Ray Peat's Newsletter - This Novel Flu Season - May 2020

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  1. md_a

    md_a Member

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    Buteyko and Other Scientific health and educational Issues

    At my request, Ray Peat, PhD www.raypeat.com Has released his recently completed May 2020 newsletter below for free distribution to those who wish to do so. He has also Similarly released his previous March 2020 newsletter which is a primer on the Impact of the new cell physiology, association/Induction paradigm, created by Gilbert Ling in the 1950s which has already Spawned many technological breakthroughs Nobel prizes In biology and medicine despite Ling not having been credited.

    It is my hope that many enthusiastic young physicians and other devoted medical practitioners and researchers may get access to this material which can help in finding several pathways to heal many of those afflicted during the present crisis and beyond from various mild to serious inflammatory illnesses as well as preventing them. NOT BY VACCINES, by a workable understanding of The roots of inflammation, the fear and confusion accelerating it, and the new paradigm in addressing those roots as well as the innate strengths and cellular wisdom imbued within all of us .

    In deep appreciation of our spirit of openness and pursuit of a better world.
    Bud Weiss

    Ray Peat's Newsletter
    “The people have no voice because they have no information.” Gore Vidal
    Copyright 2020 Raymond Peat P.O. Box 5764 Eugene OR 97405 May 2020
    Not for republication without written permission.

    This Novel Flu Season

    The argument:
    A failure of energy metabolism limits the ability of cells to return from an excited active state to a stable resting state. Unresolved excitation causes cells to emit signals indicating the need for repair, inflammatory signals. Pre-existing inflammation is associated with high altitude sickness and the ability to get sick from a corona virus, as well as chronic diseases. This implies that treatment for a so-called “coronavirus infection” should be to reduce cellular excitation and inflammation and normalize energy production. It also implies that these treatments will have favorable effects on cell aging.
    The conditions that produce inflammation activate the adaptive exosome system, a retrotrans- poson system involving a massive block of our DNA, which overlaps with the virus production mechanism. Current approaches to preventing viral disease dangerously ignore this fundamental physiological-genetic system. An important impli- cation of this system’s involvement in health and disease is that we are not defined “somas” produced once by our DNA, but rather adaptive, epigenetic, ongoing creative beings.
    U.S. history has repeatedly hinged on words that didn’t correspond to facts, for example the bombing of Vietnam based on the fictional Tonkin Gulf incident, or the invasion of Iraq based on the yellow- cake uranium and other fictional weapons of mass destruction. To explain the present destruction of the normal US economy it would be reasonable to look for some clear image to indicate that China’s new variant corona virus was more dangerous than
    preceding strains of the virus, but there has been no public information about how to distinguish infections with this new virus from other acute lung problems. According to official medical views, no specific treatment or test was known when the WHO declared the pandemic, so the FDA has bypassed its normal regulations for both tests and drugs. A test, to be useful in diagnosis, determining the exact cause of symptoms, would have to show whether any of the common respira- tory disease organisms was present, and naturally, any test has to be tested itself. The CDC has observed that half of the positives on an antibody test, in a population with low prevalence, could be false. A muddle of tests has created confusion even among experts; on May 21, the CDC acknowledged that it was mixing together their counts of antibody tests and PCR virus tests.
    In March and April, several Stanford profes- sors were arguing that the lethality of the new virus was very similar to that of the familiar influ- enzas, about 0.25% of those infected. The latest figures from the CDC, published inconspicuously on May 22, were similar, assuming that 35% of infected people could be symptom free; if a higher percentage of infections are symptom free, then the infection-death rate is even lower.
    With no public explanation of the pathophysi- ology of the “new disease,” the vacuum was filled by rumors that it was a virus escaped from germ warfare labs, alternately said to be from Wuhan or Fort Detrick, and several broadly circulated articles denied that such a virus was even possible to engineer, conflicting with articles in major journals in recent years describing exactly that engineering (de Haan, et al., 2008; Graham and Baric, 2010). In the absence of empirical informa- tion about the nature of the disease, but with the

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    rumors creating fear of a uniquely horrible disease, hospitals have been instructing doctors to treat patients with breathing problems in very aggressive and invasive, and standardized, ways.
    A couple of doctors in the US said publicly that those treatments aren’t appropriate for the real disease. Cameron Kyle-Sidell has made two videos observing that his patients’ symptoms resemble those of people with high altitude pulmonary edema, a feature of which is very low carbon dioxide as well as low oxygen. Another doctor in New York, Isaac Solaimanzadeh, suggested using calcium channel blockers and acetazolamide to treat the new disease, because of their therapeutic effect in high altitude pulmonary edema. He didn’t mention it, but both of these drugs can correct the tissue deficiency of carbon dioxide.
    In Germany, Luciano Gattinoni (Gattinoni, et al., 2020) pointed out that the standard ventilation proto- col wasn’t conforming to the best knowledge of respiratory physiology. He observed that in one conventional hospital the mortality of respiratory patients was 60%, while in a nearby hospital follow- ing his more rational method, the mortality of respi- ratory patients was zero.
    High altitude physiology is obviously confusing to the many doctors who have scoffed at the comparison of the new disease to high altitude pulmonary edema. This is because of the way physi- ology is taught. At low altitude, when a tissue’s oxygen consumption increases beyond the blood’s ability to deliver oxygen, as in an intensely working muscle, the tissue activates the glycolytic process, converting glucose to lactic acid as a source of additional energy. Carbon dioxide is seen as nothing but a waste disposal problem. This view has led to the concept of the “high altitude lactate paradox,” referring to the fact that maximal exertion at high altitude doesn’t increase lactic acid production in the normal way. Neglecting the role of carbon dioxide in suppressing the formation of lactic acid, they also neglect all of its other essential metabolic effects, including its role as the factor whose absence results in the syndromes of altitude sickness, and ventilator- induced lung damage (Sinclair, et al., 2002; Cummins, et al., 2010; Contreras, et al., 2012).
    This CO2-negligent approach to physiology has affected medicine for 100 years. When Otto Warburg discovered that aerobic glycolysis is the
    defining feature of cancer, the presence of a little extra lactate in the blood, displacing CO2, didn’t appear to most doctors and biologists to be medically important, though a little extra carbon dioxide could arouse concern. Ignoring that 30 years of slightly elevated lactate might lead to cancer or other degenerative disease, those who taught physiological chemistry also had little interest in the idea of chronic metabolic hyperven- tilation—losing a little too much CO2 even at sea level. Cumulative injury of all sorts contribute to a background of inappropriate excitation and inflammation.
    In studies related to asthma, it has become well known that abnormally low CO2, hypocapnia, constricts the airways, and elevated CO2, hypercapnia, relaxes them (El Mays, et al., 2011; Choudhury, et al., 2012); various mechanisms, affecting intracellular calcium, are known to be involved. The causes of relative hyperventilation continue to be disputed.
    The basic principles of respiration, the Bohr and Haldane effects, describe the physical equilibria of oxygen and CO2 in people who have adapted to living at different altitudes. The Haldane effect describes the fact that increased oxygen pressure decreases the amount of carbon dioxide retained by hemoglobin, and decreased oxygen pressure increases the amount of CO2 retained. A steady increase of retained CO2 with increasing altitude occurs in those who adapt. People who fail to adapt experience a loss of CO2, with an increase of lactate.
    It has become increasingly common to treat altitude sickness with carbon dioxide. A few people have argued for a long time that mechanical ventilation would be less harmful if a mixture of CO2 and O2 were used (Laffey and Kavanagh, 1999; Kregenow and Swenson, 2002), analogously to the therapeutic effect of CO2 in high altitude sickness (Harvey, et al., 1988).
    In a state of chronic stress, oxidative energy production is low, and mediators of inflamma- tion are likely to be chronically increased; there is typically a chronically increased production of lactate, and/or decreased oxida- tion of it. In this state, the increased ventilation caused by high altitude will cause an increased loss of carbon dioxide, increasing the pH of the

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    blood, which increases the formation of lactic acid. The lactate increases the leakiness of capillaries and loss of fluid, and decreases the ability of oxygen to diffuse from the alveolus to the erythrocyte. Since carbon dioxide diffuses many times more rapidly than oxygen, this diffusion barrier results in low blood CO2 at the same time as hypoxia. Even at sea level, an increase of lactate immediately increases the lungs’ diffusion barrier.
    Thinking of the infection as the disease, and therefore considering the “receptor,” “entry,” and replication of the virus to be sufficient to explain the damage to infected cells, tissues, and organs, and defining the disease as an inflammation of the respi- ratory tree and lung, the hospital system went into action. Failing to think of the intestine (which is infected as easily as the nose and lungs), the meaning of events throughout the organism, includ- ing the lungs, is misunderstood. The infection can serve as one of the factors increasing inflammation and stress, suppressing energy function, but the relevant disease to be treated is that unstable state of counter-productive, energy-depleting excitatory and inflammatory signals.
    Healthy individuals aren’t harmed by the presence of the virus, so the nature of the defect that makes some people susceptible should be the focus of attention. Some important factors have already been identified: living at high altitude provides 3- or 4-fold protection (Arias-Reyes, et al., 2020), and being a young woman is even more protective. In Italy, 70% of the deaths are men, but deaths increase sharply among post-menopausal women.
    The lungs are especially sensitive to activation of the so-called “calcium channels,” i.e., calcium uptake by cells, by hypoxia, causing constriction of blood vessels, but increased carbon dioxide, which increases during adaptation to altitude, reverses the hypertension caused by hypoxia (Baudouin and Evans, 1993; Chuang, et al., 2011). Calcium channel blockers, paralleling that effect of CO2, are effective treatments for high altitude pulmonary hypertension. Like acetazolamide, the other recognized treatment for altitude sickness, calcium channel blockers inhibit carbonic anhydrase, facilitating the body’s retention of CO2. To the medical scoffers who deny that CO2 has a constructive physiological role, the exaggerated pulmonary constriction at high altitude is the cause of the lung failure, while in the
    respiratory distress caused by Covid-19 that contriction is a consequence of the disease (Luks and Swenson, 2020), and neither is a result of a CO2 deficiency.
    The presence of lactate corresponds to some degree of reductive excess in cells, and the degree of reduction regulates the “calcium channels,” controlling the excitatory effects of intracellular calcium (Wang, et al., 1997; Iesaki and Wolin, 2000; Schach, et al., 2007). Reduction by stress and/or lactate “activates the channels,” tightening vascular smooth muscle, and activating a wide range of other cell activities, including inflamma- tion, exosome secretion, and viral replication (Savina, et al., 2003; Chen, et al., 2019). Exosome production during stress is part of the body’s normal restorative function (Zhang, et al., 2017); it’s only when protective factors such as proges- terone and carbon dioxide are lacking that their production becomes counter-productive.
    Progesterone and its neuroactive metabolites including tetrahydroprogesterone or allopreg- nanolone, are very effective “calcium channel blockers” (Todorovic, et al., 2004; Pathirathna, et al., 2005; Hu, et al., 2007). A major function of progesterone is the inactivation of the estrogen receptor; estrogen and its “receptor” are powerful activators of cellular calcium uptake (Sarkar, et al., 2008).
    Studies of progesterone’s effects on recovery of nerve function after traumatic brain damage have found that vitamin D increases its effective- ness. By improving calcium homeostasis, oppos- ing the effects of the parathyroid hormone which activates calcium channels, vitamin D (25-hydroxycholecalciferol) is coming to be considered a neurosteroid (Groves, et al., 2014; Gezen-Ak and Dursun, 2019), as well as an essen- tial factor in immunity (Pfeffer and Hawrylowicz, 2012).
    Intracellular calcium is essential for all aspects of the viral cycle—entry, gene replica- tion, maturation, and release—while also disturbing the cell’s own functions. “Evidence has emerged that pharmacologically targeting the calcium channel or calcium release from the endoplasmic reticulum ... can obstruct virus lifecycles” (Chen, et al., 2019).

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    A few doctors recognize that progesterone supplementation might seem reasonable for preventing or treating the corona virus problem, though they don’t seem to know about its already established antiviral effects (Pfahler, et al., 1987; Muñoz, et al., 2007; Hall, et al., 2016), or the mechanisms involved. Other doctors (Sharon Nachman), following their cliché thinking instilled by estrogen industry advertising, and believing that estrogen is “the female hormone” that explains women’s health advantages, have begun a study, treating the corona infection in men with estrogen patches. Old men’s estrogen levels, especially if their health is poor, can be higher than that of women of the same age, while their progesterone is always lower.
    Nitric oxide is a powerful oxidant that can destroy viruses, and it happens to dilate blood vessels. Doctors have almost unanimously recom- mended it to treat the corona virus infection; however, it is associated with inflammation (Weidinger, et al., 2015), and promotes fibrosis, and fibrosis is a sequela of coronavirus disease. An increased amount of nitric oxide in the exhaled breath is a clear predisposing factor for high altitude sickness (Ren, et al., 2015). Progesterone is a respi- ratory stimulant that increases the hypoxic ventila- tory response, and a low hypoxic ventilatory response is another predisposing factor to high altitude sickness. Progesterone inhibits the formation of nitric oxide (Wolfson, et al., 2015), while estro- gen increases it (Lima, et al., 2014).
    For years, corona viruses have been known to bind to the angiotensin converting enzyme 2 (ACE2), and that enzyme has been known to have protective effects, destroying angiotensin, and losar- tan, an angiotensin receptor blocker, has been known to be protective against corona viruses. Angiotensin increases intracellular calcium, and losartan lowers intracellular calcium. In reaction to the new corona virus, a few groups responded quickly, treating successfully with antiinflammatory things—losar- tan, cinanserin (a serotonin antagonist), aspirin, and azithromycin or erythromycin, which lower intracellular calcium. Aspirin’s effects overlap those of losartan, and it downregulates the angio- tensin receptor, ATR1 (Mitra, et al., 2012).
    Meanwhile, medical media, such as Lancet, immediately warned against the use of
    anti-angiotensin drugs, as if the authors and editors hadn’t been reading respiratory physiology in recent years. This is because of the stupefying effects of the receptor dogma. Having identified ACE2 as the “coronavirus receptor,” nothing physiological matters. Graded, holistic effects, involving simultaneous changes in many “recep- tors,” in which rising inflammation can lead to viral replication, suggesting many safe therapeutic interventions, simply don’t fit into the paradigm of product “development” and marketing.
    The closed, authoritarian nature of the medical profession makes it a perfect tool for political manipulation. Obstructing the use of rational treat- ments, the profession has been mobilized to promote the militarization of the national response to the latest respiratory virus, the history of which shows the massive involvement of the US military. Ralph Baric’s publications on the corona virus, as well as dissenting opinions among virologists and in government (Nature, Nov. 12, 2012; The Scientist Magazine, Nov. 16, 2012), make it clear that military-motivated gain of function virus research has been able to override a presidential moratorium, and the actions of Eric Schmidt and his National Defense Commission on Artificial Intelligence (proposing responses to growing Chinese power), and his recent appoint- ment by Governor Cuomo to help reorganize New York’s schools, health system, and economy, offer new perspectives on the government’s surprising actions. The fact that Italy and Iran last year signed an agreement to participate in China’s expansive trade plan might be relevant to evaluat- ing the meaning of this novel flu season.
    Since the recognition that only 1% or 2% of our DNA consists of “our genes,” and that around 48% shows features specifying retroviruses, many geneticists are suggesting that retroviruses, trans- ferring their RNA information into our DNA, are our ancestors. The reason for this crazy thought is probably to avoid as far as possible the radical abandonment of the Central Dogma of genetics, that information flows only from nucleic acids to proteins. Now that the protective and adaptive functions of exosomes and retrotransposons have been clarified, the more obvious inference might be that we are the ancestor of retroviruses, though the real implication is that we are essentially

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    adaptive, epigenetic, creative beings. The “germ line” is everywhere, not insulated in the gonads.
    Vaccine adjuvants are designed to produce systemic inflammation, and that involves some degree of activation of our innate immunity with its epigenetic adaptive potential. Recognizing that a barely recognizable background of inflammation predisposes to develop serious sickness from a corona virus, it’s important to consider the role of the recent great expansion of the influenza vaccination campaigns in Italy and the US, especially directed at older people, in the current increased incidence of corona infections. Several studies, designed to judge the effectiveness of the influenza vaccine, reported that the vaccine might be about 45% effective in reducing influenza infections, but that the vaccinated people were much more likely to have other respiratory infections, including corona virus infections.
    Focus on the induction of antibodies by vaccines to define immunity has led to a dangerous disregard for the basic facts of health. The present testing of a vaccine containing the RNA that specifies the most destructive spike protein of the corona virus, the part that inactivates our protective ACE2 enzyme, is being done in a culture that avoids consideration of the meaning of our massive endogenous system of RNA-responsive reverse transcriptases and retroele- ments. The consequences of incorporating the spike protein of the virus into our genetic repertoire are hard to imagine. The mindless activation of our huge epigenetic system of retroelements, with no knowable benefits, should be stopped.
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  2. LeeLemonoil

    LeeLemonoil Member

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    A very good letter.

    It needs concise but striking explanations how risky, how deluded, how ignorant and unscientific, against fundamental physiological and biochemical knowledge the Idea of RNA-Vaccines are. Name and shame Moderna, Fauci et al as the sharlatans they are. Not by spinning conspiracy but by factually debunking their narratives, their pseudo-knowledge. Show that they Are the least figures to be trusted with your health because they know only faulty, fantasy narratives of physiology.
     
  3. Energizer

    Energizer Member

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    Here is the PDF.
     

    Attached Files:

  4. Regina

    Regina Member

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    :darts:
     
  5. yerrag

    yerrag Member

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    This is so hard to unpack. It doesn't make sense to me.

    Why will there be increased ventilation at high altitude? Isn't oxygen already low at high altitude, so why is ventilation increased?

    Maybe it's a typo? It should read as "In this state, the decreased ventilation caused by high altitude will..." As the low oxygen availability will lead to more anaerobic respiration and that will increase the production of lactate.
     
  6. Regina

    Regina Member

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    Thx for sharing here. I feel okay to send it to a couple of MD's I know who are not really tied up with the system. They are anesthesiologists, but otherwise don't like the system. (Have hippy wives, grow their own food, live in the countryside.)
     
  7. yerrag

    yerrag Member

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    Shouldn't "neither is a result of a CO2 deficiency" read as " both are a result of a CO2 deficiency?" Otherwise, what is the point of discussing CO2?
     
  8. rei

    rei Member

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    Reading that was almost like a spiritual experience. Maybe i should order his news letter.
     
  9. yerrag

    yerrag Member

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    I'm glad we're all reading this. It is hard for me to read his newsletters at times. Because he's going over my head often and I just skip through my cluelessness.

    Take this sentence, for example. This meant that unless a substance has "specificity (not sure if it is the right term)" it won't be allowed as a treatment by pharma. By specificity, I mean that it does not specifically treat a disease. If a substance has broad effects, including treatment that disease, it won't be considered suitable by big pharma.
     
  10. jb116

    jb116 Member

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    The focal point for interpreting these passages should be based on the question of "what is it other than CO2 that causes altitude-like sickness?" Then it'll come into focus for you. Peat is making the point that in neither case of high altitude or supposed covid should we look to blame CO2 for the breathing issues. But rather we should point the finger at increased ventilation and constriction. So if we think about it, we arrive at this striking parallel:

    1. increased ventilation increases diffusion of CO2 i.e. loss of it. Higher altitudes gives us higher ventilation/but low pressure = the ventilators being worse give us higher ventilation/pressure. So in either case it's not a high CO2 issue.

    2. immediate high altitude in a state of poor health/high lactate will create constriction = covid creates constriction as it increases Angiotensin effects system in an already high lactate/poor health individual and that's not at all a high CO2 issue.

    So the reason he said neither is a result of CO2 deficiency is to highlight the point that both altitude sickness and covid should not be blamed on high CO2, instigating these stupid procedures they've been practicing in the hospitals such as ventilators but rather altitude sickness and covid are actually states of CO2 deficiency.
     
  11. Regina

    Regina Member

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    Yeah. We can discuss it here. I felt like I kinda got it but would not be able to explain it (if I ever got an imaginary audience other than my teddy bears. ;) which I line up and lecture. Just kidding.)
    I can remember when I used to be an "actor combatant" for projects in high altitude. First was in Piobbico, Italy mountain range. A woman in "perfect health" had to be sent home due to altitude sickness. A couple of months later was a project in Banff ,CA involving stunt performers from all over the world. The combatants were dropping like flies. They were being taken out on stretchers and it just got to be normal. In the back of my mind I knew it had something to do with the so-called fitness falling apart in high altitude. But I was fully ensconced in retard adrenalin stunt mode. I had completely bloodshot eyes. As in embolism. The capillaries in my eyes were burst and stayed that way the whole time I was in Banff working. I would do scenes all day, go skiing in a blizzard, drink like a sailor into the wee hours and do it again over and over for the weeks it went on.
    So, I can't explain it to my teddy bears. But I think these adrenalin junkie athletes are chronically in lipolysis. (as I was. But I was always an eater. I always ate eggs, meat, skipped salad and ate dessert). I think as hamster has learned buteyko, it takes a long time to develop. At first the control point for air hunger is short. Similarly, when thrown into high altitude, the air hunger is immediate. The air hunger is real.
    Sometimes, I think I just can't understand all this. It's too over my head. I get that the altitude sickness reveals an existing metabolic dysregulation.
     
  12. ecstatichamster

    ecstatichamster Member

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    spot on. For sick people at altitude oxygen pressure is lower resulting in the same co diction as going on a ventilator. Low CO2.

    Dr. Peat’s writing is difficult to understand. His verbal skills are remarkable in making difficult subjects simple but his writing is the opposite.
     
  13. Regina

    Regina Member

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    "1. increased ventilation increases diffusion of CO2 i.e. loss of it. Higher altitudes gives us higher ventilation/pressure = the ventilators give us higher ventilation/pressure. So it's not a high CO2 issue."
    Okay. My teddy bears are confused by the second sentence. Ray has said that in low altitude there is too much oxygen pressure...... :bucktooth:
     
  14. Regina

    Regina Member

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    "For sick people at altitude oxygen pressure is lower resulting in the same co diction as going on a ventilator. Low CO2."
    Ah friend. I am still fuzzy on this. :bucktooth:
     
  15. jb116

    jb116 Member

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    :facepalm: ahhh I'm sorry guys, here I am trying to clear it up and I made it more confusing!
    At high altitude, yes ventilation is higher, but lower pressure. With a ventilator though, it's quite worse as the pressure is also increased, is what I intended to write. This will diffuse out CO2 and in contradiction, not oxygenate better in the least. Either way, the parallel still stands and CO2 is not the issue, if anything only it's deficiency is.

    Let me clear up my post.
     
  16. JKX

    JKX Member

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    I think perhaps you've just misinterpreted the scentence...

    Re-read the first part of the quote, it provides the context for the paragraph... "To the medical scoffers who deny that CO2 has a constructive physiological role" ...

    This is not Ray's opinion, he's stating that the medical opinion is the opposite of what he believes to be correct.[/QUOTE]
     
  17. Tarmander

    Tarmander Member

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    As Peat a letter as I have ever read

    CO2 and others not taking CO2 seriously...check
    Criticize USA while covering for Communists...check
    No one is considering intestines/endotoxin...check
    Doctors like Nitric Oxide...check
    Progesterone good and estrogen conspiracy...check

    If we had carrots and serotonin this thing would have been perfect
     
  18. jb116

    jb116 Member

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    :handok: basically
     
  19. yerrag

    yerrag Member

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    Thanks. That clears things up for me.

    Part of my problem is understanding what ventilation means. Now, I think that ventilation refers to the breathing rate. If you increase your breathing rate, you increase the exhalation of CO2, so CO2 is decreased the more you breath, and this leads to low CO2.

    So, in high altitude, breathing rate (aka ventilation) increases because there is low oxygen (low oxygen pressure means less availability of oxygen).

    In a healthy person (more CO2 in blood= more tissue oxygenation), he is needing to breath at a lesser rate than an unhealthy person (less CO2 in blood = lower tissue oxygenation). The lower rate of breathing (less ventilation) in the healthy person also means that he is releasing less CO2, and retaining more CO2 than an unhealthy person would.

    This causes the healthy person to adapt better to the high elevation than the unhealthy person does. Not only is the healthy person able to retain more CO2, he is also able to produce more CO2 because he is more able to use the available oxygen in the blood to oxygenate, given his higher supply of serum CO2 (which facilitates the release of oxygen from hemoglobin to the tissues). With more oxygen available to metabolize sugar, he can enable mitochondrial respiration which is much more efficient than anaerobic (or even aerobic) glycolysis. The unhealthy person will be relying more on glycolysis, which is 1/16 less efficient in producing energy, and this person will be needing to use more oxygen to generate the same amount of metabolic energy as compared to the healthy person.

    The healthy person is able to conserve his energy because his body's metabolic state allows it. He will do much, much better than the unhealthy person. The unhealthy person has little carbon dioxide and has plenty of lactate (which he began with and added to as his metabolic state copes inefficiently with the stressful environment (at least it is to him, not as much to the healthy person).

    When the environment is that of a ventilator operated by nurses following the wrongly-placed dictates of an authoritarian medical system, you have an even more stressful environment. There is high ventilation and high oxygen pressure (which lowers CO2 in itself). The healthy patient will outlast the unhealthy patient for sure, but even the healthy patient will become very stressed with long-term ventilator exposure. But if the person is healthy, he probably will not get to that point where ventilators are used on him. The patients on ventilator are all likely to be metabolically stressed, and this contributes to the high fatal rates in ventilator-assisted patients.
     
  20. yerrag

    yerrag Member

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    [/QUOTE]

    You're right. I get it now Thanks!

    To the medical scoffers who deny that CO2 has a constructive physiological role, the exaggerated pulmonary constriction at high altitude is the cause of the lung failure, while in the respiratory distress caused by Covid-19 that contriction is a consequence of the disease (Luks and Swenson, 2020), and neither is a result of a CO2 deficiency.

    I don't know how I missed that. I kept re-reading and re-reading. I got stuck in a loop.
     
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