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EMF, an alternate Neurodiverse theory of Autism, and Glutamatergic dysfunction

Discussion in 'The EMF Rx' started by Courtney Keane, Dec 1, 2015.

  1. Courtney Keane

    Courtney Keane New Member

    Here's an idea for a new Neurodiverse model:


    A concept called Neurodiversity has come to the forefront of thought and discussion among autism advocacy groups and researchers as of late. The idea asserts that atypical or divergent neurological development should be respected and recognized as a normal human variation in cognitive function, and not considered pathology. This concept represents a paradigm shift in how we think about mental functioning. It is the answer to this conundrum: we have moved too far in pathologizing a large proportion of the population due to the epidemic growth of mental illness. In fact, it has been suggested that nearly every individual in the country may have some degree of psychiatric illness, if we include milder versions of conditions, called “shadow syndromes”. Rather than consider that the majority of the public is suffering from dysfunction and disease in their mental processing, we should think of brain differences in the same way we do cultural diversity- simply differences in human cognitive function.

    Like you, I am greatly alarmed by the phenomenal growth in psychiatric illness, and do not think dysfunction to be a normal state for any person at any point on the neurodiverse spectrum. There has been an epidemic increase and proliferation of degenerative, neurological, and autoimmune disorders of ALL kinds, in people across the entire spectrum of cognitive function. As you said, we should be looking at what has been altered in our environment sufficient to cause the problems- and certainly not trying to normalize pathology. While I don’t agree with the whole neurodiversity concept, I do think there is nugget of something helpful there.

    It could be modified- to be viewed through a non-pathological lens, but without turning a blind eye to the pathology associated with the various points. Ideally, people at any point on a diverse spectrum of normal cognitive function could exist in a homeostatic state. I believe the autistic endotype is distinct from the others, and has always existed. Theoretically, it can still exist without the dysfunction of autism or autism-like symptoms, though it is harder to find in recent times because of how the odds are stacked against them. Practically, though, the various identifiable groups along the spectrum would each have a unique constellation of dysfunction symptoms associated with them. With this model, we could begin to look at the epidemic rise of the diseased state across the spectrum, searching for similar pathological processes, mechanisms, and patterns of correlation that might help determine causation. In doing so, we might have a better chance of discovery; and in the process, we would surely gain understanding and respect for -and between- the groups.

    The next question is: What basic groups, or phenotypes, would comprise the spectrum, defining it at certain points? I will propose identification of only a few segments of the spectrum, although I’m sure there are others. The key mental domains traditionally examined are: verbal and spatial abilities, and empathizing and systemizing capacity. Brain connectivity studies have revealed striking differences between men and women in cognitive function that lend credence to some stereotypical assumptions about their behavior. Using diffusion tensor imaging, DTI, investigators were able to trace and highlight fiber pathways connecting different regions in the brain, mapping the wiring between and within structures. The study showed pronounced differences between the sexes, even though there were variations among individuals of the same sex. The brains of males were structured to facilitate connectivity between perception and coordinated action, suggesting literal, rational response; while brains of females facilitated communication between analytical and intuitive regions, providing for more empathetic and socially sensitive response. From this, we could assign phenotypes based on similar connectivity patterns and characteristics: “male” or M category, and a “female” F, category- although this is only with reference to brain connectivity and cognitive patterns seen in the majority of the group, and not an individual’s sex alone. Presumably, there could be some females in the M group, and males in the F, with a continuum between them. An idea for a third phenotype drew upon the “extreme male” theory of autism, in combination with task-based MRI imaging of brains of people with high functioning autism, or Asperger’s syndrome. This EM segment differs significantly from” normal” males in the processing of emotional input, like judging expression in another person’s eyes, by calling upon a different region of the brain. Since it is similar to the M brain in systemizing, but completely opposes F in cognitive profile with regard to empathizing, “extreme male” seems to be a fitting description, though this category certainly contains women. If these- and possibly more- phenotypes were established, then sex differences within each one could be examined, with a clearer picture as to the role of sex hormones in the development and progression of disorders associated with each group, as well as the general spectrum effect. Age of disorder onset could also be taken into account with the sex difference studies. I think we would see some interesting patterns emerge: the EM spectrum end heavily weighted toward brain neuro-inflammation appearing at or before birth and into childhood, with more severity in males. At the other end, F dysfunction appears primarily in the peripheral nervous system, with onset into adulthood, and more severity in women. These two extreme ends of the spectrum share the commonality of having less myelinated neurons. This is a very important point, which I will expand upon later. I would expect that disorders affecting the elderly would have distinct patterns, too. These phenotypes may well also be endotypes. I postulate there is something inherent in the composition of each cognitive type that predisposes the dysfunction constellation associated with it, with slight modification of gender effect due to mediation by ovarian steroids. A possible compositional difference could be the distribution and concentration of glutamate receptor types throughout in the PNS and CNS- especially the astroglia, oligodendroglia, and microglia associated with the white matter tracts providing inter- and intra-hemispheric connectivity. The common spectrum disorder factor of excess glutamate gives rationale to investigation of glutamatergic receptors.

    The role of glutamate in the body is crucial, as it is both the most prominent neurotransmitter, and the primary excitatory neurotransmitter. It is necessary for excitatory neurotransmitters to be balanced by inhibitory ones, in this case GABA- to reduce stimulation, preventing excitotoxicity that wrecks havoc on mental and physical health.

    The balance is delicate and may be disrupted by countless inputs, internal and external. Some of these include: methylation cycle blocks like MTHFR and COMT polymorphisms, GAD enzyme dysfunction, impairments in the Krebs cycle, dietary deficiencies, glutamate ingestion, insulin levels, heavy metals, halides, pathogenic infection, and stress. MMR vaccines have been shown to raise glutamate levels by 50%. When equilibrium is lost, tipping the balance drastically away from the inhibitory regulation of GABA, glutamate excess results in neuro-inflammation and cell death. The EM end of the spectrum demonstrates higher glutamate levels than other segments. This may be what makes them especially prone to imbalance from an additional glutamate load during early stages in life, as evidenced in autism and STIM behaviors. They would be the “canaries in a coal mine”, but every phenotype would have a threshold range before dysfunction. CNS glutamate has been shown to correspond fairly closely to plasma glutamate levels. If male/female phenotype norms for glutamate levels were established, then testing plasma glutamate could be utilized as a screening tool with infants prior to vaccination, and a less aggressive or alternate vaccination schedule considered for those with high levels.

    Though the EM phenotype sees problems related to glutamate earlier than others, it is a spectrum-wide concern. Glutamate excess is a primary contributing factor in disorders like ALS, Parkinson’s, schizophrenia, migraines, PANDAS/PANS syndrome, Tourettes, fibromyalgia, multiple sclerosis, restless leg syndrome, Huntington’s chorea, seizures, chronic fatigue syndrome. We see conditions like mental fatigue, hypersensitivity to sensory stimuli, ADD/ADHD, drug and alcohol addictions, polyarthropy, neuropathy, depression and anxiety, OCD, Bipolar disorder, insomnia, and stroke. Glutamate excitotoxicity, through combination with mitochondrial dysfunction and oxidative stress, could have possible implication in an even wider range of conditions related to neuroinflammation- diabetes, cancer, celiac disease, and asthma, for example.

    Given the ubiquity of the factors contributing to our glutamate load, and the pervasiveness of spectrum-wide disorder, a closer look at what conditions trigger glutamate receptor hyperactivity is imperative.

    It has been suggested that one of the first responses to overabundance of glutamate is creation of new receptors to compensate. High IQ has been correlated to greater numbers of glutamate receptors in the brain. In autism, genius is frequently observable in very restricted areas of ability, in conjunction with debilitating dysfunction from excitotoxicty. Perhaps with other pheno/endotypes, receptors multiply in differing areas of the CNS, or outside it.

    In addition to increase, glutamate receptors become hypersensitive. Exactly how and why has been perplexing. Ionotropic glutamate receptors are ligand gated ion channels. Quantum physics elucidates the loss of control over calcium voltage channels with the explanation of the biologic effect of non-native EMF. Due to the role of calcium ions, both NMDA and non-NMDA receptors are greatly influenced by non-native EMF.




    [​IMG] f_l02ca++entry.gif f_l02ca++entry.gif


    In addition, non-NMDA receptors rely upon mitochondrial function, also affected by EMF. This impairs them by reduced ability to pump ions back out of the cell, resulting in increased sensitivity of NMDA receptors to glutamate molecules. Any increase in intracellular calcium is problematic in the presence of excess glutamate, as calcium is the agent that actually inflicts harm to the cell by activating a cascade of actions that cause cell death. Glutamate may be the gun, and calcium the bullet- but now we have an idea why the trigger is being continually fired. EMF creates a scenario where calcium efflux from surrounding tissues provides abundant intracellular free calcium ions.

    GABA receptors are also ionotropic, and contribute to glutamate kindling. Even metabotropic glutamate receptors-which regulate the release of other neurotranmitter molecules and are believed to modulate gene expression- are impacted indirectly, in as much as they are linked to the ion channels and mitochondrial function disrupted by EMF.

    A few interesting observations: You mentioned that any time calcium is altered, magnesium has to react to it. NMDA receptor channels are blocked by magnesium, which is removed by depolarization of the postsynaptic cell. Schizophrenia, anxiety, bipolar disorder, OCD, asthma, allergies, ADD, autism, and diabetes are all conditions that exhibit magnesium deficiency, among others.

    EMF links glutamate toxicity, mitochondrial dysfunction, and oxidative stress intrinsically through ionotropic glutamate receptor dysfunction- underpinning a host of neuroimmunological conditions.

    Glutamate excitotoxicity doesn’t appear to be restricted to the CNS. Peripheral neuropathy is observed in diabetes and chronic alcohol abuse. Fibromyalgia patients also show evidence of small fiber polyneuropathy.

    Antibodies to NMDA glutamate receptors have recently been recognized and related to autoimmune disorders such as late onset autism, eplilepy, ataxia, and autoimmune encephalitis. Some of these disorders have prodromal symptoms reminiscent of a viral infection. Anti-basal ganglia and thalamic antibodies associated with increased levels of glycine suggest NMDA receptor contribution to hyperglutamatergia in pure OCD, although cytokine mediated inflammation may also play a role. Curiously, the ligand binding domain ionotropic glutamate receptors shares striking structural similarity to bacterial periplasmic amino-acid binding protein. Could this be the “molecular mimicry” that induces autoimmune attack in PANDAS syndrome following strep infection?

    In the same way that excitotoxicity isn’t restricted to the CNS, anti-glutamate receptor antibodies don’t appear to be either- They have been detected in various non-immunological diseases such as stroke and trauma. Parvovirus B19 infection of adult females can have decade-long symptoms of intermittent polyarthropy- perhaps from receptor involvement in the glutamate kindling phenomenon?

    Both ionotopic and metabotropic glutamate receptors are present in CNS and PNS glial cells. Astroglia, and oligodendroglia both produce anti-inflammatory cytokines that act to control inflammation. . Post-mortem findings of major depressive disorder patients indicate astroglial loss in areas of the anterior cingulated cortex, prefrontal cortex, amygdala, and white matter. Glial loss may contribute to inflammation through elevated cytokine levels, glutamate excess, and altered BBB function.

    Oligodendronoglia maintain the BBB’s integrity, regulate axonal repair, and myelinate inter- and intra-hemispheric connection. Post-mortem studies of schizophrenia patients reveal oilogdendroglial loss in the prefrontal cortex, anterioir cingulated cortex, and hippocampus, and abnormally myelinated fibers of both gray and white matter Lessened myelination due to oligodendroglial loss is crippling in the developing brain of infancy/childhood because it reduces the DC electric current, which is also it tied to calcium efflux of cells through EMF. Electroencephalogram recordings show aberrant electrical activity in autistic patients, underscoring the EMF effect. Added to all of this are anti-NMDA antibodies.

    Women have less myelin than men, which is why women have autoimmune disease more often. Schwann cells supply the myelin for the PNS. Loss of these cells from glutamate excitotoxicity results in less myelination. This is a double whammy because it causes subsequent reduction of DC current from EMF, spelling neuroimmune crisis for the F phenotype. The far ends of the neurodiverse spectrum suffer the same problem, but in variant parts of the nervous system and differing age of symptom onset.

    Ionotropic glutamate receptors have also been expressed on microglial cells of the brain, affecting activation to initiate a myriad of events, including the release of proinflammatory cyokines. These cytokines have been hypothesized to deteriorate the blood-brain barrier through oxidative stress, and affect metabolic supply for neurons, thus increasing CNS glutamate levels in a feed-forward cycle. Mcroglia may also contribute to an exaggerated Th1 response and generation of autoantibodies.

    The glial cells of the inter- and intra-hemisphere connecting tracts and their glutamate receptors are worthy of further investigation. Brain scan studies have shown that people with high functioning autism have a smaller than normal amygdala, hippocampus, and cerebellum; and the circuit between the anterior cingulate in the frontal cortex and the amygdala is not completely connected. Autopsies of Asperger brains show diminutive, tightly packed cells in the smaller-than-normal regions. This signifies immature development- not damage or atrophy- possibly resultant from under-stimulation caused by the abridged circuit. I believe these connecting tracts to be of key importance, even if there has already been damage sustained.

    Neuroplasticity may allow for the development of new connectivity and compensating function, providing that an improved glutamate-GABA balance can be established. The parts of Albert Einstein’s brain that processed visual and mathematical thought were fused together- an abnormality that may have enabled his genius. I am convinced that understanding the mechanisms of glutamatergic dysfunction is paramount for improving the health and quality of life for countless people.
     
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  2. Courtney Keane

    Courtney Keane New Member

    Men are from Mars, Women from Venus, EM phenotype from....Pluto! What I'm saying is even apart from dysfunction, this type is radically different than the others, and needs to be recognized as such. They think, feel, and act differently...even if they do have the same hormones as the others. This type does NOT need "fixing" to be made to fit the imposed societal expectation of typical male and female behavior or perspective. Only the dysfunction of autistic symptoms needs "fixing".
     
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  3. Joe Gavin

    Joe Gavin Face Everything And Rise

    Cool stuff. For some reason the role of the vagus nerve popped into my head after reading this. Appears glutamate does not cross the blood brain barrier, so it would play a role where the "digital" and "analog" light signals meet to regulate the body clock (will need to look at a previous @Jack Kruse post to get the correct regions of the brain). What if the vagus nerve was optimally stimulated to regulate glutamate in all of this? Again, cool stuff and all comes back to light (again).
     
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  4. Jack Kruse

    Jack Kruse Administrator

    Correct Joe........very correct.
    UV light is a huge problem with these kids. The environment their parents allow their germ cell lines to inhabit prior to pro creation is the major event no one wants to speak of.
     
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  5. Joe Gavin

    Joe Gavin Face Everything And Rise

    From the attached study: "We found facilitative carriers for glutamate to exist exclusively in the luminal membranes". Luminal = light.

    Facilitative transport of glutamate in the luminal membrane
    Lee et al (53) measured facilitative glutamate transport separately in luminal and abluminal membranes and found that facilitative glutamate transport exists only in the luminal border in a position to allow the release of glutamate from endothelial cells to the plasma. Luminal carriers of amino acids have no dependence on Na+ gradients (46,5458) and are therefore energy independent. Three broad classes of facilitative carriers exist: large neutral amino acids, cationic amino acids, and acidic amino acids, and each transports several amino acids (59). As mentioned, the presence of a transporter for acidic amino acids with a high affinity and a low capacity (12, 60, 61) was an enigma for many years because both glutamate and aspartate are nonessential amino acids that are synthesized and accumulated in high concentrations in the brain.


    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3136011/
     
  6. Hansen Kenimer

    Hansen Kenimer New Member

    Hey everyone. Meet my brilliant sister. :D

    Soooo.....perhaps an insult of some sort could affect the BBB, thus making it permeable to glutamate?
     
    Last edited: Dec 1, 2015
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  7. Jack Kruse

    Jack Kruse Administrator

    Glutamate has several fates, rather like tryptophan does. Tryptophan is needed to make 45 of the proteins needed for cytochrome 1. The local redox of the cellular environment is the key to its fate. It can become GABA (inhibitory), or aspartate (excitatory) when UV and IR light are absent both increase and, in excess, they become neurotoxins. Ketogenic diets seem to favor glutamate becoming GABA rather than aspartate. No one in biochemistry knows exactly why but people here should. NAD+ drops and pseudohypoxia develops when UV and IR are missing from our environment. Biochemists and PhD's often point blame to how ketones are metabolized. The belief is that ketosis favors using acetate (acetoacetate is one of the ketone bodies, after all) for fuel. This belief is not true in all light environments. Acetate tends to becomes glutamine under a blue light scenario, and this gives us the precept that it is an essential precursor for GABA. Most of you know I am not a buyer of anything done under lab lighting. This is a perfect of example of why.
     
  8. Scompy

    Scompy Gold

    I've done extensive research on the NMDA receptors and glutamate, since it's afflicted me over the years. So I'll go out on a limb here and share my findings. During my early 30s, I successfully did some temp-biohacks that worked for my condition with past capillary bursting in my retina before I understood how sunlight was my friend. For the past 5 years, I have completely resolved these issues. They #1 key for me has been morning sun. Jack is spot on to solving this root with my personal issues with missing UV and IR. In the past, I could look at a white-wall and see when ruptures appeared in my retinas, bleeding out into my vision causing blind spots for months. NDMA receptors are present in the retina and in other parts of the cardiovascular system. It's why I've read glutamate can trigger insulin release in the abscence of glucose present, due to NMDA sites in the pancreas.

    Here are my biohacks:
    1. Morning sun or any sun for that matter and avoiding artifical lighting
    2. Eating ketotic and reducing dietary glutamate.
    3. I've also noticed that hydrating and grounding really helps with my issues overall; I typically had the most problems in the past when I was ungrounded in airplanes or working in high buildings. Ironically, the worst issues I had was in 1996 working at a video game company in downtown Honolulu on the 36th floor for 14 hours each day, 6 days a week. I was stuck indoors all day under artificial lighting and the sun was right outside unavailable. That half a year working there almost killed me.
    4. Previous backup bandaids: If a spell came on, taurine and ibuprofin can bind to the NDMA receptors (or I've taken in a load of dietary glutamate unexpectidly), I'll pop around 1,000 mg of Taurine or have some eggs, as eggs are loaded in taurine.

    I suspect that because liver function can be stifled especially in people that have a fatty-liver due to much fructose and/or alcohol, the liver's ability to create enough taurine to compete with glutamate at NMDA receptors is probably gonna be limited. I.e., taurine deficiency could allow glutamate to run-wild more commonly. Sort of a Yin-Yang balance of taurine:glutamate. In felines, they rely on taurine in the diet because the liver doesn't produce much of it if any from my understanding. Ketogenic diets typically have far more taurine content, so I've suspected for years now that it's an added benefit. I've been eating ketotic for 4+ years, and it's the glutamate control that helps. Now, granted, I also avoid aged cheese that has a huge natural glutamate component and choose goat or feta. One other note here of interest I'm suspecting: babies also do not produce liver taurine until 6 months+. So let's say a baby is not getting mother's milk and is on a glutamate-loaded formula, then is injected with 20+ vaccines in the first year of life where glutamate is often a common adjuvant. Do the math as a quick way to lower redox. Plus, it's known that some autistic cases have carnitine issues, and it's in the liver where carnitine is also produced. So I'm wondering if vaccine-giving doctors should be suggesting for kids to load up on taurine before vaccinations and take more on the day of one to help balance out the glutamate-hit injected directly, unbuffered into muscle tissue.

    One other thing I've read in the past is that glutamate itself can have an isomer, and the paper I read was that the super-heating of glutamate in some foods could create it. Why would this isomer be bad? Speculation that the glutamate isomer could bind longer or stronger to the NDMA receptor site.
     
    Last edited: Dec 2, 2015
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  9. Courtney Keane

    Courtney Keane New Member

    Great comments- and very helpful! Excess glutamate is a huge issue in my family and I will take those hacks seriously. I think you're right on about the taurine and have had similar experience.. only didn't realize it until just now. Thanks for your post
     
  10. Courtney Keane

    Courtney Keane New Member

    BTW- what are your thoughts on if glutamine is converted to glutamate? I've read conflicting research. Though I realize restricting environmental/dietary glutamate and taking measures to counterbalance is just part a multi-pronged solution, it still is a part I wish to address.
     
  11. Scompy

    Scompy Gold

    Here's the big takeaway. You've just met a person online that USED to have a REAL SUPERPOWER that few understand or know about. It's why I know so much on this subject because I happen to have a Bio degree and did my homework. My past superpower was that I was a walking glutamate detector when I had poor redox, poorly hydrated and didn't get daily sun in a EMF loaded environment. I want to say that again in another way. I had the ability to detect glutamate consumption through my front vision because my visual disturbances (capillary swelling/bursting) were 100% correlated to what I had previously eaten 30 minutes in the past. Typically the swelling and issues I got in my vision lasted longer with a higher glutamate load, or shorter with a smaller glutamate load. My instrumentation for about 2 years was highly tuned and I knew exactly what foods, and specifically, what glutamate-concentration-in-foods would trigger a tiny, small, medium, large or extreme response in my vision. Tiny responses often were flashed and only lasted a minute or two, medium tyipcally lasted 30mins, and extreme responses caused blood-leakage and spot could last for days, weeks or months.

    It's the direct ingestion of glutamate is the problem I've found. Glutamic acid in that form isn't a problem to me if we're actually consuming it that way... THEREIN IS THE PROBLEM. let's talk about glutamic acid for a moment. It's highly abundant in the food supply, right? However, in my case in the past, glutamic acid load didn't seem to be too much of a problem in unprocessed foods. Look at cheese for a moment. Parmasean was previously heated when you put in on the table in a shaker. That stuff is literally pure glutamate. But if you have a lower-protein cheese, you get lower glutamic acid overall because glutamic acid is part of that protein content on the label.

    Most bread BY DEFAULT is grinded up and dried out. Why is this bad? Because 40% of the GLUTEN molecule by dry weight is glutamic acid and drying it/heating it then yields far more glutamate. In other words, bread is the absolute perfect combination of glucose chains and higher glutamate content to make it addicting. How many people do you know that can say they're able to remove all bread from their diets? It's for this synergy of glutamate and sugars for biochemical addiction.

    Another great example would be the protein powders muscle builders are getting at the stores. On the label, it says some Milligrams of glutamic acid, but it's been powderized, dried out or over-heated at some point; that label is untruthful because some % of that 'glutamic acid' is 'glutamate.' Dried fish and dried meats (beef jerky) are also ultra-loaded in pure glutamate content for this reason. Aspartame is obviously a huge issue. I couldn't even do certain bone broths in the past until I learned not to overheat them. Food prep was half of the battle in my past to learn ways to reduce glutamates as a bandaid I understood redox and contributors to my bad environment... the quantum mechanisms to cure my issues outright.

    Overheating glutamic acid --> glutamate is an analog to overheating a fat or oil to create transfat in my opinion. It's also my opinion that the body creates glutamate when it needs it and can handle tiny amounts that uptake/filtered into the bloodstream via the small intestines at a rate similar to glucose uptake. (This is why I said before the direct injection of glutamate via vaccines into muscle tissues has got to be problematic to say the least). The controls over glutamate if I remember correctly are much tighter in comparison to glucose as well in how much exists in the blood at any time.

    When you let the body operate well with a higher redox, consumption of real glutamic acid or even smaller amounts of straight glutamate isn't going to be as problematic because the body will be making glutamate when it needs it and regulating it easier. The lower the redox you go, the body has a harder time with larger/higher quantities of glutamate via the gut. But if I'm preparing my foods by heating or drying it out, I've got a big problem. Again, if liver function is stifled, glutamine regulation is also compromised.

    One last thing that's an important takeaway from my years of research on this issue. Glutamate is a suspected suppressor of taurine in the liver: the very molecule that can also compete at the NMDA receptor for potential receptor regulation. Like I said before, an insulin secretor because glutamate turns on/activates many mechanisms. Fixing organ function means fixing quantum biology. So it's my strong hypothesis, because I've literally seen it in my own life, that when a person eats ketotic and also concentrates on reduction of glutamate, more things fall into place, more weight is shed, less addictive cycles occur, etc. That glucose-glutamate synergy when it hits the bloodstream at the same moment in time from the gut is what I personally believe was a major problem for me in the past. It's EXACTLY the glucose-glutamate synergy we see in every piece of processed junk food on planet earth.

    But..., the elimination of the sugar and glutamate was just one piece of puzzle and only a bandaid to the real underlying problems. Solving the redox requires a great deal of effort, and one's personal environment is EVERYTHING in this equation. This is why the overfocus and fixing glutamate is only a temp-hack because it's a much more complex quantum issue when other mechanisms are not optimal. Solving the quantum solves it outright so the impact of glutamate in my system now in 2015 compared to 2005 is night and day. Between 1996 - 2000, migraines and blind spots in my vision was my normal. There was a 6-month period when a large dried blood on the inside of the gel in my left eye blocked most of front vision and I couldn't read with both eyes at the same time. So you see to me, this is all about truth and my past to prevent blindness. It was a powerful motivator.
     
    Last edited: Dec 2, 2015
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  12. Scompy

    Scompy Gold

    This is pure speculation and opinion about what I would do personally with my current knowledgeset...

    I'm thinking additional biohacks to reduce or ward-off late-onset autism... breastfeeding as long as possible (with the mother taking in lots of seafoods), grounding while feeding (easy for the mother to do), getting the child daily sun exposure, minimizing nnEMF by understanding all of the sources especially in sleeping-spaces, and possibly finding ways to get the child to eat more taurine and carnitine early (more chicken, egg, meats, etc.). I'd also reduce down glutamate sources of course. Baby formula is opposite of mother's milk... transfat DHA if any at all + high glutamate + high sugar + hella lotta of other perservatives and added supplements with whatever processing they are using. That translates to me as liver stifling. Pure Mother's milk that has got to be the best food on the planet with SN-2 and all of the immuno-benefits to boost.

    I'd also prevent my baby from getting vaccines until a year or two later and be spreading out vaccinations over longer periods of time. Plus, the threat-risk to individual-risk analysis should be taken into account. I don't think doctors shouldn't be in the standard practice of injecting babies in their 4th trimester. Instead, look at localized rates of disease in various cities and states, and let the parents make judgments based on real data rather than this stupidity of advocating vaccines as a one-size-fits-all approach.

    I'm not pro-vax or anti-vax for this reason. I'm pro-truth. Vaccines to me are simply medicines and all medicines carry risks and side-effects, and sometimes many permanent side-effects, and sometimes death. The public doesn't view them this way at all. Each individual vaccine concoction is unique just like any medicine. Therefore, risk/threat should play into the decision to get one. By the way, the MMR is SPECIFICALLY FORMULATED with MSG (glutamate) as an adjuvant. It's exactly the MMR that a ton of parents have complained about as the source of autism in their kids along with Jenny McCarthy. I suspect it may have been the 'MSG blast' unbuffered (no gut to buffer) into muscle tissue and could get to the brain quickly that pushed the kid over the line of autism because of all of the other combined factors of lower redox (and poor dietary choices). I want to say this is all of my speculation and could be partial-truths (not the whole story), but it's what I've come to conclude in the past few years.
     
    Last edited: Dec 2, 2015
  13. Scompy

    Scompy Gold

    Interesting... yesterday, I just found out why I've had this super-power. I have multiple mutations to breakdown GABA from glutamate (cannot do that well at all), so my blood is running hot with glutamate 24/7:

    Neurotransmitter Levels rs3749034 GAD1 A GG: 2/2 (68.6151%) Catalyzes production of GABA from glutamate High glutamate, low GABA
    Neurotransmitter Levels rs3828275 GAD1 G TT: 2/2 (7.46300%) Catalyzes production of GABA from glutamate High glutamate, low GABA

    Plus, I had calcium sensitive receptor issues:

    HPA axis / Endocrine rs1501899 CaSR G AA: 2/2 (14.7929%) Calcium sensitive receptor s7652589 and rs1501899 were also associated with nephrolithiasis in patients
    HPA axis / Endocrine rs1042636 CaSR A GG: 2/2 (1.21260%) Calcium sensitive receptor Arg990Gly polymorphism was associated with nephrolithiasis and hypercalciuria in different populations

    ^^^ links directly to nnEMF aggravation.

    In combination, I have other issues with my B12 to bottoming out easily that I'll have to resolve that also relates. Makes so much sense why egg (taurine) and eating a ton of seafood has been a friend to me, because of NMDA binding frequency when glutamic acid is made normally, and then not going away.
     
    Last edited: May 14, 2016
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  14. Jack Kruse

    Jack Kruse Administrator

    Time for some fireworks tonight. This new podcast with Wallace helps explain how vaccines MIGHT effect mtDNA and be causative to energy flows in susceptible haplogroups via the melanopsin/retinol system. A vaccine is given in the SQ space where melanopsin is and this will lower melatonin to affect mtDNA haplotypes to lower energy. None of the skeptics have a clue how this data link to the phenotype. Vaccines have adjuvants in them that draw nnEMF to them and the energies in these EMF's can disrupt the retinol from melanopsin to lower melatonin and cause more mitochondrial damage. At the 1:119 -1:23 mark Wallace lays it all out on the mitochondrial side. All the mitochondriac has to do is lay out the melanopsin side that I gave you in the Vermont 2018 talk. That is what lowers the melatonin level to lower energy flux to cause the neuronal manifestations of the disease. Black Swan Mitochondriac wisdom present here in the post. California leads the charge in new autism cases because they embrace more technology than any other place in the USA. The U.S. Centers for Disease Control (CDC). The CDC report found that autism is now diagnosed in one in every 59 American children, representing 2 ½ times more autism in 12 years and a 15 percent increase in just two years. This is DEFINITIVE proof autism is not a GENETIC disease related to the NUCLEAR genome.
    The alarming increase in autism prevalence over the past 10 years signals the need for a significant change in the federal response to addressing autism in the United States. We need advocacy for technology diets for these kids. A more accountable, effective, and strategic plan is necessary to meet the needs of those with autism and their caregivers today. Concerned Americans should be working toward a major overhaul of the current response as the Autism CARES Act is reauthorized.
    If you want to have a kid and avoid autism begin educating yourself about blue light toxicity and how it changes the epigenetic switches in your own germ line. That is where the disease begins in my opinion. Once the epigenetic changes occur it changes the free radical signals made in mitochondria which change signaling to the nuclear genome and this can hard wire nuclear changes into the offspring. Usually, this is not the case. Most of the changes associated with autism are transgenerational post-translational modifications that can be changed. The reason is obvious. They are mitochondrial defects. If you become a mitochondrion before you have sex to have a kid you can prevent this condition. If it was a nuclear genomic disease, there statistics over the last 30 years in autism would be impossible. Because the mtDNA changes 3-5 times more quickly it should be obvious this is a mitochondrial disease at its core.
    The CDC report, “Prevalence of Autism Spectrum Disorders Among Children Aged 8 Years—Autism and Developmental Disabilities Monitoring Network, 11 Sites, United States, 2014,” states that in some of the communities represented in the network, nearly three percent of eight-year-olds had an autism diagnosis in 2014. It uses the same methodology that produced the CDC’s 2010 prevalence findings of 1 in 68 children with autism.
    The extraordinary cost of autism care is expected to escalate dramatically as prevalence continues to increase. University of California Davis health economists estimates the national cost of caring for all people with autism in the billions, heading towards $1 trillion. Their forecasts for autism-related medical, nonmedical, and productivity losses were $268 billion for 2015 and $461 billion for 2025. The researchers noted that if ASD prevalence continues to increase as it has in recent years while effective interventions and preventive treatments are not identified and made widely available, the costs could reach $1 trillion by 2025.
    Notably, the economic and social costs related to the autism crisis will continue to impact every American taxpayer as funding and priorities are redirected into areas, including, but not limited to: WE need to recommend all kids AVOID all blue light devices until the brain is fully myelinated. We need to educate pediatricians, teachers, school boards, and technology companies how their beliefs are COMPLICIT in this pandemic.
    Medical and other health insurance expenditures for co-occurring conditions. Research shows that 47 percent of children with autism had at least one co-occurring condition
    Increased funding for social security disability and SSI benefits
    Training of public safety resources to manage the explosive increase in wandering and development cases, as 49 percent of children with autism wander/elope
    Programs addressing the needs of adults with autism including employment, housing, and community integration.https://www.ihmc.us/stemtalk/episode-67/
     
  15. Jack Kruse

    Jack Kruse Administrator

    More collateral nnEMF/blue light damage due to melanopsin/retinol dysfunction: Paul Allen lived in Washington before he died of a hypermethylated disease tied to melanopsin dysfunction. He got diagnosed with Hodgkin's lymphoma in 1982. Ironically this cancer was why he quit Microsoft according to his book. This was different cancer than the one he died from on 10/15/2018. In 2009, he got non-Hodgkins lymphoma, a new cancer, and it was treated successfully, at least he thought. 6 weeks ago it recurred out of the blue according to reports. He spent most of his time on the West coast near many 5G installations that have been testing networks in and around Microsoft headquarters for the last 18 months. He announced publically just a few weeks ago his second cancer had returned with a vengeance about 6 weeks ago Guess what else happened in his state in 2014 to kids with immature neurologic systems not fully myelinated or developed in their spinal cord grey matter? Another "plausible" fingerprint of nnEMF collateral damage is a recent outbreak of acute flaccid myelitis (AFM) since 2014 among children in Washington. This is the same state and location where Paul Allen lived.
    It is a polio-like disease, for those who don't know. Many ID docs have been complaining that polio-like diseases seem to be making a comeback.......they usually find out it is linked to other more obscure infectious agents. This is what the CPC patreon series told you to brace for. Infectious disease with sepsis unresponsive to treatments will be a hallmark of retinal damage.
    AFM is linked to enteroviruses and probably activated/promoted by environmental toxins like nnEMF. When Vitamin A levels are high, infectious diseases of all types become more common because the immune system undergoes severe damage. Hypervitaminosis effects of Vitamin A on the immune system are well known and published in medicine but nobody is linking the stimulus to the effect in environments known to cause hypermethylation and destruction of B12. Infectious diseases will spike in places where nnEMF is toxic. When this occurs the retinol will cause collateral B12 damage by lowering it. In children, this will lead to developmental delay in neurons, mental illness, weird brainstem tumors, anemia and many gut complaints that mimic a leaky brush border. B12 is needed in these kids for the growth of their grey matter in the brain and spinal cord. DNA methylation is an epigenetic mechanism that has been implicated in the pathogenesis of chronic inflammatory diseases as well as malignancies, by regulating the differentiation, apoptosis, proliferation, and activation of different cell types. This is achieved through alteration of gene expression and regulation of cellular phenotype. We know that phenotype links to mtDNA damage from Doug Wallace's work.........Now we have the data to link melanopsin dysfunction to free retinol which is a direct cell toxin for neurons. Do I believe this is the key to understanding the etiology in many motor neuron diseases like ALS and CTE too? Yep. Be prepared people. A tsunami is coming and no seems to see this asteroid headed for mankind. At least the dinosaurs saw their asteroid coming at them in the sky. https://www.cdc.gov/mmwr/volumes/66/wr/mm6631a2.htm
     
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  16. Scompy

    Scompy Gold

    My 22-year story has gone public and is already causing friction in several circles. Finally, it may be shattering the Conventional Wisdumb of our day: how the mainstream establishment views health and what they may never have considered before their eyes.. It's exactly what I wanted and expected nothing less. Bring it.

    https://blog.mitohq.com/my-health-advantages-leaving-the-video-game-world/
     
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  17. Alex97232

    Alex97232 Gold

    Hey Scompy, Love your guts!
     
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  18. DrEttinger

    DrEttinger Platinum

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