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Why does anesthesia affect Alzheimer's and Parkinson's patient so badly?

Discussion in 'Educating Doctors' started by Jack Kruse, Aug 10, 2016.

  1. Jack Kruse

    Jack Kruse Administrator

    A little known fact outside of medicine: people with Alzheimer's and Parkinson disease do not tolerate anethesia well. Both of the these diseases are mitochondrial disorders that link to an inability of neurons and muscles not being able to fat burn well so they default to a Warburg metabolism: Few people recall this key data about this type of metabolism: everyone focuses in on the glucose aspect of Warburg’s findings, but if you read his original papers, he also found cell use glutamine and glucose when they cannot fat burn in mitochondria and this leads to lot of ammonia released simultaneously to glucose/glutamine use. Why did he find that? Altered light spectrums cause ubiquitin up regulation creates excess protein turnover, and this leads to production of a lot of ammonia. Hospitals are filled with blue light in out OR's. When ammonia production is increased, oxygen levels fall, superoxide levels drop, while Reactive Nitrogen Species increase. These findings will alter glutaminergic metabolic pathways. Once these pathways are altered they can cause mitochondrial damage when anesthetics are also introduced. Most of the drugs we use to sleep humans have halogens in them. Cells release more ELF-UV light when this occurs from their mitochondria. Light energy and information is lost. The exclusion zone (EZ-Pollack 2013) is lost within cells and this lowers energy production in a cell and this slows recovery from anesthesia. This process is always associated with light frequencies that have too much power for a system no longer optimized in their mitochondrial function, therefore, light has to be emitted from the cell as the process occurs. This is why artificial light is problematic for biologic systems. This has been well documented in the literature by Dr. John Ott and Fritz Popp.

    Power in light waves is a function of its frequency. It is the only way the power of light can be modified in nature. When the frequency is changed, what else occurs simultaneously in mitochondrial cytochromes? The amount and type of free radical signals released also change. When nitrogen gets oxidized, this means electrons are taken away from its molecular structure. When electrons are removed from any proteins it makes them less hydrophilic and as a result, the size of the EZ in cells drops. This is also true in the MINOS that surrounds the cytochromes. The MINOS must remain reduced, ie filled with electrons, to maintain a large EZ to continue to be able to exclude protons. This is why the mitochondrial matrix is filled with protons and why there should not be a lot of free protons outside the matrix. This sets up chemiosmotic gradient between the two areas of a cell. This can be used to do work and harvest energy. When the size of the EZ drops, ammonia rises and the mTOR pathway is activated. Resveratrol, turmeric, and metformin has been shown to prevent ammonia toxicity in cells. When protons cannot be contained within the matrix or the EZ decreases the mTOR pathway is activated because beta oxidation is lost in the cytosol of mitochondria and the mitochondria have to rely on the TCA exclusively for energy. This burns out cytochrome 1 and superoxide burst. This is why mTor expression is a problem for generating longevity, because longevuity is linked to using beta oxidation over the TCA most of the time humans are alive. The process works by limiting or lowering ubiquitin marking of proteins in cells because replacing proteins costs mitochondria the most energy. With a Warburg shift you cannot replace the proteins when the mitochondria is defaulted to glucose and glutamine metabolism. With mTOR activation we see pseudohypoxia develop because ECT slows, and NAD+ levels drop in relation to a rising NADH level at cytochrome 1.

    Why should you care deeply about the nitrogen atoms present in NAD+? When nuclear NAD+ levels drop, cells lose the ability to properly regulate mitochondrial homeostasis independently of PGC-1α/β pathways. As a result % heteroplasmy in a tissue rises and energy flows slow even more. This is why anesthetics demolish brains with AD and PD. PGC-1α is a transcriptional co-activator that regulates the genes involved in energy metabolism in cells. It also effects mitochondrial respiratory protein replacement. PCG-1α is a so activated by endurance exercise and sprinting. This is why exercise helps PD and AD patients on a short term basis. PGC-1α is a major regulator of mitochondrial biogenesis and function. This pathway helps cells get rid of redox shifted mitochondria using Warburg metabolism because they cannot oscillate at 100HZ to use beta oxidation. Simply put, these tissues cannot make energy well and physiologic function craters. I spoke about them in the Ubiquitination 4-7 blogs. Those are mitochondria ruined by blue light, nnEMF, and 24/7 and carbohydrate uses sans UV/IR light. This protein interacts with the nuclear receptor PPAR-γ, which permits the interaction of this protein with multiple transcription factors to optimize energy production in cells by optimizing mitochondrial function. This protein can interact with, and regulate the activities of, cAMP response element-binding protein (CREB) and nuclear respiratory factors (NRFs). It provides a direct link between external physiological stimuli (think environment) and the regulation of mitochondrial biogenesis. This pathway is responsible in regulating muscle fiber types in skeletal muscle to optimize their mitochondria to oscillate at 100 Hz to use beta oxidation. This determines how sensitive or resistant we are to insulin and glucose and how well we can use fats. All this is tied directly the the environment the mitochondria is sensing. If the oscillation is not present you cannot use beta oxidation. It has ZERO to do with the fuels you eat. All this happens before there is any changes in the nuclear genome. This shows you that the environment dictates to the genome. It is not the other way around as modern science keeps regurgitating. http://www.sciencedirect.com/science/article/pii/S0960982216306595
     
  2. Theka

    Theka New Member

    Doesn't this mean that we will start seeing more complications from surgeries because of the anesthesia with 5G? What can a person do to mitigate the risks?
     
  3. Jack Kruse

    Jack Kruse Administrator

    We already have. The public is not aware of M & M issues like we are in medicine.
     
  4. drezy

    drezy New Member

    What does M&M mean?
     
    Theka likes this.
  5. Jack Kruse

    Jack Kruse Administrator

    morbidity and mortality It is a conference all docs have to endure
     
    drezy likes this.
  6. drezy

    drezy New Member

    Yikes!
     
  7. Theka

    Theka New Member

    I'm trying to understand anesthesia better. My husband doesn't like it and seems to require more than expected, even with local, like wisdom teeth removal. They needed to give him more. He had eye surgery as a child under general anesthesia--I believe it was ether at that time and woke during surgery. The doctors said had they had been aware of his medical history they wouldn't have scheduled it. He remembers they said something about his blood. He had survived meningitis at 4.

    It seems like the dangers of surgery are increasing as we trash our environment more, especially as hospitals are not good places to heal. A big city hospital would be worse and most leading hospitals are urban. Maybe this is another reason for medical tourism.....going to Mexico, Panama or Costa Rica ought to give a person a more optimal place to heal after surgery.
     
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  8. Theka

    Theka New Member

    I had an Aunt who despite her advanced age decided to have surgery for an aneurysm. It all went well but she couldn't manage alone afterwards and had to live in a nursing home until she died. The family said she had always been a bit different and thought she had hidden dementia well, looking back, I suspect the anesthesia was just too much. She would have been better off stopping driving and living life until it popped.
     
    Phosphene likes this.
  9. Jack Kruse

    Jack Kruse Administrator

    Anesthesia does what nnEMF does in the brain.......what Nora Volkow found in 2011. What metformin does in diabetic brains.......they increase AMPk pathways to raise glucose in arteries of the brain and this makes apoptosis easy in the low redox brain and PNS. This is why elective surgery is nuts in a 5G blue lit world. nnEMF and blue light cause increases in AMPk too..........

    A recently published study in the journal PLoS One in May of 2018 demonstrated that the anesthetic drug propofol significantly increased intracellular calcium (Ca2+) levels, induced a burst of reactive oxygen species (ROS), and activated the master metabolic regulator AMPK in C2C12 cells.

    Similar results were also obtained in a recent study published in April of 2018, wherein propofol also increased intracellular Ca2+ levels and activated AMPK in HeLa cancer cells.

    AMPK, an evolutionarily conserved kinase that is activated by the induction of cellular stress (i.e. increases in intracellular reactive oxygen species [ROS], calcium [Ca2+], and/or an AMP(ADP)/ATP ratio increase), increases lifespan and healthspan in several model organisms (yeast, worms, flies, mice, etc.)

    AMPk seems to have different effects in low redox humans. Remember Micheal Jackson used propofol to try to sleep and he died of a heart attack while anesthetized. I did a podcast with Matt the night before my Vermont talk and this came up.......you were there to hear it live. Your heart is loaded with mitochondria.......so the King of Pop had the same problem as your family.

    Interestingly, propofol is considered one of the most popular and widely-used intravenous anesthetic drugs in modern medicine to induce and maintain general anesthesia in humans. My OR team uses it all the time. I worry about it in low redox patients.

    People with low redox brains tend to have EEG's with low voltages and they tend to have low levels of Acetylcholine in their brains. That is another key neurotransmitter I have talked about long ago.

    Curiously, a recent study published in the journal Current Biology in June of 2018 by researchers from the University of Michigan demonstrated that the compound carbachol reversed anesthesia induced by the inhaled anesthetic sevoflurane (most common general anesthetic in 2018 USA) and restored wake-like behavior and level of consciousness in rats. Carbachol is a compound that binds to and stimulates acetylcholine receptors in the brain but also activates AMPK in human cells, similar to both metformin and propofol.

    Nearly every neurotransmitter that plays a critical role in promoting wakefulness, arousal and consciousness activate AMPK pathways. This is true for glutamate, acetylcholine, orexin-A, histamine, norepinephrine, dopamine, and serotonin, and melatonin. The key to redox action is what the electric charge is in the water around these proteins at the time they act. This is controlled by the bio-photon emissions in cells.......and redox potential is inversely related to the amount of light released to the water that surrounds these proteins. This idea is tightly coupled to the second paper I showed in my Vermont 2018 talk.
     
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  10. Jack Kruse

    Jack Kruse Administrator

    Several drugs that are commonly used to induce and maintain general anesthesia also activate AMPK in low doses such as propofol, sevoflurane, isoflurane, ketamine, dexmedetomidine, and midazolam. This should tell the black swan the sheer activation of AMPk is not the key metric........but the environment of the activation is MOST critical. This is why I told you all in Vermont I have been waiting 15 years for that paper to show up. I thought Pollack would be the guy to do it, but I was wrong. He refused to go as deep as he should have. If he had he might have all the money his lab needs.
    Also, several compounds that have recently been shown to promote accelerated emergence from anesthesia also activate AMPK such as carbachol, orexin-A, histamine, dopamine, dopamine D1 receptor agonists, nicotine, caffeine, and forskolin. This will seemingly confuse simple thinkers because it appears contrary until you realize how to charge (topologic charge) in water changes how matter can react.

    Nature is a lot slicker than we expect.

    AMPK has been found localized in hippocampal CA1 pyramidal neurons and glutamate, NMDA, potassium chloride, and high-frequency stimulation have been shown to induce AMPK activation in cortical and hippocampal neurons. Although an increase in Ca2+ levels is critical for neuronal activation and LTP induction, inhibition of ROS significantly inhibits hippocampal CA1 LTP, indicating that cellular stress-induced AMPK activation may play a pivotal role in neuronal excitation. This data alone tells you AMPk is not the be all end all......but it is a deep clue that topologic chare in water is big deal.

    The data in the metformin and the drugs we use in surgery was my big clue the charge in water was a lot bigger deal than anyone knows. And it turns out blue light and nnEMF change both too........When you add that cocktail together and the redox is low it should be no shock what happened to your family or Micheal Jackson.
     
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  11. Jack Kruse

    Jack Kruse Administrator

    you asked a good question........now you know why I expected paper number two.
     
  12. Jack Kruse

    Jack Kruse Administrator

    This mechanism even explains how transgenerational epigenetic activation or heteroplasmy can develop in the germ line. I know most people here have no Earthly idea why but I have been waiting patiently for this data. It is very hard to explain mtDNA damage causes childhood cancers until you understand how electric charges change the physics of water around oocytes.

    For example, Forskolin activates both AMPK and the transposable element syncytin-1 (necessary for human placental formation), increases human oocyte fertilization rates when combined with the AMPK activator cilostamide, and promotes chemically-induced LTP in hippocampal slices. The hippocampus is important in memory creation in neurons. Might forskolin TE's be telling us how maternal eggs collect and save memories of the environment they sense when this egg was first touched by your grandmother, then your mom, and then you before the fertilization of your egg?
    Huge big deal.......

    Transposable elements (TEs) are found in human oocytes, human sperm, and in human neural progenitor cells within the hippocampus. This tells me memory is tied to this mechanism. TE's are also activated and can be induced to transpose or “jump” from one genomic location to another by increases in Ca2+ or ROS. Ca2+ and ROS are mitochondrial signals.......from the matrix.

    This tells me mtDNA and the electric charge of water in oocytes is HUGE.

    .
     
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  13. Jack Kruse

    Jack Kruse Administrator

    Low dose anesthetic-induced AMPK activation may also explain the phenomenon of paradoxical excitation. Curiously, low doses of nearly every anesthetic drug have been shown to induce paradoxical excitation. As the name implies, before inducing unconsciousness, general anesthetic administration may result in a temporary increase in neuronal excitation, characterized by an increase in beta activity on the electroencephalogram (EEG) and eccentric body movements. This tells me in wakefulness when the DC electric current is present........this means the electric topologic charge in water is DIFFERENT. Who showed this? Becker experiments in salamanders being put to sleep.........

    I paid attn to Becker work better than he did. He should have dropped limb regeneration right there when he found this and went crazy for it.

    When he found anesthesia induce a loss of the DC current he found the holy grail.......in my opinion and he never realized it because of his focus on his own biases.

    I have never forgot that experiments. When we sleep we also lose the DC electric current.....and this changes the topologic chares in water in the brain.
     
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