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IS Alzheimer's disease a PHOTOelectric disease too?

Discussion in 'Educating Doctors' started by Jack Kruse, Jan 11, 2019.

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  1. Jack Kruse

    Jack Kruse Administrator

    The external manifestations of the circadian rhythm are obvious – we sleep and wake, maintain or lose our concentration, change our body temperature and use the bathroom on a regular schedule. And the social and evolutionary benefits of this rhythmic behavior are clear. Being synchronized with the planet’s rotation allows diurnal organisms such as humans make the best use of daylight hours and to constrain cell repairs and memory adjustments to the night-time. This synchronization helps living things live in groups, with everyone doing the same things at the same time. But one of the earliest and most important benefits of a circadian system was to regulate biochemistry using light as the key stimulus. The temperature of the environment became the second key stimulus.

    Concentrations of metabolic hormones like glucagon and insulin vary through the day in anticipation of eating. Intrinsic day/night differences in redox state in heart cells affect cardiac excitability via modulation of ion channels and may generate the changes in brain states that allow us to establish memories at night or erase them. Melatonin and cortisol and BDNF coordination control the memory in neurons and likely in water.

    Sometimes the internal clock mechanism is running correctly – physiological changes occur on a 24-hour cycle – but the clock is set to the wrong time of day because of choice we make around light or shift work. The response to the mismatch can cause illness. People adopt unconscious strategies to override the signals that are causing them to feel sleepy or wide awake at the wrong time. They compensate by activating the stress axis. This leads to higher levels of cortisol, lowered melatonin, lowered BDNF, and lowered NO, and increased blood pressure. All of these are powerful physiological changes that can cause damage or worsen the circadian disease. Most of these things go back to defects in how PER is effected by the epigenetic software program of light and dark.

    Light via the central retinal pathways and the ganglion cells that harbor melanopsin control small molecular signals that affect the creation of PER. We now know the very same control arm is in the skin. both places affect the RBC that flow below them to later peroxiredoxins. There are several molecules that likely help/hurt re-set the circadian clock for patients who have lost their eyes through injury or ruined their skin via tattoos or trauma to alter the optical density.

    The paradigm uses drugs to try to do this but we think we can prompt increases the levels of calcium and cAMP in the SCN which would usually result from light stimulation of the photosensitive ganglion cells. Since PBM increases ATP and cAMP it can be used to help people with AD risks. Red light is the dominant form of light in our sun too. All of these data points that AD is a photoelectric disease of a LACK of sunlight.
     
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  2. Jack Kruse

    Jack Kruse Administrator

    Another striking feature of the 24 hour oscillation of metabolic processes is the fact that the beat goes on, unperturbed, as temperature changes.

    A clock that enables flowers to open in anticipation of the sunlight would be useless if it slowed down when the temperature dropped. Even in warm-blooded animals, there is a temperature gradient between the skin and the core of the body. If the timing of metabolic processes within cells depended on where they were – and what the weather was like outside – it would be chaos.

    This temperature-independence was a major stumbling block to early acceptance of an internal clock mechanism (rather than timing based purely on external cues such as day/night). Biological reactions obey the Arrhenius relationship as surely as any other chemical process and until recently no-one could provide a convincing reason why the clock didn’t speed up when it got warmer.
    The Arrhenius equation is a formula for the temperature dependence of reaction rates.

    According to the Arrhenius equation of temperature dependence on reaction rate, in any (bio)chemical reaction, a rise in temperature increases the rate of the reaction, which eventually reduces the reaction time.

    Phosphorylation of PER2 Controls Clock Speed.

    A Phosphoswitch Regulates PER2 Degradation

    This is why adenosine controls sleep and thermoregulation because it acts a phosphorus switch in our plasma photosynthetically under the power of light, both and bad and good.

    It is remarkable that the complex yet robust phenomenon of temperature compensation is regulated by subtle differences in phosphorylation of the same protein at different sites. Notably, this finding is in general agreement with predictions of earlier mathematical models that suggested that opposing outputs with switch-like mechanisms might control temperature compensation. In the future, it will be important to identify the priming kinase that plays a central role in the phosphoswitch model. This phosphoswitch mechanism of temperature compensation may be a core feature of clocks in many species


    Recent work by Hiroki Ueda at the University of Tokyo in Japan reveals part of the answer: since the PER protein is required to inhibit the production of clock proteins – turning daytime activities into night-time rest – reducing the amount of PER will delay the clock.

    Most of the proteins in a cell have a short lifetime. Once they have completed their tasks, become unstable or unfolded, they are recycled. The trick to providing a sensitive counterbalance to thermal change is to destabilize exactly the right amount of PER.

    To understand this exquisitely balanced chemistry we must introduce another family of players – the casein kinase 1 enzyme. As part of the circadian clock, casein kinase 1 transfers phosphate groups from adenosine triphosphate (ATP) to PER protein during the day. cAMP varies day to night and this is why sleep is controlled by adenosine concentration. As adenosine rises ATP creation drops in the matrix and this increases sleep behavior and this is what likely also signals PER to enter the nucleus to be destroyed at night when light is absent and melatonin is actively repairing the damage to defective mitochondria int he brain. The added charge of the phosphate groups added on to PER makes the protein unstable and it becomes a target for ubiquitination and disposal. Now you have my ubiquitination series to consider in this dance too.......n increase ubiquitination is a sign PER cycling is defective to the clinician. Blue light and nnEMF increase this.
     
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  3. Jack Kruse

    Jack Kruse Administrator

    There are two different mechanisms at work slowing the phosphorylation of the PER protein as temperature increases. The affinity of the reactant enzyme–ATP complex to a substrate such as PER is reduced at higher temperatures. So this implies that PER is lowered in the nucleus when temperatures are increased centrally in the nucleus and kept cooler in the periphery during sleep.

    Molecular dynamics suggest that this is the result of large shape fluctuations in the catalyst slowing the binding. The brakes are also applied at the other side of the reaction equation. The affinity of the product enzyme–ADP complex is increased. These two mechanisms, acting at different sites on the same protein contribute to temperature compensation of the phosphorylation of PER proteins – and to maintain the accuracy of the clock.

    It is remarkable that the complex yet robust phenomenon of temperature compensation is regulated by a few phosphate groups that alter the charge on PER protein at night and simple changes in electrostatic charge. This simple electrostatic charge can be affected by electromagnetic pollution. CT at night time can offset this risk.

    In circadian biology we have now found the heartbeat of life with the Nobel Prize of 2017, we’ve identified the conductor (PER) and we are starting to read the score of the music of life (peroxiredoxins). Molecular-scale insights (phosphorus transfer from cAMP) will show us how to we play instruments using light frequencies (ALAN) – and who knows what variations aberrant light signals will compose for the symphony of life as evolution goes forward.
     
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  4. Jack Kruse

    Jack Kruse Administrator

    Can a ketogenic diet rescue cognition in ApoE4+ patient with mild Alzheimer's disease????: A case study: https://www.sciencedirect.com/science/article/abs/pii/S1871402118306684

    Why does this work based on the mechanism above?

    Why? Simple.....it restores proper phosphorylation to PER1 protein. What does APOE really do? It maintains the structural integrity of lipoproteins and facilitates their solubilization in the blood = RBCs peroxiredoxin repair = helps the photoelectric defect in RBCs.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4960866/
     
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  5. Jack Kruse

    Jack Kruse Administrator

    AD is a chronic decline in hypoperfusion of mitochondria. The BBB is altered and opened and this harms mitochondrial function (ferroptosis) and this affects CMRO2 and autoregulation reflex. This is why blood flow is altered in AD = this alters glucose metabolism. The arteries of the tree are damaged and they have sustained melanopsin damage = intima and media and this is hidden by autoregulation for decades in people. As charge in blood is lost platelets become more sticky to the endothelium. This is an electromagnetic defect in the microvasculature. This lowers NO release and increases turbulence and alters flow because of magnetohydrodynamics.

    Mitochondrial disease in the heart by ferroptosis also will alter cerebral flow by ultrasound and transcranial doppler.

    The link to age and AD is tied to heteroplasmy % damage in mitochondria and CCO and CGI liberation.

    Cytochrome c oxidase is three‐copper, two‐heme‐A protein found in mitochondria and RBCs.

    Heme is destroyed by melanopsin damage and this occurs in the walls of arteries, mitochondria, and RBCs.

    In RBC's cytochrome c destruction liberates CpG islands (CGI). This is true in sepsis and all types of trauma.

    I believe it is the key step that leads to damage in other organs in circadian diseases.


    Cytochrome C oxidase reduces oxygen with electrons from food that are carried by NADH (cyto1) or FADH2 (cyto2) to create water. It is an induceable enzyme meaning the presence of oxidative metabolism and the need for water creation can induce it from transcription. Sunlight and DDW I believe are inducible stimuli for CCO. Similarly, hypoxia or pseudohypoxia lower CCO production. PBM induces CCO production and regeneration and this is why it helps patients with AD and defective colonies of mitochondria. The key is to induce change by repairing redox power in the colony of the brain. CCO levels are demolished in the brain in AD; this links to heteroplasmy rate in mitochondria.

    Melanopsin dysfunction causes chronic hypoperfusion in mitochondria to cause Alzheimer's. It is an insidious chronic cumulative effect of circadian disruption that causes AD. The target of AD damage is CCO in the brain colony of mitochondria.

    CCO damage creates CGI's. CGIs represent a dispersed but coherent DNA sequence class whose members function as genomic platforms for regulating transcription at their associated promoters. These properties depend on the shared features of their DNA sequence; notably, CpG richness and a higher than average G+C content.

    When CCO is damage is too high CCO controls apoptosis via the mitochondria permeability pore and this leads to neuron cell suicide = neurodegeneration.


    What these researchers do not appear to know is that mt DNA and nuclear DNA release CPI into the blood plasma during insults. The levels of GGI is a cipher used by the colony of mitochondria to assess the damage in the system. Normally the brain is protected from these small molecular weight proteins by the BBB.

    As oxygen lowers pyruvate cannot turn into Acetyl-CoA of the Kreb cycle for beta-oxidation and NAD+ drops and you cannot fat burn. Neurons are not great glycolytic cells either. They like shunting pyruvate to lactate.

    In AD there is a paucity of electron donors as there is in aging or heteroplasmy = low NAD+/NADH. Low dose methylene blue rescues this effect by replacing NAD+ as the key electron donor. Low-dose methylene blue stimulates mitochondrial respiration by donating electrons to the electron transport chain. This property permits the cycling of electrons from chemicals inside the mitochondrial matrix to electron transport proteins in mitochondria. These transport proteins act as acceptors for electrons donated by methylene blue in mitochondria. The final acceptor of electrons in the respiratory chain is oxygen, which is obtained from oxyhemoglobin transported in the circulation. Molecular oxygen becomes reduced to water in a reaction catalyzed by the mitochondrial enzyme cytochrome oxidase (Complex IV, cytochrome c oxidase). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428125/

    In nnEMF damage, there is no protection from these insults.

    This unleashes potentially hazardous CpG-containing cell-free mitochondrial DNA (cf-mtDNA) into the cerebrovascular tree. In fact, cf-mtDNA is routinely released into the circulation and is associated with morbidity and mortality in critically ill patients. I believe it is the fingerprint of morbidity for nnEMF and it is what methylates our genome in melanopsin dysfunction.

    How the body avoids inappropriate innate immune activation by cf-mtDNA remains unknown but I have a strong belief that is cleared via our RBCs and are toll receptors because of how they work with the complement system in the innate immune response.

    Why do I say this? Because red blood cells (RBCs) modulate innate immune responses by scavenging chemokines, so this is why parabiosis studies show benefits with blood that is young and has an ability to clear these molecules, so I have hypothesized that RBCs may attenuate CpG-induced inflammation in multiple organs through direct scavenging of CpG-containing DNA.

    The innate immune system detects pathogens by the presence of highly conserved pathogen-expressed molecules, which trigger host immune defenses. Toll-like receptor (TLR) 9 detects unmethylated CpG dinucleotides in bacterial or viral DNA, and can be stimulated for therapeutic applications with synthetic oligodeoxynucleotides containing immune stimulatory “CpG motifs.” Our mitochondria used to be a bacteria so I am betting that it also works with RBC's to sense the damage to our colony of mitochondria due to the liberation of CG Islands from the cytochromes in our mitochondria that are destroyed. TLR9 activation induces both innate and adaptive immunity. The TLR9-induced innate immune activation can be applied in the prevention or treatment of infectious diseases, and the adaptive immune–enhancing effects can be harnessed for improving disease therapeutic targets.

    The family of Toll-like receptors (TLRs) appears to play a pivotal role in the innate immune system for the detection of highly conserved, pathogen-expressed molecules. To enable the rapid detection of infection, each of the 10 TLRs currently known to be expressed in humans has apparently evolved to be stimulated in the presence of certain types of pathogen-expressed molecules, which are either not expressed in host cells or are sequestered in cellular compartments where they are unavailable to the TLRs. Activation of a TLR by an appropriate pathogen molecule acts as an “alarm signal” for initiation of the appropriate immune defenses.

    A central task of the innate immune system may well be to determine whether a newly encountered pathogen is present extracellularly, as with most bacteria and fungi, in which case the “correct” type of immune response to be initiated is a T helper cell (Th) 2–like response, or intracellularly, as with most viruses and intracellular bacteria, in which case the innate immune system should induce a Th1-like immune response capable of killing infected cells. Recent studies indicate that the innate immune system accomplishes this feat, at least in part, by making use of the ligand specificity and the cellular site of expression of the TLRs.

    The innate immune system appears to use TLR9 for detecting unmethylated CpG dinucleotides, which are relatively common in bacterial and viral genomes but are highly methylated and uncommon in vertebrate genomes.

    It has also been shown in the literature that RBCs homeostatically bind mtDNA, and RBC-mediated DNA scavenging is essential in mitigating tissue injury after CpG-DNA is liberated from heme-based proteins. What kind of disease states should we expect to see cf-mtDNA elevated? Any disease where inflammation is induced by heme protein destruction = blue light hazard, nnEMF, sepsis, trauma and most mitochondrial and RBC diseases tied to alterations in circadian biology. All neurodegenerative diseases fit this bill.

    CITES:


    https://www.atsjournals.org/doi/full/10.1513/pats.200701-021AW
     
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  6. Jack Kruse

    Jack Kruse Administrator

    Who packs your medical parachute? In this podcast, 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. 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. 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.

    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 AD. 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. 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/
     
  7. Jack Kruse

    Jack Kruse Administrator

    Electromagnetic fields can activate voltage-gated calcium channels (VGCCs) via molecular resonance in the plasma membrane of cells. When electromagnetic fields activate these channels, large amounts of intracellular calcium (Ca2+) are produced. The amount produced is subject to the wave physics of the emitted light wave from the point source. If the wave is polarized this also changes the calcium efflux and its ionic resonance. Calcium is the key secondary messenger in cells for these antigens on the surface and they interact and react with RNS species like peroxynitrite (RNS radical).
    This excess calcium within the cells produces a chain of free radical chemical reactions from the mitochondria which changes the physiology of the cell at a femtosecond basis. This leads to the production of a VARYING free radical signal that causes organizational chaos in the cell. That chaos is manifested by the disruption of the incident EMF that excites and activates the voltage-gated channels in the cell. A highly variable incident EMF with produce a highly variable ROS/RNS mitochondrial signal and this results in unpredictable biochemistry in the cell. This is associated with the production of chronic oxidative stressor chemicals in the living system that cannot be buffered by the normal quenching chemicals in cells. All of this results from an environment that produces an altered electric and magnetic field around an animal/human.
    The chaotic free radical signal is capable of culminating in DNA damage and or the change in the plasma membrane to lead to pathologic symptoms and eventual disease.
    The calcium efflux causes excess calcium directly in and around the cell and in its local environment. So with respect to RBCs, it also means that this effect of electric and magnetic fields will also affect the surface of the blood vessels. Peroxiredoxins are the key peripheral circadian controller that remove CpG Island from the fragmented DNA and mtDNA that enter the blood when nnEMF is destroying cellular biology. Tight control of RBC circadian cycles links RBC antigen clearance to the innate immune system via C4. RBC become more permeable to toxins in this case and as a result, the RBC ages faster and more antigens pass through the circulatory system. This is really what happens in all mold and biotoxin disease. It is not the mold or toxin that is critical in this case, it is REMOVAL of the nnEMF field that is critical to get right. Most of the clinician out there never get this advice to their patients or the public.
    All of these mechanisms of nnEMF field exposure alter melanopsin biology in the blood and arteries to a chaotic release of nitric oxide (NO) within cells and in arteries to cause disease when it occurs chronically and affects mitochondrial function when other frequencies of sunlight are subtracted from this photic dance.
    The increase of nitric oxide is a chameleon event in the blood plasma. Endothelial nitric oxide synthetase has a quantum superposition effect on sulfur atoms in the skin, arteries, blood, and gut to protect us from dangerous nitrogenous groups in these antigens.
    This means that any pulsed or polarized non-native man-made electromagnetic signal can have a variable non-linear effect on sulfation and nitrosylation pathways in any of these organs. I covered this last night in my Feb 2019 webinar Q & A.
    It can result in therapeutic effects or detrimental effects in the blood plasma depending upon the nnEMF stimulus. This will lead to highly variable chaotic mitochondrial energy flux and fidelity signal dynamics. This is very damaging to the matrix and directly affects what biochemistry can or cannot occur. This is one reason why non-thermal electromagnetic fields (PEMF) are increasingly used in medical therapies, but they are being used without any proper understanding of how they truly operate.
    Today the sellers and purveyors of these devices think and believe that their RF/microwaves effect is always beneficial therapeutically in a wildly variable world of surrounding nnEMF. THIS IS PURE FALLACY AND MARKETiNG BuLLSHIT.
    Moreover, they fail to realize that this eNOS switch in cells is very sensitive to any variable PEMF RF pulse. This is why PEMF devices need to be strictly avoided in a 5G world. Yes, that includes all the Oura rings and PEMF devices pushed by BEMER and Dr. Havas based upon the latest NTP study on RF radiations.
    For example, if one is in an environment that fosters chronic nitric oxide release this means there will be a relative lack of sulfation of the skin, arteries, and gut and RBC's and this would favor the activation of the reactive nitrogen species of chemicals. This is particular devasting to the microbiome because NO and H2S work in unison to control the constitution of the microbiome.
    In fact, we now know that nitric oxide can also interact with the superoxide pulse (OO-) created in cytochrome one (NAD+/NADH) form altered mitochondrial function to create peroxynitrite (ONOO-) to do further damage. This is why people with gut and microbiome conditions relapse so often in toxic nnEMF environments loaded with blue light. Most of the doctors are not sophisticated enough yet to understand that things like SIBO and adrenal fatigue are adaptative and not pathologic symptoms tied to altered and highly variable EMF fields that their patients live in.
    It has been found that when peroxynitrite breaks down, it creates reactive free radicals and oxidative stress within cells and this likely leads to many of the symptoms of CV and neurodegeneration on longer timescales. In this way, both atherosclerosis, CV, and neurodegeneration can be thought severe chronic adaptive mechanisms employed by cells who have developed an innate immune allergy to nnEMF. My Q & A last night was epic in this regard.
     
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  8. Jack Kruse

    Jack Kruse Administrator

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  9. Jack Kruse

    Jack Kruse Administrator

    Do you think pulses and polarization from a smart meter have no effect on the electrical activity that is going on inside of you? This video is for that skeptic. Smart meters us a combination of RF and microwaves so they very much mimic what 5G mm waves can do. This video will serve as a warning why Uncle Jack said that the new spikes in coronary calcification lesions, widow makers, and acute onset A-fib with clotting is coming to every ER in 2019 in 5 G cities.
    The uninformed masses are hooked on cardiotoxic devices that require limitless RF/microwave pollution documented to incrementally obliterate the blood, heart, and brain and their colonies of mitochondria. This is why heart disease, atherosclerosis, and neurodegeneration all seem to be linked fundamentally. As a group, they may appear energetic and viable. But examine each person individually and uncover a resplendent array of physical impediments, abnormalities, and danger signs that plague even the very young. Within the cells, the DNA and the blood of microwave addicts there is vast evidence of radiation sickness long before they receive a clinical diagnosis.
    https://www.youtube.com/watch?time_continue=1234&v=UIobFr3m8kk
     
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