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DOES SUNLIGHT SCULPT THE MICROBIOME VIA SULFUR AND NITROGEN?

Discussion in 'Educating Doctors' started by Jack Kruse, Feb 18, 2019.

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  1. 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 change 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 via chronic LIGHT STRESS implies 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 under the power of terrestrial sunlight. Humans no longer live under terrestrial sunlight and this is why their microbiomes are being destroyed by the modern world and this changes their brains and arteries and ages their blood faster.

    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.

     
  2. Jack Kruse

    Jack Kruse Administrator

    H2S gas made by the microbiome limits the power of NO. H2S is a substrate for sulfate (SO4) production in humans. Activated neutrophils can generate sulfate from H2S while virtually all cells contain the enzymatic machinery to oxidize H2S to thiosulfate in a 3-step process in which sulfite is an intermediate substrate. Sulfite can also likely be generated from H2S via endothelial nitric oxide synthase (eNOS) which is why the post above is critical in understanding the microbiome.
     
  3. Jack Kruse

    Jack Kruse Administrator

    Sulfite, wherever it is generated, can be acted upon by the ubiquitous enzyme, sulfite oxidase, to generate SO4. Given the body’s constant need for SO4 to build heparan sulfate, to carry out phase II detoxification in the liver, maintain proper blood viscosity to prevent clotting and make sure the 93% of water in the blood plasma maintains its proper optical refraction state, and many other quantum actions not appreciated by functional medicine, It become obvious that any reduction in sulfate availability necessitates a “work-around,” a compensatory shift by the body.

    H2S produced in the gut microbiome via SFB, symptomatic though it may be, will diffuse into the blood and a portion of it will ultimately be oxidized to sulfite and then sulfate, via these mechanisms just described above. Your microbiome is built to liberate hydrogen gas to sulfate your body. That is what its main function is. So if you molecular hydrogen breath test is high all it means is you cannot absorb the hydrogen your gut biome makes. The amount of the hydrogen makes is QUANTIZED by the light your microbiome SENSES via your skin and blood compartments. That is how counterintuitive the gut really is.

    There are many reasons that sulfate might be in short supply, but by far the most common one is a LACK of sun on your skin. Rest assured there are others that many of the functional docs will try to sell you shit for but they will never tell you about the sun because it is free.
     
  4. Jack Kruse

    Jack Kruse Administrator

    H2S is also generated by the microbiome through the action of the sulfur-fixing bacteria (SFB). As with CH4 production, H2S production is a means of trapping molecular hydrogen produced upstream. In fact, the SFB has a substantially stronger affinity for molecular hydrogen than do the methanogens, which means that H2S is more likely to be produced than CH4. In this way, the methanogens and the SFB maintain a functional balance that QUANTIZED by the incident light waves to make the free radical gas to control the hydrogen producers, while at the same time supplying the body with a crucial gasotransmitter. People fail to realize that H2S, CO, and NO are all free radical gases. This means they are all carrying light information to and fro in our systems.

    H2S gas is produced from cysteine by the enzymes cystathionine beta-synthase and cystathionine gamma-lyase. It acts as a relaxant of smooth muscle and as a vasodilator and is also active in the brain, where it increases the response of the NMDA receptor and facilitates long term potentiation, which is involved in the formation of memory.

    Eventually the gas is converted to sulfite in the mitochondria by thiosulfate reductase, and the sulfite is further oxidized to thiosulfate and sulfate by sulfite oxidase. The sulfates are excreted in the urine.

    Due to its effects similar to nitric oxide (without its potential to form peroxides by interacting with superoxide), hydrogen sulfide is now recognized as potentially protecting against cardiovascular disease.

    The cardioprotective role effect of garlic is caused by catabolism of the polysulfide group in allicin to H2S, a reaction that could depend on reduction mediated by glutathione which is a protein with 3 amino acids and two of them are made from the sulfur-containing cysteine amino acid.

    Though both nitric oxide (NO) and hydrogen sulfide have been shown to relax blood vessels, their mechanisms of action are different: while NO activates the enzyme guanylyl cyclase, H
    2S activates ATP-sensitive potassium channels in smooth muscle cells. It is now believed NO might act on the bigger vessels in the body and H2S on the smaller arterial trees.

    I think H2S is critical for the brain-gut axis to operate properly. I mentioned this to Luke last night. In Alzheimer's disease, the brain's hydrogen sulfide concentration is severely decreased. In a certain rat model of Parkinson's disease, the brain's hydrogen sulfide concentration was found to be reduced, and administering hydrogen sulfide alleviated the condition. In trisomy 21 (Down syndrome) the body produces an excess of hydrogen sulfide and it might be why these kids tend to be chubby. Hydrogen sulfide is also involved in the disease process of type 1 diabetes. The beta cells of the pancreas in type 1 diabetes produce an excess of the gas, leading to the death of these cells and to reduced production of insulin by those that remain. Sunlight alters these effects telegraphing us yet again the sun is heavily involved in the sulfation of tissues.
     
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  5. Jack Kruse

    Jack Kruse Administrator

    As much as 1 liter of hydrogen is produced by bacteria of the microbiome each day. It is important to keep in mind that molecular hydrogen plays a strong anti-inflammatory role in the body. Deuterium is kept in the blood compartment because sunlight can control its movements in that compartment via the melanopsin mechanism and the uncoupling proteins in the body. The free radical gasotransmitters help control the flow of H+/D to control sulfation. They are a subfamily of endogenous molecules of gases or gaseous signaling molecules, including NO, CO, H. 2. S. These particular gases share many common features in their production and function but carry on their tasks in unique ways in different cells, which differ from classical signaling molecules, in the human body.

    For prokaryotes, methane is a gasotransmitter. Microbial methane production acts as a sink for hydrogen produced “upstream” by the hydrogen-producing bacteria in the gut.

    H2S has a wide range of functions in humans, including cognitive, neurological, gastrointestinal, cardiovascular, and others. Interestingly, its physiological effects are often opposite at low and high concentrations.

    When healthy cells are put under stress, the H2S-generating enzyme cystathionine-gamma-lyase (CSE) translocates from the cytosol to the outer mitochondrial membrane, where it uses the high mitochondrial concentration of cysteine to generate H2S. The H2S then acts within the electron transport chain to improve the efficiency of ATP production. NO reduces ATP production via its effect on CCO. The point is that H2S production is vital to cellular adaptation to physiological stress. Its adaptation is variable to an acute stressor versus a chronic stressor. Today nnEMF and blue light are a chronic light stressor to the gasotransmitter systems in humans.

    H2S is also generated by the microbiome through the action of the sulfur-fixing bacteria (SFB). As with CH4 production, H2S production is a means of trapping molecular hydrogen produced upstream.

    The terminology and characterization criteria of “gasotransmitter” were firstly introduced in 2002. For one gas molecule to be categorized as a gasotransmitter, all of the following criteria should be met.

    1. It is a small molecule of gas;
    2. It is freely permeable to membranes. As such, its effects do not rely on the cognate membrane receptors. It can have endocrine, paracrine, and autocrine effects. In their endocrine mode of action, for example, gasotransmitters can enter the bloodstream; be carried to remote targets by scavengers and released there, and modulate functions of remote target cells;
    3. It is endogenously and enzymatically generated and its production is regulated;
    4. It has well defined and specific functions at physiologically relevant concentrations. Thus, manipulating the endogenous levels of this gas evokes specific physiological changes;
    5. Functions of this endogenous gas can be mimicked by its exogenously applied counterpart;
    6. Its cellular effects may or may not be mediated by second messengers, but should have specific cellular and molecular targets.
     
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  6. Jack Kruse

    Jack Kruse Administrator

    Hydrogen sulfide binds to cytochrome oxidase and thereby prevents oxygen from binding, which leads to the dramatic slowdown of metabolism. I have a sense this is what the Russians are doing in their space program to get to Mars with their Schumann generators and artificial magnetic fields. Animals and humans naturally produce some hydrogen sulfide in their body during cold stress; researchers have proposed that the gas is used to regulate metabolic activity and body temperature, which would explain the above findings. I believe the cold stress might work best with blue and IRA light based on some hacks I have done.

    I got this idea in 2006.

    In 2005, it was shown that mice can be put into a state of suspended animation-like hypothermia by applying a low dosage of hydrogen sulfide (81 ppm H
    2S) in the air. The breathing rate of the animals sank from 120 to 10 breaths per minute and their temperature fell from 37 °C to just 2 °C above ambient temperature. In effect, these warm-blooded nocturnal mammals became cold-blooded and tightly coupled in this experiment. The mice survived this procedure for 6 hours and afterward showed no negative health consequences. In 2006 it was shown that the blood pressure of mice treated in this fashion with hydrogen sulfide did not significantly decrease. I think this process works in humans too but it is a bit more complicated.

    CITES:

    http://news.bbc.co.uk/2/hi/science/nature/4469793.stm
    1. Carabotti M, Scirocco A, Maselli MA, Severi C. The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems. Ann Gastroenterol. 2015;28(2):203-209.
    2. Buglioni A, Burnett Jr JC. A gut-heart connection in cardiometabolic regulation. Nat Med. 2013;19(5):534-536.
    3. Khoury T, Tzukert K, Abel R, et al. The gut‐kidney axis in chronic renal failure: A new potential target for therapy. Hemodial Int. 2017;21(3):323-334.
    4. Budden KF, Gellatly SL, Wood DL, et al. Emerging pathogenic links between microbiota and the gut-lung axis. Nat Rev Microbiol. 2017;15(1):55-63.
    5. Kau AL, Ahern PP, Griffin NW, et al. Human nutrition, the gut microbiome, and the immune system. Nature. 2011;474(7351):327-336.
    6. Compare D, Coccoli P, Rocco A, et al. Gut-liver axis: the impact of gut microbiota on nonalcoholic fatty liver disease. Nutr Metab Cardiovasc Dis. 2012;22(6):471-476.
    7. Brakenhoff LK, van der Heijde DM, Hommes DW, et al. The joint-gut axis in inflammatory bowel diseases. J Crohns Colitis. 2010;4(3):257-268.
    8. Clarke G, Stilling RM, Kennedy PJ, et al. Minireview: Gut microbiota: the neglected endocrine organ. Mol Endocrinol. 2014;28(8):1221-1238.
    9. David LA, Maurice CF, Carmody RN, et al. Diet rapidly and reproducibly alters the human gut microbiome. Nature. 2014;505(7484):559-563.
    10. Serino M, Luche E, Gres S, et al. Metabolic adaptation to a high-fat diet is associated with a change in the gut microbiota. Gut. 2012;61(4):543-553.
    11. Haro C, Montes-Borrego M, Rangel-Zúñiga OA, et al. Two Healthy Diets Modulate Gut Microbial Community Improving Insulin Sensitivity in a Human Obese Population. J Clin Endocrinol Metab. 2016;101(1):233-242.
    12. Duca FA, Lam TK. Gut microbiota, nutrient sensing, and energy balance. Diabetes Obes Metab. 2014;16 Suppl 1:68-76.
    13. Neish AS. Redox signaling mediated by the gut microbiota. Free Radic Res. 2013;47(11):950-957.
    14. Ghanizadeh A, Berk M. Molecular hydrogen: an overview of its neurobiological effects and therapeutic potential for bipolar disorder and schizophrenia. Med Gas Res. 2013;3(1):11.
    15. Chen X, Zuo Q, Hai Y, Sun XJ. Lactulose: an indirect antioxidant ameliorating inflammatory bowel disease by increasing hydrogen production. Med Hypotheses. 2011;76(3):325-327.
    16. Suzuki Y, Sano M, Hayashida K, et al. Are the effects of alpha‐glucosidase inhibitors on cardiovascular events related to elevated levels of hydrogen gas in the gastrointestinal tract? FEBS Lett. 2009;583(13):2157-2159.
    17. Wang R. Gasotransmitters: growing pains and joys. Trends Biochem Sci. 2014;39(5):227-232.
    18. Bures J, Cyrany J, Kohoutova D, et al. Small intestinal bacterial overgrowth syndrome. World J Gastroenterol. 2010;16(24):2978-2990.
    19. Wang R. Physiological implications of hydrogen sulfide: a whiff exploration that blossomed. Physiol Rev. 2012;92(2):791-896.
    20. Fu M, Zhang W, Wu L, et al. Hydrogen sulfide (H2S) metabolism in mitochondria and its regulatory role in energy production. Proc Natl Acad Sci U S A. 2012;109(8):2943-2948.
    21. Wallace JL. Physiological and pathophysiological roles of hydrogen sulfide in the gastrointestinal tract. Antioxid Redox Signal. 2010;12(9):1125-1133.
    22. Mitsuhashi H, Yamashita S, Ikeuchi H, et al. Oxidative stress-dependent conversion of hydrogen sulfide to sulfite by activated neutrophils. Shock. 2005;24(6):529-534.
    23. Hildebrandt TM, Grieshaber MK. Three enzymatic activities catalyze the oxidation of sulfide to thiosulfate in mammalian and invertebrate mitochondria. FEBS J. 2008;275(13):3352-3361.
    24. Seneff S, Lauritzen A, Davidson R, Lentz-Marino L. Is endothelial nitric oxide synthase a moonlighting protein whose day job is cholesterol sulfate synthesis? Implications for cholesterol transport, diabetes, and cardiovascular disease. Entropy. 2012;14(12):2492-2530.
    25. Ricard-Blum S. Glycosaminoglycans: major biological players. Glycoconj J. 2017;34(3):275-276.
    26. Seneff S, Causton NJ, Nigh GL, et al. Can glyphosate’s disruption of the gut microbiome and induction of sulfate deficiency explain the epidemic in gout and associated diseases in the industrialized world? J Biol Phys Chem. 2017;17(2):53-76.
    27. Samsel A, Seneff S. Glyphosate, pathways to modern diseases II: Celiac sprue and gluten intolerance. Interdiscip Toxicol. 2013;6(4):159-184.
    28. Neumann M, Leimkühler S. Heavy metal ions inhibit molybdoenzyme activity by binding to the dithiolene moiety of molybdopterin in Escherichia coli. FEBS J. 2008;275(22):5678-5689.
    29. Lau SJ, Sarkar B. Inorganic mercury(II)‐binding components in normal human blood serum. J Toxicol Environ Health. 1979;5(5):907-916.
    30. Waidyanatha S, Troester MA, Lindstrom AB, Rappaport SM. Measurement of hemoglobin and albumin adducts of naphthalene-1,2-oxide, 1,2-naphthoquinone and 1,4-naphthoquinone after administration of naphthalene to F344 rats. Chem Biol Interact. 2002;141(3):189-210.
    31. Rees MD, Kennett EC, Whitelock JM, Davies MJ. Oxidative damage to extracellular matrix and its role in human pathologies. Free Radic Biol Med. 2008;44(12):1973-2001.
    32. Carbonero F, Benefiel AC, Alizadeh-Ghamsari AH, Gaskins HR. Microbial pathways in colonic sulfur metabolism and links with health and disease. Front Physiol. 2012;3:448.
    33. Lauritano EC, Gabrielli M, Scarpellini E, et al. Small intestinal bacterial overgrowth recurrence after antibiotic therapy. Am J Gastroenterol. 2008;103(8):2031-2035.
    34. Waring RH. Report on Absorption of magnesium sulfate (Epsom salts) across the skin. 2010. Epsom Salt Council Web site. http://www.epsomsaltcouncil.org/wp-...report_on_absorption_of_magnesium_sulfate.pdf. Accessed September 2, 2018.
    35. Fujita Y, Fujino Y, Onodera M, et al. A fatal case of acute hydrogen sulfide poisoning caused by hydrogen sulfide: hydroxocobalamin therapy for acute hydrogen sulfide poisoning. J Anal Toxicol. 2011;35(2):119-123.
    36. Lee S, Park JM, Jeong M, et al. Korean red ginseng ameliorated experimental pancreatitis through the inhibition of hydrogen sulfide in mice. Pancreatology. 2016;16(3):326-336.
     
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  7. Jack Kruse

    Jack Kruse Administrator

    Kevin Mottus is the director of the Brain Cancer Association and he speaks about 5G millimeter wave radiation dangers at a meeting with the Council Of The District Of Columbia Committee On Transportation and Environment.

    These small cell transmitters will be located near every 2 to 10 homes, exposing families to harmful, carcinogenic, neurotoxic and genotoxic wireless radiation.
    See www.Bioinitiative.org for more info.
    Lethal levels of microwaves are filling our living space as a corrupt FCC facilitates an epidemic of brain cancer in our youth and other horrors to unfold. Our physiology is vulnerable to microwaves!
    Wifi, wireless home phone, smart meters, WLAN, and now 5th Generation 5G will flood our environment even more: Lethal Levels!
    Cell phones are known to increase the rate of breast cancer when stored in bras and shirt pockets, testicular cancer when carried in pants pockets and the FCC lets it go on because they're former hirelings of the industries they're supposed to regulate in the public interest. They have not addressed the dangers here revealed, that other countries have already appropriately dealt with.
    "People are currently getting very sick and dying with neurological disease and cancer near cell towers. There are testimonials which we have from almost every state. With the recent findings of 'Clear Evidence of Carcinogenicity' in the $25 Million US NIH funded National Toxicology Program Study and others like it, we have enough scientific evidence to re-classify wireless radiation as a Class 1 Human Carcinogen like Asbestos and Cigarette smoke. Thus we should be a warning and minimizing exposure, not maximizing exposure as we are doing with 5G which will require the installation of 800,000 new cell tower antennas."
    Contact Kevin via 5gisharmful@gmail.com
     
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  8. Jack Kruse

    Jack Kruse Administrator

    5G is going to ruin sulfation and nitrosylation of your skin, gut, and eye because it will affect surfaces first because of how these waves ruin the topology of these surfaces. It is a prediction I made about the engineered 5G RF portion of the wavefronts because of its pulse rate and polarization. Now we have more data why this prediction was made.

    Sulfated-Nitrosylation is the covalent attachment of a nitric oxide group (-NO) to cysteine thiol within a protein to form an S-nitrosothiol (SNO). Sulfated-nitrosylation has diverse regulatory roles in bacteria in the microbiome, yeast, and plants and in all mammalian cells. This process is almost always associated with massive liberation of molecular hydrogen in the gut when this process occurs. The process of parsing H+ from deuterium in the microbiome controls the growth of species in the human gut because of the effect of deuterium to control the growth of the microbiome.

    This process is run by three gasotransmitters thus operates as a fundamental mechanism for cellular signaling across phylogeny and accounts for the large part of NO bioactivity in the human gut. This would have been the topic I was going to speak about in Vermont 2019 but I changed plans and instead am heading to Munich Germany for Flowfest July 5-7, 2019.

    How do you heal a gut in an electromagnetic polluted city using this basic science? Might it be wise to eat seasonal foods with nitrates (Epi-paleo Rx) and then get in the sun to boost your exercise performance?
    Maximal nitrates come from seasonal vegetables only grown in the SUN and not in artificial light. It also is found in meats made in many of the countries of Europe.
    This is why charcuterie is a staple for me because nitrites added to meat are not damaging but quite helpful if you go outside. When you don't go outside in the sun, that's when you have problems with nitrates.

    https://www.sciencedirect.com/science/article/pii/S1089860314004510
     
  9. Jack Kruse

    Jack Kruse Administrator

    Sulfur groups come from the sulfur containing amino acids (methionine/cysteine/homocysteine/taurine) of animals foods and the hydrogen comes from the microbiome of the gut. Our gut makes over a liter of hydrogen a day and some of this gas links up to the sulfur recycled from foods to make H2S in blood. H2S in blood is a gasotransmitter.


    • In humans who have the MTHFR C667T polymorphism, all of the elevated homocysteine (sulfur containing amino acid) is concentrated among people who have poor riboflavin (B2) status. Blue light toxicity results in heavy metal collection because this slows down the methionine cycle naturally in humans. This is why understanding what free retinol does in a blue lit 5G world is uber critical. Blue light cause flavins to emit electrons when they are in solution. In humans, this causes a real problem in our blood.
    • Blue light induces liberated Vitamin A and this destroys riboflavin (B2). It is a flavin that is lowered by the blue light hazard because it emits electrons and it this causes it to become oxidized. When melanopsin dysfunction is present a wise thing to do is to eat liverwurst or pate for breakfast. The best source of riboflavin is liver, and humans rarely eat liver products any more. This is why foie gois is one of my favorite foods as my VIP members found out in Feb 2019 in Cancun especially when out at night in blue light. There are six possible combinations of the different MTHFR alleles, producing a continuous gradation of MTHFR activity from 100% of full activity in the best case to 25% of full activity in the worst. Roughly 15% or so of people fall into each one of the six combinations, leading to an even spread of MTHFR activity across the population. B2 and Mg+^2 help offset just about any MTHFR defect when we eat in the full spectrum sun. If you are indoors the opposite happens. Many believe sunlight lowers B2 but it is blue light that really is the culprit. Flavins are all blue light chromophores that emit electrons so that is why modern man has a riboflavin problem that mimics melanopsin dysfunction. When B2 is low we should always look at retinol binding protein to see the blue light link to the blue light hazard to understand that the broken sulfation problem leads to a destroyed methionine cycle.
    • 1.6 milligrams of riboflavin per day decreases homocysteine, and this decrease is highly concentrated among people with the C677T MTHFR polymorphisms who also have poor riboflavin status. Eating liver and onions weekly solves for X and is something those with metal toxicty never get told. In them, 1.6 milligrams of riboflavin decreases homocysteine a whopping 40%!
    • Creation of inorganic sulfate is activated by ATP so PBM/LLLT/SUNLIGHT all improve sulfation.

    The free radical gasotransmitters help control the flow of H+/D to control sulfation. How?
    The presence of strongly hydrated, kosmotropic anions (for example, SO4^2-) results in decreased 1H/2H exchange, suggesting less free water, decreased protein solvation and increased protein stability whereas increased 1H/2H exchange is found in the presence of weakly hydrated, chaotropic anions (for example, ClO4-), correlating with increased protein solvation and decreased protein thermal stability.

    Sulfate is a kosmotrope in humans and this means that it forms a gel like liquid crystalline structure inside of cells that is used in a variety of ways.

    The terms 'kosmotrope' (order-maker) and 'chaotrope' (disorder-maker) originally denoted solutes that stabilized, or destabilized respectively, proteins and membranes; thus chaotropes unfold proteins, destabilize hydrophobic aggregates and increase the solubility of hydrophobes whereas kosmotropes stabilize proteins and hydrophobic aggregates in solution and reduce the solubility of hydrophobes. Sulfate stabiize proteins in our blood plasma when the sun hits our skin and eyes.



     
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