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Parkinson's disease begins as an PHOTOelectrical defect.......

Discussion in 'Educating Doctors' started by Jack Kruse, Jan 6, 2019.

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  1. Jack Kruse

    Jack Kruse Administrator

    Glucose had long been thought to fuel oxidative metabolism in active neurons until the recently proposed astrocyte-neuron lactate shuttle hypothesis (ANLSH) challenged this view. According to the ANLSH, activity-induced uptake of glucose takes place predominantly in astrocytes, which metabolize glucose anaerobically.

    Lactate produced from anaerobic glycolysis in astrocytes is then released from astrocytes and provides the primary metabolic fuel for neurons. The conversion of glucose to lactate is thought to be stimulated by glutamate and the concomitant high intracellular Na that ensues.

    Why is that important?

    What does glutamate stimulation do?

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  2. Jack Kruse

    Jack Kruse Administrator

    This is broken in PD.........this is why dopamine is not being made.

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  3. Jack Kruse

    Jack Kruse Administrator

    So..........what exactly is this Black Swan saying about PD?
  4. Jack Kruse

    Jack Kruse Administrator

  5. Jack Kruse

    Jack Kruse Administrator

  6. Jack Kruse

    Jack Kruse Administrator

    All PD patients have mitochondria that are redox shifted from their photoelectric defect = pseudohypoxia = low NAD+

    The Astrocyte - neuron lactate shuttle seems to boost more ATP supply to the neuron under hypoxic conditions.
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  7. Jack Kruse

    Jack Kruse Administrator

  8. Jack Kruse

    Jack Kruse Administrator

    Astrocytes (top) can take up glucose from the blood circulation through glucose transporters (GLUT1), a process that is enhanced upon glutamate release from neurons and glutamate binding to astrocyte-expressed glutamate transporters (GLT-1).

    Let us put it all together now.........

    Of all cells, human erythrocytes express the highest level of the Glut1 glucose transporter. However, the regulation and function of Glut1 during erythropoiesis are not well known because nobody studies it.

    We now know that glucose transport actually decreases during human erythropoiesis despite a >3-log increase in Glut1 transcripts.

    In contrast, Glut1-mediated transport of L-dehydroascorbic acid (DHA), an oxidized form of ascorbic acid (AA), is dramatically enhanced.

    Recent studies have identified stomatin, an integral erythrocyte membrane protein, as regulating the switch from glucose to DHA transport.

    Notably, though they found that erythrocyte Glut1 and associated DHA uptake are unique traits of humans and the few other mammals that have lost the ability to synthesize AA from glucose. ARE YOU PAYING ATTENTION. Might stomatin have a circadian cycle in RBC that gets destroyed by melanopsin dysfunction?

    Yep......how? Since Stomatin is in the cell membrane of RBC its circadian biology must be linked to the RBC entrainment. What entrains them? The heme protein peroxiredoxins. Remember all heme proteins are destroyed by melanopsin dysfunction.

    Research using red blood cells as their source cell found that peroxiredoxins, highly conserved antioxidant proteins, undergo ∼24-hour redox cycles, which persist for many days under constant conditions (that is, in the absence of external cues). Moreover, these rhythms are entrainable (that is, tunable by environmental stimuli) and temperature-compensated, both key features of circadian rhythms. This is how PD begins folks. As it goes the melanopsin dysfunction destroys more and more photoreceptors and this leads to a gradual picture of scurvy in dopaminergic neurons because their RBC circadian biology is destroyed.

    Accordingly, it has been shown that mice, which is a species capable of synthesizing AA, express Glut 4 but not Glut1 in mature erythrocytes. Thus, erythrocyte-specific coexpression of Glut1 with stomatin constitutes a compensatory mechanism in mammals that are unable to synthesize vitamin C.

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  9. Jack Kruse

    Jack Kruse Administrator

    With PD, like all diseases of aging NAD+ drops due to the pseudohypoxia and we have a serious mitochondrial problem.

    How do we solve for X, David Sinclair? Do we give people NAD+ in nature or do we use an endogenous pathway?


    Supplement makers take note.
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  10. Jack Kruse

    Jack Kruse Administrator

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  11. Jack Kruse

    Jack Kruse Administrator

    Why is PD linked to gut issues so much?

    Hominids in a house, job, car, with PD = primates in a zoo - not enough NO in the system.

    What doesn't this guy know? Light in the primate zoo is very similar to light in the hominid zoo and the results are the same. It is painfully obvious what he is missing. How long do you think it will take for him to get around and reach Jeff Leach's work in Science on this topic? Light at the equator does not vary and no matter what you did to the Hadza their microbiome there was rock solid. Wild primates and wild humans have a lot in common. The most interesting thing is the zoo humans have no idea they have a lot in common with the confined primates because they are being forced to live indoors under blue light. The very same light stress environment we see in US zoo humans in neighborhoods. #mitochondriacwisdom https://www.youtube.com/watch?time_continue=1&v=FW3198J83RQ
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  12. Jack Kruse

    Jack Kruse Administrator


    Animal photosynthesis requires it.

    Could melanin make photosynthesis likely in animals? Photosynthesis in plants is considered the most important chemical reaction in the world because is the first step in the food chain. The first clues of the process were detected by Lavoisier and others during the XVIII century, but the exact nature of the chemical reactions involved remain poorly understood. Moreover, dissociation of the water molecule constitutes the very first reaction of photosynthesis in plants, and was unsuspected, even unthinkable in human beings, until we found it in human retina in the 1990s. The discovery of the amazing capacity of our body to makes the dissociation of the water molecule breaks the paradigm: Plants and human beings have the same very first reaction as the origin of life. The impact in the field of molecular biology is huge; therefore the role of the water and glucose must be redefined, glucose is just a source of biomass, instead water is the real source of energy of the eukaryotic cell, and neuron cell is not an exception. The main source of energy of the CNS is the CSF and therefore the ventricles and subarachnoid space. Blood vessels are merely source of biomass. By the analogy with the process in plants, our discovery was named human photosynthesis. Human being begin to lose the capacity to split the water molecule at 26 years old, ca. 10 % each decade, and after the fifties goes into free fall. Our research along these 23 years thought us that medical modulation of human photosynthesis has extraordinary therapeutic results in CNS´s diseases.
    Melanin is a human chlorophyll; Melanin is to animal kingdom as chlorophyll is to plant kingdom. Both molecules have the amazing capacity to split the water molecule at room temperature. Both of these chemical makes is possible to burn water to liberate electrons. Photosynthesis is the only known process that is capable of actually burning water. But the process in chlorophyll is irreversible and melanin makes the process work in two way. The first is the dissociation and reforming of water molecule with the consequential release of energy.

    The human body has a photosynthesis system composed by Light/ Melanin/ Water, arranged in order of abundance in nature. Melanin is able to absorb the full electromagnetic spectrum, from radio to gamma rays, in contrast, chlorophyll just absorbs blue and red light (400 to 600 nm). This is why plants are surface quantum machines and animals are full thickness solar machines. Secondly, melanin has the intrinsic property to split and reform the water molecule using hydrogen peroxide, and the reaction happens as follows:

    2H2O ↔ 2H2 + O2 + 4e
    Melanin has the astonishing capacity to split the water molecule at room temperature, for instance, in the laboratory, it is necessary to heat up water at 2000°C in order the reach the separation of hydrogen from the oxygen atoms. Melanin is a biogenic amine like dopamine, melatonin, serotonin, and histamine. Moreover, melanin supports the reunification of water molecule giving off liquid water and four high energy electrons. The reaction is not symmetrical in time or optically because, like any other chemical reaction, depends of the photochemistry of the microenvironment

    Human Photosynthesis and the eukaryotic cell breaks the ground of the cellular metabolism, the energy released symmetrically in all directions by melanin is a real source of photonic energy of the eukaryotic cell, and the neuron cell is not an exception. All melanocytes are from neuroectoderm. There is a misconception in photosynthesis that the creation of glucose as is the main source of energy. This bad idea comes from the observation that in plants glucose is the main product of energy absorption photosynthesis. The traditional diagram of photosynthesis must changes as follows:

    6CO2 + 6H2O → C6H12O6 + 6O2 + Energy
    Thus, instead of energy, the word biomass should be used: In this way, light is turned into matter and mass by slowing down as the electromagnetic field changes to suit the form nature requires in the transmutation of energy from one form to another. Electromagnetic fields are the shape shifters and speed controllers of light waves. Mother Nature has optimized how to use them in life forms.

    6CO2 + 6H2O → C6H12O6 + 6O2 + Biomass
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  13. Jack Kruse

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  14. Jack Kruse

    Jack Kruse Administrator

    Vitamin K2 is a mitochondrial electron carrier that rescues PINK1 deficiency. This implies to the linear thinkers that Parkinson's disease begins in the gut due to the microbiome. The implication is short-sighted. This disease is fundamentally photoelectric on that affects several surfaces we have, the gut being just one. This is one of the key surfaces where human diseases begin when light and that surface do not mesh properly from a circadian coupling. Human UBIAD1 localizes to mitochondria and converts vitamin K(1) to vitamin K(2). Vitamin K(2) is best known as a cofactor in blood coagulation, but in bacteria, it is a membrane-bound electron carrier. Whether vitamin K(2) exerts a similar carrier function in eukaryotic cells is unknown.

    In the literature UBIAD1/Heix as a modifier of pink1, a gene mutated in Parkinson's disease that affects mitochondrial function to lead to high heteroplasmy rates. Researchers found that vitamin K(2) was necessary and sufficient to transfer electrons in mitochondrial models.

    Heix mutants showed severe mitochondrial defects that were rescued by vitamin K(2), and, similar to ubiquinone (CoEnQ10), vitamin K(2) transferred electrons in these mitochondria, resulting in more efficient adenosine triphosphate (ATP) production. Thus, mitochondrial dysfunction was rescued by vitamin K(2) that serves as a mitochondrial electron carrier, helping to maintain normal ATP production via the Q cycle.

    Since Vitamin K2 is produced by the microbiome and is recycled within the gut of animals like humans this is why "THEY say" it is reasonable to believe that Parkinson's disease often begins in the gut. I don't. https://www.newscientist.com/articl...may-start-in-the-gut-and-travel-to-the-brain/
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  15. Jack Kruse

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  16. Jack Kruse

    Jack Kruse Administrator

    Folate is protected by melanin in our skin........Melanin is a batter for sunlight and water.

    What happens when folate drops because of photoelectric topologic effect in the skin?

    Folate deficiency leads to harmful chromosome abnormalities causing cells to inherit the incorrect amount of DNA and can even lead to the loss of an entire chromosome.


    This means you need a lot of sun to stimulate alpha MSH people if your brain is functioning poorly for any reason.
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  17. Jack Kruse

    Jack Kruse Administrator

    Is there another animal photosynthetic pathway that links the skin, gut, and brain?

    Who packs your medical parachute? In this podcast below, you are lead to believe you are hearing groundbreaking ideas on neurodegeneration. I am going to tell you-you are not hearing anything truly worthwhile if you're a Black Swan. Why do I give this scathing criticism?

    What do most clinicians and biochemists understand fail about the biophysics of nitric oxide(NO) production and physiology?

    How light and NO work in us. Share this with your clinicians to upgrade their knowledge so they can help you get to optimal. Nitric oxide and LLLT are interesting bedfellows. Light-mediated vasodilation was first described in 1968 by Furchgott, in his nitric oxide research that leads to his receipt of a Nobel Prize thirty years later in 1998. Later studies conducted by other researchers confirmed and extended Furchgott's early work, and demonstrate the ability of light frequencies to influence the localized production or release of NO, and to stimulate vasodilation through the effect NO on cGMP. This finding suggests that properly designed illumination devices may be effective, noninvasive therapeutic agents for patients who would benefit from increased localized NO availability. However, the wavelengths that are most effective on this light-mediated release of NO are different from those used in LLLT, being in the UV-A (320-400 nm) and in some cases light frequencies present in the low blue range just above UVA.

    UVA light also marks the time of the day where PER1 gene is transcribed and found in its HIGHEST CONCENTRATION in the blood plasma to affect all tissues ability to tell time well. Without this frequency of sunlight, PER1 activity is poor in the plasma and cannot turn out the proper endogenous cycles in the cytoplasm of cells to optimize the timing of metabolic pathways in biochemistry. Just knowing the pathway matters little in this situation because you need to understand what is controlling its kinetics because altered kinetics come from bad circadian timing in cells. This = broken circadian mechanism = poor redox state = poor solar exposure. This is why food gurus and biochemists continue to trip over the dogma.

    Some wavelengths of light are absorbed by hemoglobin, and that illumination can release the NO from hemoglobin (specifically from the nitrosothiols in the beta chain of the hemoglobin molecule) in red blood cells (RBCs) Since RBCs are continuously delivered to the area of treatment, there is a natural supply of NO that can be released from each new RBC that passes under the light source and is exposed to the appropriate wavelength of photon energy. Since the half-life of the NO released under the area of illumination is only 2 to 3 seconds, NO release is very local and focal, preventing the effect of increased NO from being manifested in other portions of the body. Vasodilation from NO is based on its effect on the enzyme guanylate cyclase (GC), which forms cGMP to phosphorylate myosin and relax smooth muscle cells in the vascular system. Once available levels of GC are saturated with NO, or once maximum levels of cGMP are achieved, further vasodilation through illumination will not occur until these biologic compounds return to their pre-illumination status. This system is designed to feedback upon itself. Again, the wavelengths that have been shown to mediate this effect tend to be in the UV-A and blue ranges, not the red and NIR wavelength ranges that are mainly used for LLLT.

    Many people are unaware that cytochrome c is a heme related protein and contains 4 red light chromophores. This is critically important in understanding how light and mitochondria work at the most fundamental level. The activity of cytochrome c oxidase is inhibited by nitric oxide (NO). This was a surprising discovery to those who do understand how mitochondria work with light and sleep. They found it 'shocking' that the body could and WOULD poison one of its own enzymes; in fact, it was initially shrugged off as an imperfection of experiment, but a few years later, several groups reported that mitochondria produced an enzyme that synthesizes NO, that was identified as the neuronal isoforms of NO synthase.

    It was proposed that evolution crafted cytochrome c oxidase to bind not only oxygen but also to use the NO as a braking mechanism for electron flow and power in the mitochondria. The effect of slowing respiration and electron flow in some locations was to divert oxygen elsewhere in cells and tissues where mitochondria were working better. Since O2 is paramagnetic and drawn to magnetic fields, O2 will naturally flow without much effort of extra needed energy to move toward mitochondria where magnetic fields are generated due to good redox power. What biochemists do not realize is that UVA light is never present when IRA light is not. This means that the NO-CCO mechanism is a shunt to get rid of poor mitochondrial engines using Carnot Thereom and the chiral heat effect. This all assumes RED light from the sun is present to drive autophagy for engine replacement. This is why indoor living is devasting to those with high heteroplasmy.

    Since NO blocks respiration in the endothelial cells lining blood vessels, and this helps to transfer oxygen into smooth muscle cells in these vessels where it is needed and required by physiologic demands. This effect is very misunderstood in the etiology of PAD and atherosclerosis damage. A lack of sunlight with UVA light is the FIRST STEP in these diseases. This is why most people with PAD and atherosclerosis have low Vitamin D status and poor redox.

    This inhibition of mitochondrial respiration by NO can be explained by direct competition between NO and O2 for the reduced binuclear center CuB/a3 of cytochrome c oxidase and is reversible. Many people do not even realize that cytochrome c is inducible. Details matter in quantum biology. It was later proposed that laser irradiation could reverse the inhibition of cytochrome c oxidase by NO by photodissociating NO from its binding sites. Because this coordinate binding is much weaker than a covalent bond, this dissociation is possible by visible and NIR light that has insufficient energy to break covalent bonds. This ability is used in optogenetics. This ability is also used in PBM.

    The dissociation of NO from COX will thus increase the respiration rate ("NO hypothesis"). The experiment has now proved, light ALONE can indeed reverse the inhibition caused by NO binding to cytochrome oxidase, both in isolated mitochondria and in whole cells. Most clinicians are unaware of this ability of UV and IR light. This is incredibly important in CAD, PAD, atherosclerosis, and all neurodegeneration because this is HOW THEY ALL BEGIN.

    When you do not get out in the sun in nature it alters the redox state of the arterial wall and the RBCs in the artery. This ruins the peroxiredoxin heme proteins in the RBC's and they lose their DHA, Vitamin C, and ability to induce the COX enzyme. All of these things age the blood cells faster and lower their ability to carry oxygen and CO2 while keeping the innate immune system activation status in the blood plasma active. This ruins how Toll receptor proteins work and also can lead to autoimmune conditions like Crohn's disease and neurodegeneration like PD.

    Most of the beautiful things in nature appear to be done effortlessly. Do you think nature worked hard to freeze Lake Michigan to create a work of art from above?


    Grass doesn't strain to grow, does it? It is effortless because it is designed well. Nature never tells us about her efforts. She just shows us continual results of her designs. Looking at the macroscopic anatomy of the viscera in the gut would never give you a clue how these organs work with the skin and brain. Solar light links them all. For humans, depth and substance can be easy to obtain.......it's just not effortless to attain in life. Choice of the light you use determines that journey.

    You should no longer be surprised how effortless nature really is below your level of understanding. Light can also protect cells against NO-induced cell death. These experiments used light in the visible spectrum, with wavelengths from 600 to 630 nm (and others). NIR also seems to have effects on cytochrome oxidase in conditions where NO is unlikely to be present. This is why parabiosis studies show the effects they do. These are the things we do for our clients at Kruse Longevity Center. https://peterattiamd.com/franciscogonzalezlima/
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  18. Jack Kruse

    Jack Kruse Administrator

    What else don't most biochemists know about UVA and NO in neurodegeneration?

    Tina Kuru has explained that during light excitation of electronic states, a noticeable fraction of the excitation energy is inevitably converted to heat. When heat is thermalized we know from quantum mechanics coherence is usually altered and no quantum mechanical actions are likely to occur. This is a signal where macroscopic thermodynamics of heat movement tied to Carnot or the three laws of thermodynamics take over with their equilibrium bias because of Boltzmann's equation for entropy with movements of heat. In quantum thermodynamics, the story is quite different. When heat is not thermalized quantum mechanical action of the process dominate and it appears macroscopically that the cell can controvert the second law. It does not. It is using the stochastic basis of the second law to benefit to drive process in electrons and protons not possible in a noncoherent state. Quantum tunneling is one such example. This is why biochemists remain befuddled with quantum biology.

    Now classical heat thermodynamics governed by Carnot Theorem and the 3 classical laws state, that when heat moves it causes a local increase in the temperature of the absorbing chromophores. This induces the chiral heat effect in tissues. What is that you ask? It is a quantum mechanical process that allows free movement of hydrogen in the matrix among TCA anions that are critical to making more heat and water (DDW) while it improves your Carnot mechanism. This is why evolution created uncoupled haplotypes when humans left the equator. For those who did not see my 2017 webinar on the chiral heat effect and how it links to this chapter: In all cases, raising the temperature, invokes thermal vibrational and entropic effects inside of living cells. This tends to preferentially stabilize H+ over deuterium bonds in our TCA anion intermediates in our colony of mitochondria in a specific tissue to vary the metabolic rate. Mitochondria used to be bacteria, and nature turned it into a Carnot heat engine for its use. Mother Nature knew exactly what she was doing when she turned the stolen bacteria at our core and innovated uncoupling proteins and haplotypes variations to improve the efficiencies of our heat engines as the environment got cooler the further we left Africa. Carnot showed us a few hundred years ago how a heat engine really works. His work showed that the best way to increase the efficiency of a heat engine was to: 1. increase the difference in the temperature from the heat source (matrix) inside the engine. Or 2. lower the exterior environments surroundings while keeping the thermalized heat production stable. This is why a car engine runs better than a steam engine, and why a jet engine runs better than a car. The temperature differential is the key to how it operates efficiently. With modern disease states, we lose that temperature variation because of indoor living and the change to the incident EMF (sun) we live under.
    The hotter an engine can run the more thermally efficient it is.

    The more heat you liberate the more deuterium your colony excretes because it does not allow much deuterium into the matrix via UCP-2 to lower the temperature in the matrix. the temperature slows because deuterium slows kinetics because of its KIE compared to H+. This is why the TCA has so many enzymes. It is trying to hand select H+ over deuterium at every step and the UCP are the carburators of the heat engine. As a result, the more H+ that cycles in the matrix, the faster ATP is made because the spin rate of the ATPase increases as heating in the matrix increases and as a result, the TCA/urea cycle performs like a Ferrari and not a Nissan Sentra. When the matrix cannot make heat well, the mitochondria have to default to using glucose for fuel and NAD+ drops and pseudohypoxia results. This is when UVA light from sunlight helps the matrix. NO inhibits CCO and the red light in sun still spins the ATPase fast because of what Kuru's work has shown us. https://pubs.acs.org/doi/abs/10.1021/ja9530376

    This idea of Carnot has guided engineers for 200 years but it still seems to perplex doctors who treat people with mitochondrial damage. Human diseases are associated with a loss of heat in the matrix. This occurs when heteroplasmy rises. These ideas are laid out by McManus and Wallace's theories on how the IMJ's change their geometry. This is also not well understood by biochemists because it is a quantum mechanical effect that works with UCP-2 and other heme chromophores. It is a big deal with deuterium biology in the matrix at Krebs bicycle. This is how different colonies of mitochondria in tissues vary their kinetic cycling in different tissues. I spoke about this in the Vermont 2018 video.

    When heating occurs over any appreciable time or space averaged heating of the sample can be prevented by controlling the radiation frequency intensity and dose appropriately. This is the basis of power density in heat entropy systems using light. Light can act coherently or non coherently and this is yet another way the biochemists trip up. They do not realize that coherent light has no flicker just like the sun and coherent light has what appears to be an unlimited orbital angular momentum (OAM) to store information and energy. That energy will not be thermalized and it will be stored for use later. This is the key to understanding the thyoalkaloid membranes and the mito matrix in cells. Cells seem adept at taking sunlight and creating coherent light with it within the cellular apparatus.

    Medicine can use this idea to use laser light to replace most drugs if they wised up to the implications of Kuru's work.

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  19. Jack Kruse

    Jack Kruse Administrator

    I just did my February 2019 on another neurodegenerative disease called ALS that has the very same findings in this paper. When redox potential of the cells that control the Blood-brain barrier or the cervical spinal cord barrier is low the barrier opens and lets things get in that should not and this leads to many nonlinear collateral effects. The Mitochondriac play is never to let the barrier become leaky, to begin with, it. We know that the barrier in the CNS and PNS remains open after many different types of stressors for close to 4 weeks in rodents. The same study needs to be done on humans. Allen Frey showed us in the 1960s that nnEMF made the BBB leaky just from simple exposure. I wonder when they'll make the connection to why AD and ALS are spiking in a blue-lit nnEMF world that opens all the barriers in humans? https://www.sciencedaily.com/releases/2019/01/190114130825.htm
  20. Jack Kruse

    Jack Kruse Administrator

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