Is nighttime and DAYTIME technology devices use to blame for the etiology of most diseases in humans? Yes, I believe it is today. WOW. That is a big statement, Uncle Jack. How and Why? Here is a recent slide from a presentation I gave to shock my audience below.

Melanopsin, like the cone photoreceptor, is a PHOTORECEPTOR TOO FOR BLUE LIGHT. ALL OPSINS in humans are bound to retinol, and when the photoreceptors are damaged it is because of the atomic changes in retinol when the weak covalent bound it broken by light out of the normal circadian cycle.

What is the take home? The blue light hazard associated with man made light or the light present in all laboratories globally today generates massive levels of mitochondrial ROS and oxidative stress occurs directly in the outer segments of photoreceptors after blue light irradiation leading to disease. The cites below show that this statement is not hyperbole. It is now PEER reviewed published reality.

If you want to know where melanoma begins read the last cite in listed below. Melanocytes sense blue light and regulate pigmentation through Opsin-3 = melanopsin.

It took 90 years for “medical science ” to rebut the claim that linoleic acid is essential in any human diet, a claim that has led to an incalculable mischief in terms of dietary advice and disease prevalence, In the last two centuries. How many decades will it take for the average physician or your physician to read those papers covering the nutrition debacle? How long will it take to change their advice or their practice of the healing arts?

I believe it might take several hundred years to get people to understand that blue light from man made devices is more deadly than any other stimulus man has created in the last 120 years because our focus in in nuclear DNA and not on the mitochondrial DNA mutations cause by blue light.

In 1998, we found melanopsin in the retina. In 2009 we found neuropsin in the skin and cornea. In 2014, we found melanopsin in the arterioles of the human body. This tells us all we are creatures of light who capture and transform the light of the sun into energy that cells use to create life and health.

In December 2017, we found melanopsin in the skin and subcutaneous fat of humans. This was huge news to those who understand leptin and that leptin the fat hormone is also found within the subcutaneous fat of MAN. The data is telling us why we have an obesity crisis and it has NOTHING to do with food or exercise but it has a lot to do with circadian arrhythmia of light in our eye and skin and subcutaneous fat mass.

The nighttime and daytime light environment has changed dramatically due to modern technology. Increased usage of mobile devices during ANYTIME OF THE DAY can disrupt your circadian clock. PEOPLE forget that the melanopsin receptor is regenerated DURING daytime!!!! So if you are around man-made blue light during the day you are still ruining your melanopsin photoreceptors. The intense light emitted from technology devices in screens has the potential to alter the timed release of factors within the eye, leading to chronic insults and susceptibility for visual damage. What does this mean to melanopsin photoreceptors?

I gave you my answer in the Vermont 2018 video.

Recent findings cited below to suggest a functional role for the circadian clock in mammalian cone photoreceptor development and provide evidence for a continuing role for thyroid hormone (TH) signaling in cone photoreceptor maintenance. These researchers have said their findings may be of relevance in OTHER tissues where human photoreceptors are as well, where the circadian clock could alter tissue function by directly regulating enzyme type 2 iodothyronine deiodinase (Dio2) expression and thus TH signaling.

THAT is WHAT the data I presented in VERMONT 2018 is all about. I hope you view the talk. It is well worth it to further your education. Once you realize and know where melanopsin is, and follow the damage in its wake, you begin to see where mitochondrial disease begins for the very first time in your life. It happens where clinicians least expect it and that is why they always miss it and the public cannot be helped via a prescription pad. That is where the data is now……..it is not in food/exercise choices, it is made in the light choices we make.

With this new information, researchers can begin to ask questions such as, “How else can we change the photoreceptors in humans using light evolution has never used? Are there other factors that can improve photoreceptor function and help extend their viability that we have failed to consider in science and industry? The BLACK SWAN among you now knows this answer. It should be as clear as the nose on your face, because this new data is telling you disease generation is not what your doctors were taught in medical school.  Your light choices form your medical destiny.  







CPC #49: Mondini’s dysplasia and Tinnitus

  • Mondini dysplasia can cause chronic tinnitus. This defect comes from a defect in the Fibonacci sequences during embryogenesis and can lead to defects in melanosis that can profoundly affect hearing and tinnitus generation in the dysplastic brain.
  • The Fibonacci numbers form a sequence of numbers defined by a relationship mathematically.  What this means, in English, is that it is a sequence of numbers whose relationship is this: after the first two numbers, each proceeding number is the sum of the previous two numbers. For example 0, 1, 1, 2, 3, 5, 8, 13, 21, 34, 55, 89, 144, 233…..and so on. Quite simple, really.
  • Fibonacci numbers are not purely artifact, they are also found in nature in an uncurling fern, the branching of trees, and leaflets of the pineapple. The Fibonacci sequence also describes the “golden spiral,” which is when a “golden rectangle” is subdivided in smaller and smaller golden rectangles —the result being a predictable spiral.
  • Fibonacci numbers have an interesting property. When you divide one number in the sequence by the number preceding it, you are left with a number very close to 1.618. This number is called the “golden ratio,” and rectangle whose sides is equal to the golden ratio is known as a “golden rectangle.”
  • One example of a biological structure in the mammalian body which is very close to a “golden spiral” is the cochlea.  You can see that spiral below in blue.

  • The Mondini malformation and Mondini defect is an abnormality of the inner ear that is associated with sensorineural hearing loss and tinnitus. This deformity was first described in 1791 by Mondini after examining the inner ear of a deaf boy. The Mondini dysplasia describes a cochlea with incomplete partitioning and a reduced number of turns, an enlarged vestibular aqueduct, and a dilated vestibule. A normal cochlea has two and a half turns, a cochlea with Mondini dysplasia has one and a half turns; the basal turn being normally formed with a dilated or cystic apical turn to the cochlear. The hearing loss can deteriorate over time either gradually or in a step-wise fashion and it can lead to debilitating tinnitus as hearing is destroyed. Destroying the ear with deafness operations might actually make the tinnitus worse. Cochlea implants might be a better way to deal with dysplastic auditory cortex.

About one in five people experience tinnitus, the perception of a sound—often described as ringing—that isn’t really there. Tinnitus brain mapping has revealed just how different tinnitus is from normal representations of sounds in the brain.

Perhaps the most remarkable finding from the brain mapping experiments was that activity directly linked to tinnitus was very extensive and spanned a large proportion of the part of the brain that researchers measured from during brain surgery. This tells us that tinnitus is really not a peripheral disease but a sensory processing disorder.

Only a few groups in the world have the expertise and collaborative infrastructure to conduct these neurosurgical experiments. It is possible because patients who require invasive brain mapping in preparation for epilepsy surgery also volunteer to participate in research studies. The University of Iowa has the ability to do this because of their epilepsy program.

It is such a rarity that a person requiring invasive electrode monitoring for epilepsy also has tinnitus. Some people do not have epilepsy but have been found to have other neurovascular abnormalities that might the cause of the tinnitus.

Iowa’s epilepsy team puts a recording platform into the patient’s brain for clinical purposes and they can modify it without changing the risk of the surgery. This allows them to understand functions in the brain in a way that is impossible to do with any other approach.

Iowa researchers contrasted brain activity during periods when tinnitus was relatively stronger and weaker. They found the expected tinnitus-linked brain activity, but they report that the unusual activity extended far beyond circumscribed auditory cortical regions to encompass almost all of the auditory cortex, along with other parts of the brain.

The sheer amount of the brain across which the tinnitus network is present suggests that tinnitus may not simply ‘fill in the gap’ left by hearing damage, but also actively infiltrates beyond this into wider brain systems based on the findings of this paper below.

These new insights should help to inform treatments such as neurofeedback or optogenetic therapies, where patients learn to control their “brainwaves,” or electromagnetic brain stimulation.

A better understanding of the brain patterns associated with tinnitus may also help point toward new photobiomodulation approaches to treatment.

The team included the University of Iowa researchers Hiroyuki Oya, Gander, Sedley, and Howard and Christopher Kovach, Kirill Nourski, and Hiroto Kawasaki, as well as Timothy Griffiths at Newcastle University. The research was supported by grants from the National Institutes of Health and the Wellcome Trust and Medical Research Council in the U.K.

Tinnitus appears to be a sensory processing disorder whose causes are multiple but all lead to a sensory processing disorder in the thalamus and auditory cortex.  Mondini’s dysplasia is one of many things that cause this cortical dysfunction in the auditory part of the brain.




DO TINNITUS, PD, and AD all RELATE TO blue light and nnEMF via hypoxia?

In the human ear, there are melanocytes present in the hearing mechanism which are cells that form melanin. Melanin is a UV light-absorbing pigment that can be made from tyrosine or phenylalanine. You can see from the picture above that the action spectra of light from both aromatic amino acids is 220-300nm light which is deep in the UV range. This implies the light frequencies are somehow linked to how and what we hear. Tinnitus is a warning symptom that your nnEMF environment is sub-optimal. The question is for the inquiring mind, is why did evolution put this photochemical in our hearing apparatus?

Might melanin be how we tune into our environment first before sound affects us?

Remember light travels way faster than sound so from a physics standpoint using light for the afferent sensory reflex loop makes a lot of quantum mechanical sense. It just offends your doctor’s common sense. That is a good thing for a Black Swan. We ask questions few people do.

In this system, full-spectrum solar light is critical because it contains the 200-400 nm light tyrosine/phenylalanine that needs to create melanin. Melanocytes make melanin from aromatic amino acids (tyrosine) that all have hexagonal rings of carbon that absorb UV light from 220 nm to 300 nm. For this mechanism to tune properly, you first need AM balanced light in the visible spectrum that has no UV light present. The dose of the blue light present is stimulatory to the pituitary gland but this pro-growth stimulus is always protected and balanced by the 42% of IR-A present early in the AM. The next light that shows up diurnally in solar exposure is UV-A light in the AM. when it shows up varies based upon your latitude. This explains why tinnitus is rare inside the tropics where light is more stable. I expect this will change as people inside the tropics begins to use technology from the US. This will ruin their afferent reflex loops.

Melanosomes in the ear pay attention to UV light’s arrival by having melanin’s electrons become excited by the sun rays. To activate the system the ear pinna and external auditory canal need the full day spectrum solar light to develop naturally. This includes IR-A, UV-A, and UV-B based upon your latitude and altitude.

The human ear effectively “measures” the light radiation environment you allow via your choices and helps fine tune your hearing by reacting with the photon traps in tyrosine and phenylalanine with the formation of melanin as hearing protectors. If the radiation environment is disturbed (by man-made light), limited or no melanin is formed in the pinna or in the external auditory canal.

Without this initial stimulus, human hearing becomes affected and our hearing becomes susceptible to an improper energy transformation.

People forget that when light collides with melanin the electromagnetic wave becomes and electro-mechanical wave or an electromechanical wave called a phonon/soliton. What is the target of this phonon or soliton? Look at the picture below. Is there a pigmented vascular layer in the inner ear? Yes, there is. Why do we have light pigments in our cochlea? And why do we have melanin in our pinna and our ear canal? These are questions Black Swans ask themselves to understand why their hearing is altered.

Those phonons are targeting pigmented cells in the body of the cochlea by a process of chemiexcitation. If solar light is absent and man-made light dominant in your environment the transformation these light waves into mechanical-acoustic signals (phonons/solitons) is disturbed. This is how tinnitus begins quantum mechanically in my opinion. The afferent reflex arc is disrupted by nnEMF light waves sensed on the external ear and in our ear canals.

Melanin is a pigmented polymer with a known role in dermal solar protection. In vertebrates, melanogenesis has been reported in leukocyte population of cells suggesting a potential role in innate immunity. An altered innate immune response is one of the first things ENT surgeons should suspect in people with tinnitus but few do because they do not know about this link.

The presence of melanin in the inner ear was established more than a century ago, but the exact biological function of the pigment in the labyrinth has yet to be determined in medical textbooks. This is why tinnitus remains a mystery for docs and their patients afflicted with it.

Special attention should be drawn to the composition of melanin. Melanin is a biological reservoir for divalent ions like calcium and as an ion exchanger, as well as an intracellular buffering system for calcium. nnEMF alters the resonance frequency of this atom. nnEMF also alters voltage-gated channels that control calcium flow. This explains why melanin and nnEMF are likely linked to the symptom of tinnitus. It should be pointed out to the non learned that melanin is capable of binding ototoxic drugs. Finally, morphological responses of melanocytes happen when local disturbance of Ca++. Below you can see how calcium is quantized to the light that affects the afferent loop in this reflex.

One last link of Ca2+ release to another ear disease is Meniere’s disease which is often linked to tinnitus.  An altered level of melanin or an imbalance of its functioning can create an imbalanced Ca2+ homeostasis in the inner ear.   This has been demonstrated using  endolymphatic hydrops (EH) as an animal model for Meniere’s disease. These models have shown us that there is a  possibility of a receptor-mediated Ca2+ transport across the pigmented epithelial layer, especially the light cells, and the presence of a ‘chemical signal’ as an initiating modulating factor in the disturbance of Ca2+ homeostasis.  It appears light tunes the cochela using calcium as the electromechanical lever.  It is pointed out numerous times in the PEER reviewed literature that melanin is capable of binding calcium and may act as a buffering system in hearing and in balance.

Quantum mechanics rarely extends to molecular medicine. Recently, the pigment melanin was found to be susceptible to chemiexcitation, in which an electron is chemically excited to a high-energy molecular orbital. In invertebrates, chemiexcitation causes bioluminescence; in mammals, a higher-energy process involving melanin transfers energy to RNA and DNA and mtDNA without using photons.  This can create lethal and mutagenic cyclobutane pyrimidine dimers that can cause many diseases. This process is initiated by the free radicals NO and O2-. Their formation can be triggered by nnEMF light and/or inflammation. Several chronic diseases share two properties: inflammation generates these radicals across the tissue, and the diseased cells lie near melanin. I have said for 15 years that that nonquantized chemiexcitation may be an upstream event in numerous human diseases that lead to mitochondrial damage.


Nuclear DNA repair of UV pyrimidine dimers in Chinese hamster ovary cells (CHO cells) is very selective with preferential repair of only sequences containing actively transcribed genomic regions. In essence, the literature over the last 30 years has shown very little repair mechanisms of these dimers in the entire mitochondrial genome of any animal tested.  Nuclear DNA repair mechanisms are quite rapid and very accurate.  Direct nuclear DNA action is likely not the mechanism that leads to disease.  Research has shown, even actively transcribed areas in mtDNA do not appear to be repaired in mitochondrial DNA. This data is in agreement with that previously reported in HeLa cells and in yeast  where a lack of repair of pyrimidine dimers in mitochondrial DNA was also observed.

The chemiexcitation path to diseases is a new quantum mechanical idea. It has long been known that photons of ultraviolet radiation from sunlight can be directly absorbed by DNA, where they excite DNA bases. If two excited pyrimidines (thymine or cytosine) are adjacent in RNA, DNA or mtDNA, a double bond forms automatically by the action of light. UV light can do this but it blue light is also quite capable of doing this as well.  When blue light creates ROS and RNS it opens thymine or cytosine to form two single bonds between the bases and makes a cyclobutane pyrimidine dimer (CPD); this [2+2] cycloaddition reaction can only happen if the bases are in an excited state by light.  Sunlight normally can lead to cell death via apoptosis.  It can also stimulate NK cells to take out the altered cell filled with mitochondrial disease and viral loads.  Alien light does not stimulate immunosurveillance in the same “quantized way” that sunlight does and this can lead to cancers or other mitochondrial disease.  This is often associated with co-morbid hypoxia in the cell.   Immunological surveillance is a monitoring process of the immune system to detect and destroy virally infected and neoplastically transformed cells in the body.  This is why altered melanosis is linked to both viral illness and cancers.

The CPD disrupts base pairing and distorts the DNA helix, leading to cell death or – when DNA replicates – a C→T mutation. Mutations in oncogenes and tumor suppressor genes are required for disease generation like cancer. Chemiexcitation instead excites the DNA bases long after light exposure has ended because of how melanin operates with light. In this situation, light radiation serves to activate enzymes that synthesize the radicals NO• and O2•−for hours afterward. These radicals form peroxynitrite, which oxidizes melanin or its monomer DHICA (5,6-dihydroxyindole-2-carboxylic acid) and allows ambient O2 to create a dioxetane on the melanin. The dioextane moiety, is a strained 4-atom ring containing –C–O–O–C–, is unusual in being able to release large amounts of energy in a single reaction, creating long-lived, high-energy, electronically excited triplet states (denoted by * below).

This triplet energy can transfer to RNA/DNA/mtDNA, resulting in a CPD without the involvement of photons. Thereafter, an unrepaired CPD would again result in mutations or cell death. The same radicals are formed during normal cellular inflammation from nnEMF damage, creates the same end product can be created by enzymes like horseradish peroxidase (HRP), prompting the idea that chemiexcitation can occur in internal organs leading to a myriad of diseases that today have no explanation of what causes them. This mechanism is likely why RF and microwave radiation damaged the ears and brains in people stationed in the Cuban embassy a couple of years ago when and Electromagnetic device was aimed at our emabassy to cause damage to US citizens.

Human mitochondria have their own DNA, which is double- stranded, circular and contains —16,569 base pairs. The mitochondrial genome has been sequenced in its entirety and consists of genes that code for 13 subunits of the respiratory chain complexes, 22 tRNAs and two rRNAs. Until recently, the only mitochondrial DNA defect that appeared to be of significance was that of a mutation in one of the mitochondrial ribosomal RNA genes which conferred chloramphenicol resistance. However, within the past 30 years defects in the mitochondrial genome have been described in a number of human diseases. The initial description by Holt et al. of deleted mitochondrial DNA in patients with mitochondrial diseases has been confirmed by  numerous studies which found that mitochondrial deletions occurred in > 90 % of cases with Kearns—Sayre syndrome. Additionally, mitochondrial point mutations have been associated with Leber’s hereditary optic neuropathy, Pearson’s syndrome, autism, T2D, and some cases of chronic progressive external ophthalmoplegia. Accumulations of mutations in mitochondrial DNA have also been reported in the brains of patients with Parkinsonism and Alzheimers disease. These findings suggest that mitochondrial DNA defects are of biological importance in modern medicine.  It makes you wonder why medicine keeps ignoring these links.

What does all this imply?  If you live at a high latitude, with poor sunlight, have too much nnEMF in your life that causes hypoxia, or you live in a large city with many people addicted to technology, you are at risk for hearing loss and tinnitus.  It also might be a precursor symptom to macula degeneration and neurodegeneration in the brain.  Anywhere melanin is located, chemiexcitation can cause mtDNA damage and cause a hum in your ears.


Chemical excitation of electrons: A dark path to melanoma.Premi S, Brash DE.DNA Repair (Amst). 2016 Aug;44:169-177. doi: 10.1016/j.dnarep.2016.05.023. Epub 2016 Jun 1.PMID: 27262612


Do you know the purpose of the unusual construction of the mitochondrial membranes? Did you know that the inner mitochondrial membrane is the ONLY membrane in humans that is DEVOID of DHA? Do you know why the membranes in the mitochondria are built by Nature to be extremely hydrophobic? Do you know that these membranes can carry voltages close to 30 million volts because of this build-out? Do you know that one of these membranes actually makes water from food? Did you know that the atomic construction of this water also has to be specifically depleted of a certain isotope? Do you know why all these things exist in your mitochondria?

The answer might shock you. Uncle Jack is going to tell you that all these things occurred 650 million years ago to suspend the laws of physics to allow nature to do things not even gods could fathom. Nature figured out how to use nanoscale spaces to suspend physics to build the possibility of life.

Did you know when a thin layer of water is squeezed between two hydrophobic surfaces, the laws of classical physics break down? Well, I have been teaching my members this since my epic April 2016 webinar on what life really is up too. Now you have more data I am on the right track and the paradigm and all my critics remain myopic.


So Nature built cells to have the ability to suspend what we should expect to give us the most improbable answer why life really exists and happens. She figured out how to suspend her own laws using things she built. How is that for counterintuitive?

That is why I teach Black Swans how to think. Black Swans are rare. They go deeper to find wisdom than others would. I call these people Black Swan mitochondriacs. Humans that actually take the time, to read, research, and read about science that on the surface seems superfluous, but is foundational to our health on the submolecular quantum level.

Nature does not employ any “balanced protocol” in her usage. She is all about unbalancing the scales to favor the tasks that cells need to accomplish. NEVER FORGET IT.

And anyone who says otherwise will have to explain this new finding.

People who have open minds to accept new data that blows your paradigm of beliefs apart.

Why do living things prefer the lighter isotope of hydrogen than the heavier version of hydrogen called deuterium?

Heavier things make quantum mechanics “less probable”.

In the early 1980s, researchers first noted an unexpected effect when two hydrophobic surfaces were slowly brought together in water. At some point, the two surfaces would suddenly jump into contact—like two magnets being brought together.  No one knew why or how it happened.

Part of this research challenge was to realize that the hydrophobic interaction is unique to liquid water.   No other solvents are capable of this effect.  Living things are most made of water.    Your colony of mitochondria make water.

The smaller an object/atom is, the less strictly it is governed by the laws of classical physics, and the more it is subject to quantum effects. A tiny hydrogen atom is a quantum object—sometimes behaving like a particle, sometimes more like a wave. Deuterium, twice as heavy as hydrogen, is less subject to quantum effects. The consequence is that D2O is less destabilized than H2O when squeezed between two hydrophobic surfaces and the hydrogen bonds between water molecules get broken. It turns out life wants to shapeshift water’s hydrogen bonds with light to create the magic that life uses.

When mitochondria are non optimal they are making less water and they become hypoxic. This changes the delta psi or the electric charge on its membranes and this lowers the redox potential. We can see this effect via our endogenous glutathione levels on testing. This lowers the probability of these quantum nuclear effects in water making illness more likely over health.

This tells us that this effect is important in creating the living state.  This new research work shows how quantum nuclear effects in water become substantial on the nanoscale.  that is the scale your cells operate in.

Nature is capable of a lot more than we believe.


“Nuclear Quantum Effects in Hydrophobic Nanoconfinement” by Buddha Ratna Shrestha, Sreekiran Pillai, Adriano Santana, Stephen H. Donaldson Jr., Tod A. Pascal and Himanshu Mishra, 31 July 2019, Journal of Physical Chemistry Letters.
DOI: 10.1021/acs.jpclett.9b01835





When a wise person speaks he understands fully the intent of the words, but what the ignorant person hears is subject to their present set of knowledge. There is an inherent disconnect. There is always a loss of information and energy transfer in this case which is why social media is not the ideal place to explain yourself in order to teach.

This requires the student to have skin in the game to understand things well and it is best done in person. Where misunderstanding dwells, misuse will not be far behind in the under-educated mind. It is far safer and wiser for the quantum biologist to remain on the solid ground of the physics of light and eschew the shifting sands of philosophic extrapolations found in modern physics. The ignorant among us can know things, but the point of life is to understand how all things link back to the fabric of nature and life.

Life also has another surprise for those with natural wisdom: When we talk sense to a fool they often try to label you foolish only because of their own ignorance. If your audience is not wise this can lead to meme creation and control of many other lean minds. The goal is to make the curious wise with nature’s wisdom quickly to overcome the wasteful inertia of a paradigm’s core beliefs. This is why I am allergic to a closed mind who buries curiosity. What is the core message for a curious mind? Just because you don’t understand it, doesn’t mean or imply that the truth is not being delivered to you. Your wisdom myopia does not trump the deep truths buried in nature’s laws. There is a science of light out there to understand, and to bring it to biology is to brighten everyone’s perspectives. Today, biology is in the dark ages of understanding how light works with and within cells and innovates life from abiotic atoms.

This must change if medicine is to advance. An age in science is called dark, not because the light fails to shine, but because people refuse to see what is already published in the literature but still have yet to understand how it links back to life. Their educational myopia allows them to remain in the dark because they continue to misunderstand the implications of this data.