.

The answer was to isolate deuterium from H+.  The lesson of the periodic table was a huge piece to this puzzle.

I came back two years later and showed how a cells in our skin and circulatory system can make VUV light. I showed the mechanism used in the blood and skin. I sent this Tweet message out and link to the Mourou Nobel Prize talk and asked this question what happens to foodstuffs when you add a neutron to H+?  Is the food the same healthy food or does it become a poison?  I mentioned that processed keto food that all the guru sold via MLM schemes sets off the RF detectors at airports too.  I asked them why?  I asked them does it matter?

Radio silence.

I asked a simple question, “If one takes the nucleus of an atom in food, it is also made up of protons and neutrons like nuclear waste. If we add or take away a neutron, does it change the food?  

ANSWER:  it changes absolutely everything we think we know about food and its properties because the atom is different. What does that mean if you are a mitochondria? Do they react to it like glyphosate?  

Might we be blaming a lot of bad food ideas when the real toxin is the food just eaten out of season or shipped from another hemisphere where it is summer

After all, as Mourou said, it is no longer the same atom, and its properties will completely change, and a mitochondrion won’t be able to process it the same. This is what light does in photosynthesis between H+ and deuterium.  Photosynthesis puts deuterium in certain places on the backbone of food carbons and enzymes subtract the deuterium away to shunt them from the matrix.  

This is why biochemistry has all those enzymatic steps in the slide above people.  Everyone opens a biochemistry book but no one thinks to ask the question that is obvious.  Why is Nature doing all these steps?  Does she make errors?  Does she add enzyme steps to drive medical students crazy during their first year of training?

The matrix pays attention to this change EVEN when you do not at WHOLE FOODS on 12/31.  What happens?  The lifespan of disease creation is fundamentally changed in human mammals from far off when you are old, to diseases rapidly showing up in children and teens.  This is why I can see diseases of aging in 20-year-olds in my clinic.”  HEALTHY foods can be toxins when you have this perspective.

Now let’s review again what Mourou said in his acceptance of the Nobel Prize speech on the same topic.  He said high-intensity endogenous light made in a lab could cut the lifespan of nuclear waste because it is fundamentally changed, and we could cut this from a million years to 30 minutes.

Why do Mourou and Kruse sound familiar on this topic about neutron additions?  Because they understand the physics behind the actions in Nature.  Most do not because they suck at observing what she is doing at the smallest levels of science.  Therefore, they call us crazy motherfuckers when it’s the ignorance of centralized systems of science who are out of line with their outdated thinking.

So when you hear me say something about food ever again…………remember this blog passage.  Tape it to your forehead and maybe tattoo it on a body part.  No one understands food like a mitochondriac.  NO ONE.

The implications of my podcast with these two men goes way deeper than most of you can fathom. I’m still warming up.

Nature’s food lesson for us all: Just because something seems logical about food, doesn’t mean it’s wise. Something can make sense in and of itself, but when tested against reality yield an undesirable or inefficient outcome. Being seduced by impractical logic is antithetical to wisdom, you just feel smart despite being wrong. Nature is absurd in how she uses isotopic variations in food in mammals.

BACK TO THE PERIODIC TABLE SCULPTING MAMMAL STORY

Post-KT event, the absence of UV light allowed melanin to move from the exteriors to the interiors where melanin adaptation and renovation were maximized.  The results were seen in massive alterations of mammalian body plans within ten million years. These changes required energy.  Where did it come from?  Well, the sun returned and now melanin was inside and outside most mammals.  50% of the energy-consuming processes of the normoxic cell in these animals can be accounted for by ion pumping. This is even true in a neuron.  The transformation of light energy to chemical energy by melanin inside of the body’s tissues serves this need for energy. It decreased the need for membrane ion leakage to generate energy. This ability contributed immediately to a major energy saving,  This allowed for organ expansion and rearrangement like encephalization seen in mammals post-KT event.

Theoretically, the power to the inside of the cell depends partially on ATP as Ling always believed.  Melanin filled the rest of the thermodynamic gap Ling saw in his calculations of ATP stoichiometry.  Internalized melanin gave mammals the ability to transform all light energies into chemical energy by means of water dissociation into hydrogen, oxygen, and 4 electrons. H+ is used to spin the ATPase Fo head to create ATP and a magnetic field. Mammals create massive amounts of H+ from melanin’s ability. This helps explain why Ling was furious with Peter Mitchell for decades. He had no idea about what melanin was really doing in a cell because I asked him about it. Energy production in mammalian cells relies on massive additions to the energy balance sheet because of melanin.   When you look at Ling’s numbers for ATP stoichiometry, the math didn’t add up.  I knew right away, why Ling was right.

TYING IT ALL TOGETHER

H+ and magnetism help explain why we use the atoms we do on the periodic table. The key ones that make VUV light are all paramagnetic. They are drawn to the mitochondria because that is where melanin is to make H+. Many people want to understand how magnetism fits into the 3 legged stool of life. Free radicals are all drawn to magnetic fields too because this is where mitochondria and melanin are in mammalian cells. These areas in cells are where the sun buries its magnetic flux in cells and connects with it wirelessly.

It uses H+ creation via melanin and matrix water to do it. Magnetism is the essential force that determines the form of plasma or ionized matter taken in an environment. The hydrogen regions around galaxies are also considered plasmas, despite their degree of ionization being small. The degree of ionization in interplanetary space varies between unionized states or can morph into fully ionized states in other regions of space. In space, however, even the weakly-ionized plasma in the hydrogen region reacts strongly to electromagnetic fields. Mitochondria at small scales have a massive electromagnetic field with respect to H+.

Magnetized plasma, such as that contained in the hydrogen region, is the dominating state in the universe as a whole. Our sun produces massive amounts of plasma it spits out into the solar system as the solar wind or a coronal mass ejection. The sun’s plasma is contained by the high electric and magnetic fields of the sun. So is the H+ in our mitochondria to create ATP. This makes your colony of mitochondria filled with H+ a wireless antenna for the sun’s photons. Our circulatory system connects us to the magnetic flux in the sun.

NOETHER’S THEOREM EXPLAINED FULLY IS A FUNCTION OF POMC LOCATION

Melanin captures that energy from the sun buried in our blood. As the energy is captured, Noether’s theorem is used to bend space-time in cells to tell matter how to act in cells. This is covered by the field of general relativity (Einstein), which treats gravity as a bending of space caused by mass and energy.

Einstein’s theory seemed to have a serious problem at its core: Energy caused the bending of space, but gravity itself was energy in his model. Thus, it would seem that the energy of bending space made yet more energy. Presumably, this would bend space more, resulting in more energy transformation. It seemed like the theory could cascade in this manner to the point that energy would grow forever. And because this didn’t happen, there needed to be a solution to the problem. Emmy Noether’s solution to the problem is now called Noether’s theorem. Her theorem revolutionized physics, but her theorem has yet to hit biology because biology still doesn’t realize that all biochemistry is quantized by light via non-linear optics in cells.

Light, captured by melanin, tells cells how space-time bends at the electronic level inside of us. ——-> POMC CHANGES SPACE TIME IN YOU!

This is how the wide band gapped semiconductors are organized quantum mechanically below your ability to sense it from atoms and by relativity to make light waves stronger than the sun provides inside of us. To decipher the electric and magnetic codes you need wide-band gapped semiconductors to get Nature’s recipes to run your cells. This light is what keeps cells operating far from equilibrium to satisfy the second law of thermodynamics.

This arrangement is really interesting in the RPE of the eye and the choriocapillaris. In mammals, moderate hypoxia or pseudohypoxia (14%) significantly increases the extracellular concentration of dopamine, prior to retinal depolarization in retinal ganglion cells. This hypoxia is critical in degrading melanin into DOPA to create dopamine in the eye to keep the globe round and not myopic while also helping regenerate photoreceptors with melatonin which is created in the mitochondrial matrix. Dopamine and melatonin are both assisted by DHA breakdown products in the eye in preserving photoreceptor regeneration.  I believe DHA is critical in melanin renovation as well. Why?

Uncompensated oxidative stress is often an early event associated with retinal, neuronal or heart cell death, and the retinal pigment epithelium and retina are under continuous stress by nature’s design.  One of my mentors in neurosurgery, Dr. Nicolas Bazan, found that elovanoids created from the photooxidation of DHA have unique structures and that they enhance the expression of pro-survival proteins in cells undergoing uncompensated oxidative stress by controlling autophagy.

Bazan and his team at LSU found that ELVs are made from 32 or 34 carbon-length fatty acid precursors produced naturally in human retinal pigment epithelial (RPE) cells. Most of the known lipid mediators or messengers are derived from 18, 20, or 22 carbon-length fatty acid precursors, including prostaglandins, leukotrienes, lipoxins, endocannabinoids, resolving, and docosanoids. Elovanoids have structures reminiscent of docosanoids but with different physicochemical properties and alternatively regulated biosynthetic pathways.

That elovanoids are longer than all known mediators may be the key to their potency. Dr. Bazan spoke to me this week and told me he just discovered two more ELVs that are 43 -46 carbons. He was very excited about their potential use in TBI cases.  The longer elovanoids may be able to reach and bind for a longer period of time to receptors in cells necessary to induce cell survival.  I have a sense these longer ELVs may protect the non-visual photopigments in the retina, brain, and carotid system.  This will become important later in the series.

People forget the reactions on the top line of the slide below are bidirectional and hypoxia controls which way we go, right to left = normoxia, but left to right is done in hypoxic environment causing melanin to degrade. Hydrogen atoms force this change at melanin interfaces because they are atomic chameleons.

Not too hard to understand once you see it laid out in this blog.

SINCE WE CREATE LED LIGHT FROM VUV SEMICONDUCTORS…….WHO IS THE LIGHT SHOW FOR INSIDE OF US?

If you remember the dialogue between Dr. Huberman and myself on melanopsin he remarked boldly that no one in his PEER group could believe in the early 2000s that humans had rhabdomeric opsins from non-vertebrates in our body plans. Although the melanopsin system of mammals has received the most recent interest, the founding member of this new branch of the opsin gene family was in fact isolated from the photosensitive dermal melanophores of Xenopus laevis, a frog in 1998.

You guys could not see my face during the podcast but I had a real big smile on my face as he said it. Why? I thought everyone knew the story of where mammals came from. I learned it as a young boy in NYC museums. I was taught although there was no abrupt transition to ‘true mammals’, the general idea is that the tetrapods (vertebrates with four legs) divided into amphibians (that lay eggs in water) and amniotes (that lay eggs on land).

Amniotes then split into sauropsids (including dinosaurs) and synapsids (including mammal-like reptiles), which eventually led to mammals. Once the dinosaurs were gone, early mammals could stop living nocturnally and flourish in the many forms we find today. So for me, having frog melanopsin in the human brain made total sense It also told me we had to have deep chromosomal stability in the mammalian genome. It turns out my hunch was right (below).

HYPERLINK

The discovery in the early 2000s by David Berson’s group at Brown University of other cells in a mouse retina that responds to light and has nothing to do with a vision came as a shock to centralized science. Dr. Huberman confirmed this in Malibu. None of them thought non-visual photoreception was possible at this time.

Many mocked Suzanne Sommers when she reported in the 1990s that a penlight behind her knee affected her melatonin level and disrupted her sleep. Even stranger discoveries became commonplace in many laboratories demonstrating that these cells contained a new class of opsin proteins called melanopsins, never before seen in vertebrates (but similar to those of many invertebrates like fish). Non-mammalian vertebrates retain two quite separate melanopsin genes, while mammals have just one.  Here is the screens for all the light show created by your interiors.

Every modern mammal, from a platypus to a blue whale, is descended from a common ancestor that lived about 210-180 million years ago if they are a mammal. We don’t know a great deal about this animal, but the organization of its genome has now been computationally reconstructed by an international team of researchers. The reconstruction shows that the mammal ancestor had 19 autosomal chromosomes, which control the inheritance of an organism’s characteristics outside of those controlled by sex-linked chromosomes, (these are paired in most cells, making 38 in total) plus two sex chromosomes.

KEY TAKE HOME:  Mammalian chromosomes have been more stable than scientists predicted before the human genome project was complete.   It turns out, Darwin was wrong.

The researchers found nine whole chromosomes, or chromosome fragments in the mammal ancestor whose order of genes is the same in modern birds’ (therapod dinosaurs) chromosomes. It seems it is very likely there was some crossing of genomes between birds and mammals at the KT event since these two animals made it through the last extinction event together. Their genomes show this connection. This only deepens my theories about melanin.

More proof these animals are linked to POMC biology: The researchers found in contrast, regions between these conserved blocks contained more repetitive sequences and were more prone to breakages, rearrangements, and sequence duplications. Ancestral genome reconstructions are critical to interpreting where and why selective environmental pressures vary across genomes. This study has now established a clear relationship between chromatin architecture, gene regulation, and linkage conservation.

It does something else centralized science doesn’t like. It provided me with hard data to say publically that the foundation for assessing the role of natural selection in chromosome evolution across the mammalian tree of life isn’t Darwinian.

It follows a quantum periodicity that links it to the periodic table of elements and the amplification of the use of paramagnetic atoms to build semiconductors in cells. Why? Chromosomes are filled with base pairs that are magnetized by UV light.  That periodicity is in where hydrogen is and isn’t and what hydrogen’s atomic weight is in that zip code, and what its magnetic moment is while in that zip code.  You’ll see why this idea is on solid footing soon enough.

In the study, they found that the rate of chromosome rearrangement differed between mammal lineages. For example, in the ruminant lineage (leading to modern cattle, sheep, and deer) there was an acceleration in the rearrangement of these chromosomes 65 million years ago, when an asteroid impact killed off the dinosaurs and led to the rise of mammals.

Centralized sciences call this a “remarkable finding” because their theories from Darwin wouldn’t have predicted it. I chuckled when I read the paper in late 2022. It shows definitively, that mammals have enjoyed evolutionary stability of the order and orientation of genes on chromosomes over an extended evolutionary timeframe of more than 320 million years.  The doesn’t sound like natural selection as it was taught to me.

We now know that melanopsin is the most common opsin in the human brain even though blue light cannot penetrate the bone in our skull. It can only get in via the eye and has to pass the RPE of the retina before it gets deep into the substance of the brain.

SUMMARY

Centralized researchers forgot Nature’s lessons. Molecular oxygen (O2) is essential for vertebrate life. Strikingly, certain species are able to survive for periods lasting several months in anoxic conditions and are able to recover full function at the end of this time when O2 is restored.

The freshwater turtle Chrysemys picta is a well-studied example. It spends long periods during the winter in ice-covered ponds without access to the surface, often in water or mud with little or no O2. Mammals evolved 210 million years ago to live underground outside of the sun in a hypoxic environment. It seems melanin helped them navigate these environments.

This pseudohypoxia was linked to the NAD+ levels of their mitochondria and when oxygen was low and blue light dominated Earth’s surface and the dinosaurs were gone this allowed melanocytes to migrate inside of us. This brought melanin closer to our colonies of mitochondria where the real action began in energy transformation to create a human brain.

I’m closing in on the recipe of light I mentioned in the podcast.  It turns out the beginning of Genesis never told us the shadows in life hold the light in our perception of reality.  It might turn out that evolution theory and Genesis both contain half-truths.

CITES

My cerebral cortex

 

QUANTUM ENGINEERING #41: MY QUEST IN HACKING THE PERIODIC TABLE PART 1

If you listened to the beginning of part two of the podcast, I mentioned the large band gap needed to charge separate water.  This single issue sent me looking at the periodic table.  I found that answer there, but in reality, I stumbled into a bigger reality.  I finally realized how we humans evolved.  Here are the details of that POMC story.

LIGHT AND WATER BECAME THE FIRST TWO LEGS OF THE STOOL OF LIFE

Water is made from two atoms so I began with hydrogen on the periodic table because water has 2 H in its chemical formula.  As soon as I went deep I found some interesting trends about hydrogen.  Science depends on compelling narratives, and few people seem to know the real story behind hydrogen. This really explains why even today biology ignores water’s role in a cell.  In fact, in a cell Nature has shown us that hydrogen can act as a metal or non-metal.  Hydrogen makes life a cooperative quantum dance and it can make other elements do things they normally would not do.

It turns out how hydrogen acts chemically,  depends wholly on the environment it is within.  Does this means hydrogen can take different forms in our body if the environment of that region is controlled by information in some way? Is it a donor or a collector of electrons? Is it a metal or a gas?  The answer is yes.

This is why on Earth hydrogen always seems to hang out exclusively with carbon and oxygen in life. The hydrogen ion (proton = H+) and electrons go to reduce (or fix) carbon dioxide into the carbohydrates and biomass of photosynthetic organisms using both the C3 or C4 pathways, which feed herbivores, and down the food web, the vast majority of animal species. The air-breathers break down carbohydrates by oxidizing them (with oxygen) in the mitochondria of cells to obtain energy for growth and reproduction, regenerating carbon dioxide and water. This completes the living dynamo of photosynthesis and respiration that turns inanimate substances into living organisms.

The measured ionization energy of H2 is 1488 kJ mol-1. This number is primarily important in comparison to the ionization energy of a hydrogen atom, which is 1312 kJ mol-1. Therefore, it requires more energy to remove an electron from the hydrogen molecule than from the hydrogen atom; the electron, therefore, has lower energy in the molecule. To pull the atoms apart, the energy of the electron must be increased.  I knew electrons can only be powered by light because of Einstein’s photoelectric law of the universe.  So I looked up how much power by light was needed to break this bond. I began to understand why we needed over 12 electron volts of light power to split water into its substrates.  Hence, a lot of energy is required to break this bond. So I went looking for an answer on how photosynthesis did it.

MAGNETISM THEN BECOMES THE THIRD LEG OF THE STOOL OF LIFE

Next, I looked at oxygen.

The oxygen molecule is a particularly interesting case, O2, to study.  This study was detailed in my 2014 conference talk at Dave Asprey’s event that you heard Rick Rubin talk about in the podcast.  Asprey banned the talk because essentially it told everyone who heard the talk everything Dave was selling was snake oil.  Props to Rick for telling that story.  I would have died with it.

When I looked at oxygen I drew out its complete molecular orbital energy level diagram, and I noticed that the last two electrons must either be paired in the same 2p π* orbital or separated into different 2p π* orbitals. To determine which, it is important to note that oxygen molecules are paramagnetic—meaning they are strongly attracted to a magnetic field. I did not know that prior to this moment.  It turns out that moment was going to change my life.  To account for this paramagnetism, I recalled from my high school chemistry class that electron spin is a magnetic property. In most molecules, all electrons are paired, so for each “spin up” electron there is a “spin down” electron and their magnetic fields cancel out. If all electrons are paired, the molecule is diamagnetic, meaning that it responds only weakly to a magnetic field.  then I thought about the Earth.  We have a magnetic field and so does the sun.  Then I thought about the ATPase in mitochondria and knew it had one from the spinning Fo head where ATP was made.  Immediately I realized oxygen was being drawn to mitochondria because of magnetism.

If the electrons are not paired, they can adopt the same spin in the presence of a magnetic field. This accounts for the attraction of the paramagnetic molecule to the magnetic field. Therefore, for a molecule to be paramagnetic, it must have unpaired electrons.  This thought stopped me dead in my tracks because I knew we had some chemicals in us that had unpaired electrons called free radicals.

Are all free radicals created in human biology paramagnetic because they have unpaired electrons?

It turned out in my research of organic chemistry, all radicals are paramagnetic, but all paramagnetic species are not radicals. Take for example the metal Nickel. Nickel is paramagnetic, and therefore has unpaired electrons, but at the same time is not a radical because it is a stable atom and does not react with other elements. Radicals are unstable by nature and they react by donating their electrons.  I thought to myself, is this donation of electrons how a semiconductor operates.  I looked into it and found that is exactly how a semiconductor works.  That created an idea and I wrote this down on a piece of paper that became this slide below.

I left the normal periodic table of elements and then looked up the magnetic table of elements.  Here I found, Ca2+, Mg2+, K+, and Na+ are also paramagnetic. Mo is used on the inner mitochondrial membrane and is also paramagnetic. The thought crossed my mind that it seemed biology was specializing in using atoms in biochemistry that might dope semiconductors.  I knew collagen was a wide band gap semiconductor from Becker’s bone work.  I began to realize atoms doped to carbon and surrounded by water are all wide band gapped semiconductors.

Then I looked at other atoms used in cells.

H, C, N, P, S. Se, Cu, I are all dimagnetic.

It seemed immediately that H and O differ in their magnetic powers. What about water that acts as a semiconductor in cells? Water is not paramagnetic even though oxygen is, due to the absence of unpaired electron (s) in its molecule. Here is hydrogen pulling its magic tricks again on another atom. Water is reported as a diamagnetic substance with a susceptibility of − 9 × 10 ^− 6. This implies that when it is submitted to a magnetic field, it will tend to repel the field lines.

Then I thought about iron and hemoglobin and all the heme based proteins in cells like the P450 system, catalase, and peroxides in mitochondria.

Fe, Co, are ferromagnetic

Oxygen is paramagnetic.

All free radicals are paramagnetic.

Anything paramagnetic is drawn to magnetic fields and inside cells this draws them to mitochondria.

Then I thought about Mammals. What did I know about them? I knew about the asteroid event.

The rocks found at the K-T boundary, whether they are found in Europe, Canada, or the United States, all show a very high level of the element iridium. This iridium layer has been located in over 100 different spots on Earth, both on land and under the ocean. Iridium, which defines the KT boundary is also paramagnetic.

Does anyone see a trend here that I found in hacking the periodic table?

HYPERLINK

Most of the key atoms were paramagnetic and this told me semiconduction was the key to understanding how cells work.  I then looked at proteins differently and remembered about Szent Gylogi’s talk in 1941 where he said all proteins were semiconductors and Becker proved him right 25 years later.

I went back to hydrogen and proteins to see a link.  I found it in chlorophyll, hemoglobin, and melanin.

What thoughts filled my head that day?  The retina has melanin in its RPE and it creates massive amounts of ROS at the choriocapillaris.  I thought to myself……..is melanin creating a stream of electrons in the eye to electrify the brain?

When electrons are not paired, as they are in ROS/RNS they can adopt the same spin in the presence of a magnetic field around them.  The brain is filled with mitochondria that creates magnetic fields. Might this accounts for the attraction of the paramagnetic molecule to the a mitochondria’s magnetic field? Might these free radicals be key to explain how tissues are sculpted and changed?  I knew for a molecule to be paramagnetic, it must have unpaired electrons.  I went looking for a protein that was paramagnetic and could transform light into chemical energy in the form of free radicals and I found melanin.

Melanin is a paramagnetic bio-polymer that has revealed in testing to exhibit strong and stable paramagnetism.  It is loaded in mammals skin and in their eyes.  I also found out that melanin synthesis is an oxygen-dependent process that acts as a potential source of reactive oxygen species (ROS) inside pigment-forming cells.  I knew I was onto something.  Melanin was able to transform light energy into chemical energy, and this has been accepted by the countries of the first world patent offices.  I wondered it melanin could create hydrogen and oxygen in a cell. I found that it can.

Hydrogen is the rogue element in the periodic table that breaks all the rules we expect, and this is why life uses it in her designs. When a hydrogen bond forms between two water molecules, the redistribution of electrons changes the ability for further hydrogen bonding. In this sense, a hydrogen bond can be electrostatic. Hydrogen bonds, however, can become covalent as well.  Iodine’s addition to hydrogen favors the formation of covalent bonding in water.  You heard about this in the podcast.  This is a fancy way of saying hydrogen makes other atoms do things they normally might not want to do. Hydrogen’s will is strong because of the closeness of its one electron to its nucleus. This gives hydrogen lots of differentisotopes. This is when I found out the addition of deuterium, a heavier isotpe of hydrogen changes how water absorbs light.  I did not know this.

Water with deuterium in it absorbs less IR-A light and hardly any UV light at all.

These facts meant something more interesting.  It meant hydrogen had to invoke Einstein’s relativity theory more than any other element on the periodic table! You might not understand why now just yet, but more on this aspect shortly to fill in your gaps.

Magnetic Type for all the elements in the Periodic Table

Hydrogen normally has one proton that is encircled by one electron that buzzes in its electron shell.  Its valence shell is designed to hold two electrons. So you need to ask yourself is the shell half filled or half empty?  Other atoms want to know this too because this is how they decide how they react with hydrogen. This is why hydrogen can be a chameleon. Most elements either gain or lose their electrons in chemical reactions. The pathways that hydrogen electron takes determines the chemical abilities of the atoms in this dance. Hydrogen swings, either way, depending upon the environment it finds itself in.   This makes it a very interesting player in biochemistry. It’s no wonder hydrogen is an integral part of life’s plan. Hydrogen is found in all amino acids and semiconductive protein polymers.  It also makes up 2/3 of water.  Imagine that.  Without water depleted of deuterium, you cannot convert sulfated cholesterol to Vitamin D 25 D (OH) because the photoisomerization step needs it.

When hydrogen is ionized or charge separated………however, what can happen in life at the cell level changes in a big way……….hydrogen becomes the superman of flow.  When hydrogen is ionized and loses its only electron it becomes a proton cation.

This makes H+ the lightest cation in chemistry and given the small size of the proton, explains the unusually high diffusion rate of the proton relative to that of other common cations like potassium (K+).  When hydrogen loses its electron it becomes an ionic plasma that acts like a liquid metal.

Ionic plasmas have special abilities.  One ability is called proton jump conduction or protonicity.  These rules are governed by something called the Grotthuss mechanism.   Hydrogen is a chemist’s conundrum, a biologist’s enigma, and a physicist’s dream because it can lose or gain this single electron. I have always been of the belief that hydrogen did not really belong to any group in the periodic table based on this ability. Remember all that talk about the periodic table I did to Rick and Andrew.  Do you think that work was wasted now that you see the details in the story they missed?

After many thoughts on this topic,  I realized under some environments it can be placed into group 7 or group one in the periodic table. All known elements of group 7 are halogens. The group 1 elements compromise the alkali metals. Hydrogen is often placed in group one of the periodic table by convention due to its electron configuration,  but it is not considered by many to be an alkali metal.  Why?

Hydrogen rarely exhibits behavior comparable to that of alkali metals. For example, all the alkali metals react with water, with the heavier alkali metals reacting more vigorously than the lighter ones. The word “alkali” received its name from the Arabic word “al qali,” meaning “from ashes”. These particular elements were given the name “alkali” because they react with water to form hydroxide ions, creating very basic solutions (with pH > 7), which are also called alkaline solutions.

Hydrogen forms water with oxygen directly and does not form a basic solution. Adding more hydrogen to it does not cause a special reaction at all, as it does with the other metals in group 1.

Why is hydrogen fundamentally different? Water is most famous for forming hydrogen bonds with other water molecules and with other ions dissolved in it. A hydrogen bond consists of hydrogen shared between two electronegative atoms like oxygen or sulfur. The compound that donates the hydrogen to the chemical reaction is the hydrogen donor, and the acceptor atoms is the hydrogen acceptor.

Water is unique because it can be both an acceptor and a donor of hydrogen. It means water can be a switch hitter in many biochemical reactions.  This is why water is the universal solvent on Earth.  In fact, water can even donate two of its hydrogen’s if need be! This makes the water molecule take on the tetrahedral structure in its frozen form linked in a crystalline hexagonal array in crystal ice.  When I realized water had a crystalline structure I knew immediately it had to be part of the cells construction plan for its own wide based semiconductors.

All of a sudden biology took on a new meaning to me with this new perspective.

I told you in the podcast that hydrogen can also act as a group 7 halogen.  It can mimic iodine element 53.  It means it can gain electrons to become a nonmetal.  Non-metals can become semiconductors.  It was here that I realized the water was acting as a semiconductor between sulfated cholesterol and Vitamin D in our skin to change the structure of matter.  When hydrogen does this in water when it is associated with iodine it forms an ionic liquid.

Ionic liquids are now receiving special attention in science, owing to their unique properties such as high ionic conductivity, non-volatility, and non-flammability.  This ability makes these fluids versatile alternatives to conventional solvent-based systems used to make batteries, fuel cells, and supercapacitors that hold large charges.  They are also quite helpful as heat-transfer fluids to move infrared energies within a system.  This is when I realized why iodine was being used in the breast, brain, and thyroid gland with melanin and tyrosine.  Iodine and water create another semiconductor that is transferring energy from the sun to us.

Iodine addition to iodide-based ionic liquids leads to extraordinarily efficient charge transport, vastly exceeding that expected for a standard viscous system.  Hydrogen and iodine form an ionic plasma within the CSF of the human brain. The choroid plexus of the human brain is designed to add iodine to CSF.  CSF, you will recall is an ultra-filtrate of blood plasma and is made up of 99.9% water.  When iodine meets water that has been charged separated by IR light or by the hydrophilic proteins within the dura matter a massive amount of H+ is made in the CSF of the brain.  H+ is equivalent to a proton.  Using the Grotthuss mechanism, iodine is able to move protons closer together than we would normally expect,  to alter their hydrogen bonding network to allow them to form superconducting proton cables that act like a positive charge electric current.  The mechanism allows for charges to be transported not by the movement of particles, but by the breaking and reformation of chemical bonds. As water is charge separated by IR light or by hydrophilic substances, many excess H+ ions are made adjacent to the exclusion zone of water. Gerald Pollack’s experiments have shown this exquisitely.  The excess protons can then diffuse through the hydrogen bond network of water molecules or other hydrogen-bonded liquids (iodized CSF)  through the formation or cleavage of covalent bonds.  Iodine helps UV light get from the sun and our skin to the brain.

A biological cell is a dissipative system by its very nature. You heard this in the podcast when Rick said, “I don’t know what that means.”  I said I will tell you.  Now I am retelling it to you here.  This implies it has the role or purpose to break symmetry and create a metastable system to react to all environmental possibilities that the cell may face. Breaking symmetry tells biology something about Noether’s theorem.  A cell uses hydrogen and oxygen to un-condense our protein polymers, ever so slightly, to allow life to exist.  It changes the size and shape by moving charges, of electrons and H+.  Gilbert Ling tripped over this in the 1950s.  I mentioned him in the podcast.

When we sleep our semiconductive proteins are designed to be fully condensed and small.  This implies that life can only exist when our protein polymers are slightly unfolded during wakefulness.  Ling is the guy who brought the idea of unfolded proteins to centralized science.  This unfolding of protein semiconductors happens when electrons are withdrawn from proteins.  Free radicals add electrons to the holes that ATP creates to create a current.  In fact, any paramagnetic atoms can add their electrons to the semiconductor to operate it.  UV light creates hormones and hormones are tides of electrons controlled by our star.

Cortisol from ACTH in POMC do this and so does ATP made in the matrix.  Cortisol and ATP are both electron-withdrawing semiconductive biochemicals.  Gilbert Ling was the first scientist to realize what ATP did to proteins.  ATP allows for amino acids to unfold to allow for water binding sites to open to the water hydration shells around proteins.  Water is also a semiconductive protein because of the action of hydrogen bonds in water.

Ling had no idea what he found but the guys at FONAR did because they made an MRI machine from the idea.  When I read Ling’s books I realized what he was saying.  Water is a semiconductor in human’s and it needs specific proteins adjacent to it to operate and unleash solar energy in the electronic state.  Again, when I met Ling I asked him questions to see if he really knew what he found. He did not, and if he did I think he’d have Peter Mitchell’s Nobel Prize now.  He deserved it.

WIDE BAND GAPPED SEMICONDUCTORS ARE SPECIAL BECAUSE THEY CAN SENSE UV LIGHT AND USE IT TO TRANSFER ENERGY AND INFORMATION.

When we are awake our proteins have to be somewhat unfolded and un-condensed (larger).  This means during the day we are less thermodynamically efficient.  The sun’s light has to bridge the gap and this is why we evolved wakefulness from sleep.  This is why I told you in Cold Thermogenesis 2 that I believed that life’s primordial condition was sleep. I believed we evolved wakefulness when we gained the ability to unfold our protein polymers and engage in semiconduction.

Within this sliver of semiconductive protein unfolding is where the magic of life happens.  Similarly, a cell is designed to break symmetries by using hydrogen and oxygen to its advantage.   This ability must be associated with a specific molecule capable of breaking symmetry.  H20 can “unfold” or ‘charge separate’ into H+ and -OH with the addition of infrared heat from the sun or when it lies adjacent to hydrophilic substances.

Proteins are made more hydrophilic with the addition of electrons to them.  They are made more hydrophobic when electrons are removed.   It turns out all proteins are hydrated in life.  Our proteins are the first smart device ever built by nature.  This might be why DNA only codes for proteins using specific amino acids.  Those amino acids work with the visible spectrum of our star.

When we die we lose that ability and our muscles get hard in stiff in rigor mortis.  Liquid water is the perfect chemical to break symmetry with all the protein polymers in all life forms. The reason is found in water’s molecular 3 D molecular arrangements. Liquid water has perfect symmetry in that no matter from which direction you look at the molecules, the view is the same from a molecular standpoint. But water, can and does, lose its symmetry in nature naturally.

During my 18 months of unlearning to relearn, I found out that symmetry in crystals is key.  When symmetry is broken by any phase transition in chemistry (water) energy and information transfers must occur by nature’s laws.  This was how sunlight info and energy entered our bodies.  I realized melanin, Vitamin D, T3, T4, RBCs, etc…..all were semiconductive crystals transferring data from the sun.

This data informs the biomolecules in biochemistry how to act because all of them have hydrogen the chemical chameleon I mentioned above.  This occurs many times in the biochemical reaction pathways of cells. And as such, all breaks of symmetry require a transfer of energy by the laws of physics to satisfy the Second Law of Thermodynamics. Symmetry is also broken any time temperature rises or falls or when electrons or protons are moving in any biochemical reaction. Any transfer of energy/information has the potential to break symmetry and therefore to give rise to emergent properties in the protein polymers or products of these reactions.  This explained why Cold thermogenesis worked to create new stronger light inside of us: VUV using melanin water and these elements on the periodic table.

The line between metal and non-metal status in any element has become quite blurred because of hydrogen. Physics is now awakened to this issue.  This is a new problem for modern chemistry. Its implications have not yet been appreciated by biology.  When you consider that hydrogen is involved in most biologic reactions, this has massive implications for the biology of you and for life in general.  I am no longer in the biochemical silo of belief and I make fun of those who are toying in that cesspool of misunderstanding:  Ray Peat and the food gurus.

When I was a student growing up, hydrogen had a clear distinction in chemistry.  Sodium and hydrogen are group 1 elements.  Not only is hydrogen capable of switching teams but so is sodium its neighbor. Sodium is also used by life in a big way in extra and intracellular ionic fluids.  Now we know that hydrogen and sodium “switch teams” based on their local environment.  When the conditions of existence in these atoms’ environments are altered, they can change their chemical abilities. This action seems very counterintuitive, yet it has been proven by experiment.  This makes them “metastable atoms”. Life appears to like to use atoms that are cationic, small, and metastable. Ling realized this too.  Ling was a smart cookie.

I went back to the periodic table.

We all think hydrogen is a clear gas. But on Jupiter, hydrogen is under so much pressure with an altered temperature, it becomes an extraordinary superconducting metal. In mitochondria, H+ becomes a metal-like plasma as well.  MEG data shows that the two tissues with the highest mitochondrial densities have large magnetic fields, namely the brain, and heart.

This is why Jupiter is believed to have a stronger magnetic field than the sun. Hydrogen gas is diamagnetic on Earth while its dance partner gas oxygen is paramagnetic.  One repels a magnetic field while the other is drawn to one.  So hydrogen acts differently on both planets because each planet fosters a different environment.  In space, hydrogen also acts differently magnetically. Hydrogen is a plasma in space. When air or gas is ionized, it loses its electrons, and plasma forms with conductive properties similar to those of metals. We see this in our ionosphere with aurora.

Plasma is the most abundant form of matter in the Universe because most stars are in a plasma state. Heating a gas may ionize its molecules or atoms by reducing or increasing the number of electrons in them, thus turning it into a plasma.  A plasma contains charged particles: positive ions and negative electrons or ions.  I’d like to remind you here that your mitochondrial matrix is filled with H+.  This is a hydrogen proton missing its electrons.  Mitochondria also liberate light in the form of infrared light or heat.  They also create WATER!  That water is needed to fabricate our wide bandgapped semiconductors.   It too acts as an ionic plasma in you.

These were all the connections I was making that fateful day in the library of the medical school.

Here is how cells bury the sun’s magnetic flux in cells.  It uses H+ to do it.   Magnetism is the essential force that determines the form of plasma or ionized matter taken in an environment. The hydrogen regions around galaxies are also considered plasmas, despite their degree of ionization being small. The degree of ionization in interplanetary space varies between unionized states or can morph into fully ionized states in other regions of space.

In space, however, even the weakly-ionized plasma in the hydrogen region reacts strongly to electromagnetic fields.  Magnetized plasma, such as that contained in the hydrogen region, is the dominating state in the universe as a whole.  Our sun produces massive amounts of plasma it spits out at us into the solar system as the solar wind or a coronal mass ejection.  The sun’s plasma is contained by the high electric and magnetic fields of the sun.

So is the H+ in our mitochondria.  This makes your colony of mitochondria an antenna for the sun’s photons.  To decipher the electric and magnetic codes you need wide-band gapped semiconductors to get Nature’s recipes to run your cells far from equilibrium to satisfy the second law of thermodynamics.  Not too hard to understand once you see it.

SUMMARY

Modern semiconductor technologies are only 70 years old but have already transformed human society. At the heart of the technologies are the physical characteristics of the semiconductor materials themselves: their fundamental electronic and optical properties that enable electrons, holes, and photons to interact and control each other in a wide variety of device architectures and operating environments. For the first 40 years of semiconductor technology, through the late 1980s, the major semiconductor materials were Ge, Si and the “conventional” III-Vs elements of non-metals. The Ge- and Si-based technologies were spawned in 1947 by the demonstration of the first transistor. The early devices were discrete and modest, but further development enabled the replacement of bulky, inefficient, and slow-turn-on vacuum tubes in applications that began with civilian radios and walkie-talkies but quickly expanded to police radios and later military communications satellites. Shortly thereafter, these devices were followed by integrated microelectronics, enabling the rise and spread of computer technology. By 2015, Si technology, dominated by Si complementary metal-oxide semiconductor (CMOS) architectures. The “conventional” III-Vs refer to the narrower-band gap subset of compound semiconductors composed of elements from columns III and V of the periodic table. None of them were paramagnetic.

In electronics, the discovery in the 1970s that the AlGaAs/GaAs heterojunction could give rise to a two-dimensional electron gas (2DEG) was pivotal, enabling the first high-electron-mobility transistors (HEMTs) in GaAs5 and thin pseudomorphic strained InGaAs6 channels. In the 1980s, these devices and their cousins, GaAs- and InGaAs-based heterojunction bipolar transistors (HBTs), quickly began setting records for unity-current-gain frequency (fT) and output power above 10 GHz. In 1989, recognizing these benefits, the U.S. Defense Advanced Research Projects Agency (DARPA) launched its GaAs-based monolithic microwave integrated circuits (MIMIC) program. In optoelectronics, the invention in the 1960s of the laser diode was just as pivotal. A long chain of progress led, among other devices, to the single-mode InP-based laser diodes that now power the broadband dense-wavelength-division-multiplexed (DWDM) optical fiber networks, and which in turn are the backbone of the modern Internet.

By hacking the periodic table I found out in the late 1980s and early 1990s, a series of pivotal materials breakthroughs were made by Isamu Akasaki, Hiroshi Amano, and Shuji Nakamura, for which they were awarded the 2014 Nobel Prize in Physics. Their breakthroughs, built upon the efforts of many earlier researchers, were completely unexpected: seemingly “magic” AlN and GaN buffer layers on sapphire that dramatically reduced dislocation densities; methods to activate p-type Mg doping of GaN; and the remarkable resilience of InGaN quantum well luminescence against structural defects. Magnesium doping was the key to my hacking eureka. Magnesium also doped chlorophyll. My search for other atoms to dope carbon was open full bore.

The KT event caused a brownout on Earth with respect to photosynthesis. This meant less food for the big dinosaurs but it also meant less oxygen for all life. Why did mammals do so well in this environment?

Mammals began to specialize in using paramagnetic atoms with unpaired electrons to control their cellular circuitry. This helped make them more hydrogen, oxygen, and electrons instead of having to rely on their ATPase. Melanin crystals they absorbed from their surface were their innovative event to give them superpowers.

Oxygen is considered critical to nearly all life on earth, as the end electron acceptor in mitochondria that makes, theoretically, mitochondrial oxidative phosphorylation possible, and thereby energy production. This is modern centralized dogma. Is there another pathway to oxygen that mammals specialize in? Anaerobic energy sources can only temporarily supply ATP and maintain cellular function before substrate depletion, energy shortfall, or end-product poisoning that threatens survival. In most vertebrates, the limits of anoxia tolerance are short, on the order of minutes, because of the urgent dependence of the heart and central nervous system on a continuous supply of O2. Modern humans can only handle 4 minutes of anoxia before neuronal cell death occurs. What happened 65 million years ago with mammals is interesting because their hearts and brains were small organs and not energy dense. Today that is not true.

This brings up the key question, what did early mammals look like and how were they sculpted by melanin moving in their bodies from their surfaces to their interior organs?

That story continues in the next blogs.

CITES:

My cerebral cortex.

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

IMPLICATIONS OF THE RUBIN/HUBERMAN MEETING?

What hit the cutting floor?

What do centralized healthcare providers need to know?  History of their profession so they can make better adaptations for patients.  If you listened to the Huberman/Rubin podcast I just did on Tetragrammaton you’ll want more of the details that lead me to POMC and melanin.  Here is the part of that story that EVERY MD needs to assimilate.

I wrote this blog last night after doing a consult for a centralized MD.  I hope it helps many of you.  Check out my latest article: HOW I GOT ON THE POMC/MELANIN TRACK AFTER MY MICHELANGELO EUREKA?  https://www.linkedin.com/pulse/how-i-got-pomcmelanin-track-after-my-michelangelo-eureka-jack-kruse

I made this public.

SHARE IT.  If you want your doctor to adapt you need to help them by pushing them.

QUANTUM ENGINEERING #39: MELANIN CONTROLS EVOLUTIONARY TRAJECTORY IN MAMMALS

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The “regressive evolution” of living a species on Earth has spawned interesting new ideas in new species.  The most interesting regression to me is now seen in humans on social media.  It is hiding right in plain sight and you can only see it if you maintain the wide band gapped semiconductors in your brain.  Improving them in your body no longer is operational.  Darwin is attributed to the quote that survival is linked to the survival of the fittest, but 20 years ago I realized his perspective was myopic.  I believe it should now be about the survival of the wisest.    INTELLECT IS NOT WISDOM.

Only wise humans who can see the loss of human superpower happening at breakneck speed will survive this “backward evolution“.  Wisdom for today’s mammals is born inside their melanin sheets inside their skulls.  Wisdom makes you the most adaptable creature in a rapidly changing environment.  What is changing fast?  Light is.

Light is the creative “Source” in the universe.  To some “backward evolution” may imply a loss of complexity, misleading you to believe, that evolution has a goal of creating more complex forms. It doesn’t However, evolution merely favors features that make a poster “more fit” for a particular current environment.

Consider cave-dwelling fish in Mexico below.

Look at the fish.  Implications of the picture?  What you do isn’t what you think. Let me explain the creative process buried at the core of life.  The evolutionary process doesn’t retrace its steps in “regressive evolution”.  It just appears it to those who do not carefully observe the process.  You have to go deeper than the facade.  Cave-dwelling creatures have frequently undergone “regressive evolution”,  due to their unique light environment.  Remember fish are not mammals, but they have lessons for mammals to learn.  These fish have lost many complex features, like eyes, that are not needed in dark environments. But eye loss in cavefish, for example, doesn’t mean an exact return to a primordial ancestor without these organs. The eye remnants remain.  They are atrophic and lie in wait until the light, the “Source code” returns.  Instead, processes that previously produced the eye stop partway through the process, leaving a vestigial eye overgrown with skin.

I believe the same process occurred in the primate clade of mammals in Africa 2-4 million years ago to explain our species.

To a surface thinker with low dopamine, due to degraded melanin sheets in their skulls, things can look like they’re going into reverse when they aren’t. The eye didn’t go in reverse. It just stopped going forward.  Might humans represent the same thing in the chimp family?

Might it even be more complex today compared to our own genesis?

I believe this is exactly what is happening to human mammals today.  They are no longer moving forward, and their epigenetic toolbox which relies on UV light to drive mitosis, is also regressing.  What does that imply?  The cavefish doesn’t face this now because it is not a mammal and it is protected fully from man’s use of artificial light.

What is happening to mammals that aren’t in Nature and are subject to man made light?

That is how it looks on the primate side who doesn’t talk, how does it look in their cousins who can speak?

What was perfection 520 years ago in stone?

As humans have degraded the melanin sheets inside their skulls with the use of clothing and indoor dwelling with fire use they have become more creative.  Creativity is a regressive evolutionary creation in my opinion of regressive changes in the frontal lobes.  This regressive change has had a positive connotation which can be seen in the Louve in Paris.  Melanin degradations created various levels of dopamine in our frontal lobes that lead to new things on Earth.  There is a lesson here.

Losses in biological complexity may accompany less-obvious increases in complexity in other areas of humanity.  This manifests in novel ways, such as the biochemistries parasites use to get inside hosts and sculpt changes in us by changing light frequencies in our cells.  How big a deal is this?  Men’s face change due to toxoplasmosis.

The sex of offspring change when women infected get pregnant.  What happens to the mitochondrial DNA of women with POMC deficiency over several generations since they control mtDNA inheritance.  Do you understand what “regressive evolution” really means?    I think autism is the first step in new speciation.

It’s very easy for people who do not understand science to think of evolution in terms of what you see; what the morphological features are in living things. But there are also lots of other features that we don’t perceive at the physiological and the biochemical level.  It turns out POMC is working at the biophysical level.  This is well below the classic world of reality.  It is well hidden by Nature.

In cavefish, lost eyes may similarly obscure alternative complexity. Organs responsive to vibrations appear in great quantities in these fish, providing another way to sense in dark environments. And in the already-overstuffed head, these organs found available real estate in the fish’s empty eye sockets.  Nature is efficient in how she operates even in regression.

When Alan Turing turned his mind to biology in 1952, he proposed a model for how biological patterns could stem from the interaction of just two molecules. New work hints that it’s what all vertebrates use to grow hair, feathers, and other skin structures that links to melanin biology.

In 1952, well before developmental biologists spoke in terms of Hox genes and transcription factors, or even understood DNA’s structure, Alan Turing had an heretical idea.

Turing wanted to understand the underlying mechanism that produces natural patterns. He proposed that patterns such as spots form as a result of the interactions between two chemicals that spread throughout a system much like gas atoms in a box do, with one crucial difference. Instead of diffusing evenly like a gas, the chemicals, which Turing called “morphogens,” diffuse at different rates. One serves as an activator to express a unique characteristic, like a tiger’s stripe, and the other acts as an inhibitor, kicking in periodically to shut down the activator’s expression.

How would this work?

Imagine a field of dry grass dotted with grasshoppers. If the grass were set on fire at several random points and no moisture were present to inhibit the flames.  The fires would char the entire field. If this scenario played out like a Turing mechanism, however, the heat from the encroaching flames would cause some of the fleeing grasshoppers to sweat, dampening the grass around them and thereby creating periodic unburned spots in the otherwise burned field.  A pattern would develop.  POMC operates the same way on the body plan genes to sculpt us.  This is where our new frontal lobes in the brain came from and where bipedalism came from.  It also explains why POMC is heavily expressed in our skin overlying our gut that shortened by 30 feet from our cousins.

Some centralized biologists remain skeptical that Turing mechanisms are sufficient to account for these periodic patterns, particularly because there are other viable models, including one proposed by Lewis Wolpert, an emeritus developmental biologist at University College London. In Wolpert’s model, cells interpret their position in space based on how much of each morphogen there is, resulting in stripes, spots or digits. Furthermore, Wolpert says, “no one has yet identified the molecules that work for a Turing mechanism in development.”

Uncle Jack thinks alpha MSH and ACTH/blood glucose are the morphogen and activator in the Turing mechanism of mammals and UV light from our environment and inside of our bodies powers the process of building the mammalian body plan to explain morphogensis.

Centralized biology ignored this paper for decades after Turing’s death.  Only mathematicians toyed with it.  In my 18 months of unlearning to relearn, I realized what Turing found.  He found a way to allow mathematics to bridge the gap between reality to the quantum world.  How?

POMC is a gene made out of atoms.  Since the beginning of the universe, we know one thing for sure.  There were quantum subatomic particles present at genesis.  First and foremost, this implies that a quantum evolution began as a by-product of some type of supernova blast.  All atoms come from these blasts.  This quantum mechanism evolved into a chemical evolution with the construction of atoms.  From this chemical evolution emerged biochemical evolution directed by light some 3.8 billion years ago.  No one is following these clues back to how all things began except Turing.

Atoms are in everything that makes us, especially proteins which come from genes like POMC.  Every part of you is made up by atoms right now.  All atoms are controlled by light at some level = they are quantized.  The laws of the universe scale from the quantum level to the macroscopic level.  Quantum mechanics is foundational to everything in this universe.  This implies that, in order to have a fundamental understanding of life, you must have a quantized molecular mechanism to prove your theory.

Darwin has nothing to prove anything with what he wrote in the Origin of Species. He provided us with observations that correlated to morphologic change.  This was correlative data, not causative data.  Lots of people forget that basic fault because of guys like Huxley and Dawkins.

When you are dealing with atoms, you are dealing with quantum mechanics.  This is an area where Dawkins will have to trick you to believe Darwin’s ideas.  Nothing in Darwin’s theory talks about nature’s basic quantum language because it was not discovered yet.  Darwin gets a pass on that but Dawkins does not from me.  Feynman famously said that if your theory does not match your experiment, no matter how elegant the theory,  it is wrong.  Well, I am going to show you Darwin was, in fact, wrong.  I am going to use quantum mechanics to show you why.  The key to understanding how evolution occurs is to understand the fundamentals of Einstein’s mass equivalence equation E =mc^2.

The mass equivalence equation shows us the wide reaching impacts of failing to understand how small changes in quantum mass can create widespread changes in energy.  How does math scale to the quantum world?   Avogadro’s constant is the only scaling factor we have that allows us to go between the macroscopic world to the quantum level (sub atomic scale).  This allows us to link observations we make in nature, with respect to atoms, directly to the mathematics of the quantum realm.

You heard me mention this relationship in the podcast I did with Max Gulhane, MD from Australia when I talked about how much water is created from Fats and carbohydrates and I mentioned that fats created double the amount of moles of water than sugar does.  One mole of a substance is equal to 6.022 × 10²³ units of that substance (such as atoms, molecules, or ions). The number 6.022 × 10²³ is known as Avogadro’s constant.

Just from common sense, quantum mechanics describes nature as absurd.  hen the quantum experiments have validated nature’s absurd behavior, we must accept Lady Evolution as she is; bizarre and  absurd.   QED seems counterintuitive to evolutionary biology because she asks you to read the mass equivalence equation right to left in order to understand her.  Life is fundamentally a thermodynamic problem to solve, not an evolutionary one.  E=mc^2 means that 2 x3 = 6 just like 3 x 2 = 6.  Few realize that is built into Einstein’s mass equivalence equation.

The key for quantum evolution is to know how the molecules of life, namely proteins, change over time.  Subatomic particles change the charge and change the size and shape of molecules and this leads to new emergent properties macroscopically in animals.  POMC is the mammalian gene that introduced charge variation and size and shape changes to proteins to cause them to act differently.

Biological diversity, across the board, is based on a fairly restricted set of principles that seem to work and are reused over and over again in evolution.  This seems especially true in the evolution or mammals and therapod dinosaurs/birds over the last 65 million years. Nature, in all its exuberant inventiveness, may be more conservative than we thought in creating changes in morphology.

SUMMARY

Part of the reason evolution doesn’t retrace its steps is that adaptations lead to other changes. That makes simply dialing back a specific change extremely complicated.

If you’ve made a change, you’re going to fine-tune that adaptation, and that adaptation will have to interact with other genes to sculpt out a solution with staying power.  Now, if you reverse that one change, all of the other genes are still going to have to be changed to reverse evolution.

In cavefish, for example, the original development of an eye may have come with changes not only to the semiconductive proteins needed for eyes but also to skull structures of an eye socket. A mutation affecting an eye protein wouldn’t cause an organism to revert to one without the socket.

Changes in the the environment always predates changes in the semiconductive fab plants in cells.  When thought of in this way, you can see why Nature never makes mistakes. Evolution is always progressive in that it’s selecting for features that improve the fitness of the individuals in which that variation is being expressed.

If DNA genes matter so much why is it that most, not all, circadian gene regulation occurs at a post transcriptional time frame?  Post-transcriptional regulation is the control of gene expression at the RNA level. It occurs AFTER the RNA polymerase has been attached to the gene’s promoter and is synthesizing the nucleotide sequence. This means the gene is not the key to change.  It means the process after gene expression are the key to how wide band gapped semiconductors in you sculpt tissues.  Therefore, as the name indicates, it occurs between the transcription phase and the translation phase of gene expression.

These controls are critical for the regulation of many genes across human tissues. It also plays a huge role in cell physiology, being implicated in pathologies such as cancer and neurodegenerative diseases in humans.  This tells us that these diseases are caused by environmental changes and not GENETIC ones.  This is why I told Dr. Huberman and Rick Darwin was wrong in his approach and the neo Darwinists like Dawkins are really wrong.  I can give Darwin a pass because quantum mechanics was not discovered until 50 years after his penned his theory.  I cannot absolve Dawkins of this.  His self gene book was penned over 50 years from the discovery of quantum mechanics.   The implications for you care clear.  Centralized science still acts like Darwin was correct.  This makes no sense from a scientific point of view does it?  Darwin said small changes in genes called mutations leads to variation of species.  This is a huge problem for neo-Darwinians. Why?  A post transcriptional protein results in a non-functional protein for life.  Proteins must have all four bends to work properly in cells.  So how could life’s stage be gene based?

Life is like a photograph; it develops from the negatives in the environment.  What is next for humans on Earth?

I now believe creativity, and most mental diseases, are a regressive evolutionary creation in my opinion of regressive changes in the frontal lobes.  Many modern diseases are evidence of proteins undergoing semiconductive engineering inside your tissues to change the frequencies of light in your tissues.  This leads to new and alien bends, charges, and alteration of atoms in your tissues that change the morphology of your body and the physiology of your tissues.  The most powerful changes are occurring in the POMC gene family and all the peptides it creates by light frequency cleavage.

CITES

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3363033/

https://www.science.org/doi/10.1126/sciadv.aau5484

https://www.newscientist.com/article/mg25834344-900-the-shocking-decline-of-earths-microbiome-and-how-to-save-it/