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Ray Peat Interview Ray Peat On The Coronavirus, Immunity, & Vaccines 2020-03-18

  1. Ray Peat on the Coronavirus, Immunity, & Vaccines

    Date Recorded: 2020-03-18

    John Barkhausen: What do you think is going on right now (about COVID-19)?

    Ray Peat: First of all, I am not sure any special is going around, in the virus, and infection world, it’s definitely happening in the media and politics. Mexico isn’t getting excited and they have, I think, 16 mild cases. CDC for years has been reporting the annual respiratory or flu like death rate has being in the tens of thousands of deaths per year in USA, so hundred or two hundred, the average number of deaths from respiratory disease being say 40000 or 30000. If you look at historical percentage of those respiratory diseases, about 10 to 15 percent are historically a coronavirus infections and the others are things as simple as rhinovirus, or respiratory season virus, things that range from mild sniffles up to serious pneumonia, but historically, about 10 percent are corona type virus, so if 30000 or 40000 people are expected to die from flu like respiratory disease we will expect to have 3000 or 4000 deaths per year from a coronavirus respiratory infection, so I don’t see any evidence at all that anything is happening on a real biological level.

    JB: You are saying that in a giving year we should see 3000 to 4000 deaths from coronavirus?

    RP: Yes, that could still happen, we can get up to the average mortality associated with corona viruses, but we are not approaching that by long way so far, so lower than average year as far the actual figures that exist indicate, so just looking at the actual numbers it looks like we are slightly deficient in cases and deaths of respiratory problems associated with that virus.

    JB: Have you checked the Chinese or Asian data, is the corona death up from average?

    RP: They haven’t talk about the average for corona, they weren’t gathering that data, but they say, this is just slightly more deadly than a typical influenza virus or the other things causing respiratory disease, so it is somewhat according to their figures just slightly more deadly, but the problem is Italy has always as twice as many respiratory disease or flu-like death per year per capital as USA, so it isn’t unusual for them to be especially hard hit, but what make the number go up is that they have been primarily testing sick people in hospitals and its same with cancer diagnosis, if you go all out to look for cancer in population of middle age and old age and cancer range you will find 100 percent cancers if you really go into diagnosis, so the more you diagnose the more you can find, people die at the same rate unless you treat them, if you increase your treatment for cancer as you increase the diagnosis, the treatment is good in kill more and more, but you can make your treatments look better by diagnosing more and more cases which are harmless, same with the flu, or the coronavirus, if you test everyone in population, you will get all this people with very mild reactions, so it look like… In South Korea for example, 0.6 percent, because they tested more people, so the dying people are become a smaller percentage when you test it one more representative cross-section of the population.

    JB: So, maybe it’s just an accident, because they are looking for diseases, and most of them are vulnerable, so they test the sick people first.

    RP: YES, so that if restricted to the people in hospital on respiratory, then you will find that most of them have serious viruses probably, multiple respiratory viruses.

    When you very sick, various viruses that have been carrying harmlessly, will pop to the surface and get measured.

    JB: What`s the difference between virus and bacteria, and particular about the coronavirus?

    RP: Almost all bacteria are free-living in a sense that can generally live outside the cells, if you feed them right stuff and giving them the right temperature and other conditions. They have the apparatus to reproduce their own genetic material, and the virus depends on entering a cell either bacterium or higher organisms cell, and taking advantage of their machinery like ribosomes that can produce proteins for nucleic acid, so this viruses putting their bad? of nucleic acid, once that can get into the cell and that is process on ours? ribosomes endoplasmic reticulum and proteins are added to the replicated nucleic acid and then is excreted as a finish particle by our ordinary cell excretory system, secreting system.

    JB: So, in a healthy person if you encounter a virus, even if it’s a new virus, do you think we are able to conquer that, or at least isolated so it’s doesn’t do any harm?

    RP: Yes, for example on the surface of respiratory in our lungs and the tubes leading to air sacs... the air sacs are in line with epithelial cells that can secrete their cells around the air sacs that secrete mucus that cover the epithelial cell and to reduce the surface tension so the air sacs will stay open. There is a protein called surfactant protein that has an oil loving liquid filling fraction so it acts like a soap, but the water loving part of the protein dissolves in this mucus layer on the cell lining the air sacs, and the oily surface reduces the surface tension so the air sacs can stay open but without extreme tension, and that surfactant protein contains groups that will collect the sugar like surfaces of the viral proteins or other any pathogen possibility that hits that surfactant protein will get gluten? down by this binding particles, so it’s our first layer of defense, then in our around of epithelium layer we have reactive parts of the immune system, the angiotensin converting enzyme is one of the early parts of our immune system that sets up an inflammatory reaction that will set in action a whole chain of events, if the pathogen gets trough and is actually a treat, then you activate this proteolytic protein that create angiotensin witch is like a transmitter of a panic reaction to the organism, and it happens this coronavirus is able to bind to one of this angiotensin converting enzymes, there is one with is only pro-inflammatory and the other one that backs that up, which undoes, inhibits the inflammatory damage done by the first angiotensin producing enzyme, this is called ACE2, and ACE2 happens to be attacked by this particular virus witch binds to that enzyme, and that’s receptor its vulnerable point of organism as far this fire is concern, and binding to that ACE2 means that it leaves the ACE1 which produces angiotensin, it leaves that free to act, and ACE2 is capable in inactivating angiotensin breaking down to the first seven amino acids, they call it angiotensin 1-7, and this is a defensive anti-inflammatory peptide, so if your ACE2 is knocked out, angiotensin has a free range to cause damage, so the virus increases the inflammatory reaction by sticking to the defensive enzyme, and that enzyme combined with the virus, than acts to enter the cell by way of the angiotensin receptor which is called the AT1, that are two known receptors by which angiotensin can do damage. Angiotensin 1 is strictly an inflammation producing system, the angiotensin 2 produces somewhat defensive reactions, but it happens that the virus enzyme combination entering the cell by way of angiotensin receptor 1, AT1, and that turns on a whole range of destructive processes, nitric oxide, serotonin for example. And, so, just looking at the effects, its obvious you can defend by anything that defends you against nitric oxide and serotonin, so anti-inflammatory things are the known treatment for this kind of virus that Chinese for years have been using, cinanserin which is a serotonin blocker for other treatments, and they find that is helpful for people with the established respiratory corona infection, and losartan witch is high blood pressure drug is the most well-known blocker of angiotensin 1 receptor.. losartan is cheap and widely available.

    Basically the virus just activates an inflammatory process that many other things activate, so things that would primarily activate nitric oxide production or serotonin production, or histamine, or prostaglandin production, any of this tend to end up in the same condition, so, I think without knowing more about the nature of infection, I think people who are taking aspirin for example it has wide range of antiviral properties it's already known to reduce infection from a standard influenza virus, hepatitis C virus, rhinovirus, African well-known viruses, are blocked by common aspirin. There was a study on HIV, when they saw beneficial effects from aspirin. Vitamin D, one of its effects, like progesterone and aspirin, all are known protective pro immune, but an anti-inflammatory things, lower the expression of angiotensin receptor 1, so they predispose us to be less inflammable.

    JB: So, when it enters the lungs, your cells put out kind of lipid, or some kind?

    RP: Well, naturally, once we are born and start breathing, we depend on the production of surfactant protein, so it’s everywhere normally, and our intestine has similar layers of defenses right about surface mucus will be a barrier against infection, and then surface layers of cells and so on, and this viruses, the coronavirus don’t just specialize on the lungs, they can infect the mucus membrane in the nose and the intestine, so some people been saying that runny noses aren’t connected as precursor of the lung infection, but, Russian virologists sad, looking at tens of thousands of patients, he saw that runny nose was a typical precursor to the rest of the lung and infection symptoms, and the intestine is just prone to infection as the lungs.

    JB: Its possible to eat the virus and could attack the intestine, it’s what you say?

    RP: Yes, if you get in your mouth and swallow it, will infect those as well.

    JB: Even if your stomach acid will think we`ll take care of it?

    RP: Not necessarily, stomach acid doesn’t break down the nucleic acid.

    JB: …in the healthy person, if the mucus is working correctly, is able to kill the virus?

    RP: The surface cells including the mucus have proteins analogues to the surfactant in the lung, proteins that collect the surface groups of pathogens and bind them together as like putting flypaper on.

    The hydrophobic surface its itself tends to disorganize some of the invaders.

    JB: For instance, they tell us to wash our hands all the time, how a soap kills a virus?

    RP: Taking the proteins, dissolving, making relatively insoluble things soluble, because the soap has hydrophobic fraction that sticks to hydrophobic insoluble parts of an organism and dissembles inside out.

    JB: Its COVID-19 a little better break in our system, then a normal cold which is also a corona virus. I heard cold is also a coronavirus, it’s that true?

    RP: No, cold can be caused by any of this... if your immune system is good, like one study found that almost half of all of the respiratory infections, they couldn’t identify a particular cause, but the rhinovirus was the biggest, about 30 percent, that’s the most common cold virus that they identify, but are lots of unknown things that cause those symptoms, and then then coronavirus is in a range of somewhere between 5 and 15 percent of those respiratory infections.

    JB: Do you think the reaction of the government at this point is over the top?

    RP: Unless there was a purpose to create international chaos for example to try to finish off Iran by cutting of their medical supplies.

    JB: That’s write, the top administration is intensifying sanctions at this time.

    RP: Yes, you would suppose that would get in their plans, and if it's not really a threat, otherwise it becomes a threat to do all of this and say things, for example I just heard that all of my favorites brand of milk have been discontinued for the duration of the panic.

    JB: Really? Why is that?

    RP: I don’t know

    JB: They are claiming as a carrier?

    RP: No, but I notice that over last several weeks, the certain brands that I normally get, they reduce to one little row in the supermarket, and wont replenishing that, and today they said they will be discontinuing that

    JB: Whoa, that’s annoying

    RP: Yes

    JB: I am sort of puzzled by their reaction, and everybody around here is, you know, trying to cope with it

    RP: The media, including the big media like Nature International Science magazine, they are getting kind of excited in denying that it was an intentionally created virus which was leaked either accidentally or intentionally, they just, I think, yesterday published a paper explaining technically way will be impossible for them to done it, but the fact the rushing so fast to deny that it could have been leaked accidentally out of lab, but when you look at the fact the normally they say that it takes over a year to produce a vaccine to a new respiratory infection, but already now, within weeks saying that they have a vaccine ready to test, the purpose of CDC patenting the coronavirus 17 years ago was delivery to create pathogens experimentally to unable them to anticipate a pathogen so they could create to have a vaccine ready, so their intention was to have a vaccine ready by creating a pathogen, but now they saying they couldn’t possible of creating this but they do happen to have a vaccine almost ready to used, by their own declaration, it sounds very suspicious.

    JB: I feel like there is tremendous conflict of interest in CDC..

    RP: Yes, same with WHO, on January 29th sad it’s not a pandemic and then, next days, sad it is a pandemic. I think something happened to him politically.

    JB: I see. A pandemic is supposed to reach a much higher bar as my understanding then we reach at this point.

    RP: Well, as I said, I don’t see any evidence, or anything different from last year or 10 years ago.

    JB: Maybe you can explain the conflict of interest of WHO, I am not familiar with that.


    RP: People working there who have close connections to the vaccine industry, I think Robert Kennedy Jr. website has information about the conflicts of interest.

    JB: And CDC, you mention they have a pattern of coronavirus, why would they patent that?

    RP: Well, so they can license a vaccine, I suppose.

    JB: That gives them the sell right to license a vaccine to treat that…. And Trump assistant… he was saying that it will be a least a year and half to put out a vaccine, you thing is out of the loop?

    RP: No, that’s what have been saying, virologists in general is saying it takes time to develop. And, to do actual testing I think that’s a very optimistic idea because if it really had to test it, it will take a generation… The way they test it, the safety of it for example, is in a control group to use the same adjuvants, aluminum adjuvant for example, which is the most dangerous component, so they are using fraudulent safety test, you can't have a test without a controlled group.

    JB: Explain what an adjuvant is?

    RP: It creates derangement, in this case in the muscle were is injected, and anything you inject in the muscle is going to damage it, start an autoimmune correcting process, but they found that just pathogens particles were enough to really tear up the tissue to produce a violent immune reaction, so they found that aluminum oxide particles creating a terrific immunological storm that would sometimes create a little tumor, or abscess at the site with such an intense damage, but that extreme inflammation at the point of injection activates a better more systemic immune reaction, it turns your whole body into inflammatory system, so people very often have a fever for a couple of days after getting a shot.

    JB: So that’s way when some people when are getting a flu shot, they feel that they have a mild flu.

    RP: Yes, it’s the same thing, systemic inflammatory reaction which is the whole purpose of the adjuvant, it would not be an adjuvant if it didn’t damage your whole inflammatory system.

    JB: So, you are saying that when they do the testing, they don’t have a control group that doesn’t receive the adjuvant?

    RP: Yes, in many of the studies, that wasn’t universal situation, but several of the very important studies were completely fraudulent by not having a controlled group

    JB: That’s consider standard in double-blind testing, isn’t it?

    RP: Yes

    JB: They keep coming back with Spanish flu, I think it was 1918, they took it a tremendous toll in lives I think over a year, it was blamed on Spain, like Trump is blaming on China, but it turn out, it actually came from US army base and I just red recently that so-called flu that started in the army base for this for soldiers who just been drafted and then were shift over Europe, that may have been caused by a vaccine that the Rockefeller center was testing on those soldiers who were basically draftees. Have you heard anything about that?

    RP: I haven’t heard any more than what you sad, but do you know about the movie Vaxxed, there is information in that about the Gulf War syndrome and the anthrax vaccine. The people were getting the Gulf War syndrome without leaving the US, following the anthrax vaccination.

    JB: And also, the nurses who was giving them felt terrible about administrating them. I just gone read a little thing about this article I found.. it's looking at research was done about the Spanish flu, and this scientist who looked into it, look back at the autopsy and found that all people who diet of flu supposedly tested positive for bacterium pneumonia, so for some reason they all got bacteria pneumonia, and that’s what this person believes killed them. That’s different from the flu?

    RP: oh, defiantly yes, but the CDC counts pretty much, that will fall into unknown category of severe respiratory syndromes, so they, to get their annual 40000 deaths that they can scare people, saying that’s flu, get your flu shot, it obviously, isn’t the flu, its pneumonia from partly unknown causes and partly from a variety of viruses that have nothing to do with the flu shot.

    JB: And virulence from that situation is from worse environment, even packed into barracks, or ships to Europe, or trenches.

    RP: Yes, the conditions was from first world war, were not helpful in general, much of the world was influence by the war conditions, so stress itself it’s a cause an epidemic, shortage of food will increase the incidence of infectious diseases.

    JB: es, that’s a really good point, so right now if it’s true that this is a pandemic, its seems to me that people all around the world are under tremendous amount of stress. Do you thing its possible a cause, actually is the case of its coming?

    RP: Yes, if anything unusual is happening in the disease world, I think you can blame sanctions as one of the big causes, dislocating the world economy, if you cause unemployment you gone increase infectious diseases

    JB: You mean poverty causes infectious diseases?

    RP: Yes

    JB: Also, someone referring to sites of 5G deployment, the new telecommunications standard that involves new millimeters waves, basically being everywhere in environment so you cannot escape from these microwaves. Do you think that could contribute to declining immune system?

    RP: Yes, I saw a good take on hour-long lecture by Devra Davis, she did a good book on cancer, The Secret History of the War on Cancer, this is a very good analyses of the electromagnetic damage, mostly they are claiming that is safe on bases of absolute no research, but the animal research that exist shows that there is a real danger.

    JB: That there is a degradation of the immune system from, like cell phone for instance?

    RP: Yes, for example, some studies, just the mild field from setting up an electric sewing machine they found that people who worked on electric sewing machine for 20 years had a very high rate of dementia, and anything that affects your nervous system is affecting your immune system.

    JB: Right, so another reason to go on rolling machine or a bicycle.

    RP: Yes

    JB: How much role endotoxin plays in regards to viral infection and the effects of endotoxin are increased in the presents of the virus?

    RP: Endotoxin is a protein with fatty acids and carbohydrates attached to it, it’s called lipopolysaccharides, but is just part of the coding of bacterium so its being produce in the living process of the bacteria, and normally our intestine filters out most of it, but when you are under stress more of it reaches the liver and the liver is always doing a fairly good job of detoxifying but some of it always circulating and activating the immune system a little bit, but when you under stress your liver gets overwhelm with this bacterial material and lets it produce inflammation and stress interfering with oxidative metabolism everywhere in your body and its activating because is interfering with mitochondrial energy production, its overlapping with what the angiotensin is doing anyway, but it activates the angiotensin system, so viral infection and anything stressing your intestine enough to make it permeable to bacterial materials will end up the same place making you having inflammatory symptoms, sometimes with … ? symptoms, other times with lung and head syndrome? symptoms.

    JB: Yes, I didn’t believe you years ago when you said intestine is connected to other organs but I do believe you now, and if you look at the map of nerve system your intestine is connected with all those.

    RP: Yes, it’s partly chemical leaking through and partly inflammatory substances like serotonin and histamine produced by the intestine itself getting in the blood stream, tremendous flood of serotonin shows up and circulates in the platelets, and the nerves directly can transmit signals such as secretion of mucus and production of histamine and serotonin and nitric oxide right up in the nose membrane and throat membrane, so you can treat the symptoms at the source by swallowing this things?, that’s way I recommend the raw carrot, because carrot being indigestible will help to wash out some of the bacteria that are producing endotoxin, but if you take anti-inflammatory things with it, such as olive or coconut oil, or aspirin or anti-histamine, or antibiotic, the carrot will deliver that down all the way through the intestine offering protection and anti-inflammatory effect. An early US 20th century gastroenterologists demonstrated that … ? temper, which saw as lung and respiratory disease, he found that before any bacteria or any virus occurred in any of this respiratory membranes it was

    already well establish infection of the intestine, and they will start drooling and sniffling because of nervous or chemical signal from an inflamed intestine, so no pathogen was present in this inflamed respiratory membrane, it was all coming from the intestine. I think that’s a very generally neglected in people treating respiratory sicknesses, they let them go on eating things that are known to favor bacterial growth in the small intestine for example.

    JB: I notice when I eat something my nose started to get moist inside, maybe is my age, I am almost 65, but when I eat something now, doesn’t always happen, but from time to time, I started to get slightly runny nose

    RP: Yes, that was something I notice about some years ago, when I worked in the woods, I would come in to eat something in the restaurant, and I notice day after day I would see someone eating paya ? or milk shake and by the time they got to the… they will be sniffling… I things it was loosening up, mucus producing sort of therapeutic cleanse reaction when they got their blood sugar up, the first stage of inflammation increases circulation but it can dry up the membranes, and the mucus that they secret becomes gummy and hardened and produces a dry coughs, but when you get your blood sugar up the process can complete itself, seems to need enough energy to produce a good flow of blood and mucus production, so it can wash away the histamine.

    JB: What about the theory the virus is simply ..? or stomatitis from bacteria and viral infections are really caused by a cold ? intracellular bacteria.. it must be a cold bacteria associated with HIV?

    RP: Those things do exist, but I don’t think he was right in that blaming at all on cold bacteria. We are loaded with potential viruses, its several percent of our genome, some people have identified as potential viruses or retroviruses, and this are DNA that has been built in our system by an exposure to the environment. There is a lab in Germany that shows that you can identify beef DNA after you eat beef, in the blood stream and then you can find it integrated in our genome. What we eat it has DNA in it, is likely to be able to enter cells and be integrated as a potential of resource, when we put in the stress, is something that Barbara Mcclintock was very unpopular in 1940s and 50s when she talked about the jumping genes, but she show the stress causes genes to come out from the chromosomes and move around to a different place, and since we have this retroviruses, I think is almost certain to under stress we will express retroviruses that have been in us for generations, and if you look for them, you look like got o viral infection from outside, this is what Peter Duseberg is been saying for the last 40 years …. When the people with the test for HIV virus have looked from blood store of army recruits in 1960s and 70s. Every year that the stored blood showed roughly about 1.5 percent HIV infection, every year the same, and current more recent test have been in the same range of the general population. If you look at sick people you will find a higher percentage so it looks like an epidemic, even in Africa were people are under stress and exposed to many infectious diseases you will find a very high infection rate, so called HIV virus, but the standard healthy population historically has been 1.5 percent, and if you straw up the organism and cause rearrangement of the genes as Mcclintock showed the stress induces the expression of what we can call viruses, retroviruses.

    JB: I heard the immunity after the infection with the coronavirus is quite short lived, does Mr Peat have any opinion on acquire immunity to coronavirus?

    RP: No, not at all, but one thing that is known is that after this kind of severe respiratory infection there was a great increase in the risk of pulmonary fibrosis, just because inflammation leads to fibrosis and reduce lung function, so apart from any future risk, I think the real thing to worry about is to stop the progression of that angiotensin related inflammatory production of tissue fibrosis and stiffness

    JB: I see, anti-inflammatory will do that

    RP: Yes

    JB: What’s the best easy to deliver anti-inflammatory to the lung?

    RP: I think through the mouth just eating like little losartan?, and the Chinese are recommending a variety of things, they including some virus killing chemicals, but I think the main their recommendation are losartan and cinanserin the anti-serotonin things being very broad spectrum protective anti-inflammatory, so I things cyproheptadine Is a good safe drug, and a lot of people are recommending the old approach to viruses, the idea of killing the virus, in the 70s and 80s, antiviral based on the idea of nucleoside analogues to mutate the DNA of the virus, acyclovir and ….? for example, and at that time, a lot of people were saying if you mutate the DNA-ARN of the virus aren’t you likely to be mutating the human DNA? and the FDA, proved studies they say absolutely not going to mutate, your gonadal DNA, but in recent years, 40 years later, the studies are saying yes, definitely injure the gonads and mutate human DNA, so people are now recommending wide spread use protectively nucleoside analog antivirals, but I think wide spread use of that is going to create genetic damage to the reproducing population.

    JB: To sum up what the best course of action to protect ourselves?

    RP: My first recommendation was is to eat well and make sure your vitamin D level is up around 50-60 ng/ml on blood test, which often take 5000 units per day, and to use a very safe antiviral such as aspirin, but if there is a sign of infection then I think Losartan and the anti-serotonin things will be appropriate to limit the degree of inflammation and not to worry about killing the virus or becoming immune to some future variant because your immune system is a lot better than vaccines but still the immune system doesn’t necessary keep up with the mutating virus.

    JB: Ok, so losartan and cyproheptadine is good thing to take if aspirin is not working

    RP: I thinks so, the Chinese recommend cinanserin, I don’t know if might be better than cyproheptadine

    JB: You can also get vit D from sun light

    RP: That’s the best thing.

    http://www.radio4all.net/index.php/...vLEBLCe0OS3CvVPM1ItMFiiv7BZJnQiSff_Av2rGJHNJ8
     
  2. Doing some digging, thought this was interesting, from military times.
    Oops, meant to post this on the other thread.
     
  3. Thanks, great interview. The part about stress causing dormant viral particles to come out into circulation I totally believe, its why being sick is so often conflated with being "infected", when the sickness is in most cases rather caused by chronic stress.

    Still, seems what is going on in Italy is pretty out of the ordinary.
     
  4. Great interview.

    I think Peat might be a little bit crazy tho lol. Seems like he was suggesting the “authorities” intentionally got rid of the brand of milk he likes just to spite him, but I didn’t listen so he was probably making a joke
     
  5. It didn't seem like he was suggesting he was being targeted, it sounded more like he was just sad that his favorite milk is gone and wanted to tell people about it
     
  6. He must be back in the states. That was always a Safeway brand. We should note Safeway was bought by Albertsons last year. And they are more a hedge fund than interested in food.
     
  7. Ray Peat drinks the Safeway Select milk?! I’m a downright pre-madonna by comparison.

    Also, two easily definable camps here: one of them is advising vitamin d, which I upped while shutting myself in for one more day of working from home.
     
  8. :disrelieved:I just found out that my respiratory therapist friend who was exposed last week now has it and is quarantined to her home.
    Edit: make that two friends.
     
  9. prima donna* :D
     
  10. Just got done listening to that interview......very interesting.
    It still amazes me how much information he has in his head.
    What if Ray Peat is the internet?
     
  11. How to interpret the advice on aspirin? To take as a preventative, but not to take if you feel sick already....?
     
  12. Why not take aspirin if you feel sick already? I didn't get that message from reading the interview, but maybe I missed it. I don't think RP puts much credence in the "avoid NSAID ibuprofen message from France & CDC.
     
  13. Has anybody here been taking supplemental D3 for a good while with good results in general?
     
  14. Might give some kind of visual Peat was saying in regards to Angiotensin, ACE 1 and 2, etc.

     
  15. I would have ( perhaps superficially) interpreted this as an allergy or sensitivity. Can somebody tease apart the nuances ?
     
  16. Oh yes, I totally forgot about this part. I was/am most intrigued by it. What I think he is getting at is that there was inflammation earlier in the day, possibly from exhaustive work, and that the increased circulation caused by inflammation causes the mucus to sort of dry up. Once the blood sugar is increased by the end of the day meal the mucus becomes wet again and can sort of finish what it was doing earlier.

    Also, I'm glad my question got asked about endotoxin!! :cool
     
  17. Debunking Nature Magazine's "COVID-19 Definitely Didn't Come From A Lab" China Propaganda

    or

    China owns Nature magazine’s ass – Debunking “The proximal origin of SARS-CoV-2” claiming COVID-19 definitely wasn’t from a lab
     
  18. Excellent video, thank you.
     
  19. I'm going to send it to Peat, if someone hasn't already, to see what he'd add or takeaway (besides cell membrane talk.)

    This stuff is fascinating. If everyone just used this time to really understand how all it works, so many more would be empowered and know can be done.
     
  20. Thanks this helped I was getting confused when ray said Losartan blocks angiotensin receptor 1 and Wikipedia say it blocks II.. both are correct? Either way sounds like Asian countries are having better results by using ABRs and Europe is struggling while keeping people on their ACEIs.
     
  21. I do not know if it is correct, but I try to understand, apparently the acute accelerating lung fibrosis induced by COVID-19 infection can be justified through ACE – ACE2 - AT1 overactivation caused by the virus. Losartan is an AT1 antagonist with a selective, competitive function which decreases the end

    organ responses to Angiotensin II. It is a common anti-hypertensive agent which is currently prescribed for high blood pressure patients, particularly those who are prone to diabetic nephropathies. Losartan may lead to protection of lung fibrosis through other molecular mechanisms such as downregulation of TGF-β1.

    After entrance to the body, COVID-19 fuse their envelopes with membranes of the host cells, then transport their genetic material into the affected cells. This essential fusion is mediated by glycosylated spike proteins on the surface of the virion interacting with proper surface receptors on the membrane of host cells. Angiotensin-converting enzyme 2 (ACE2) receptor is a known surface human cell proteins on which COVID-19 spike proteins are specifically bound.

    The activation of RAS is triggered by secreting of renin from kidney, through juxtaglomerular cells. Renin is a protease that cleaves angiotensinogen, the precursor of angiotensin, which is made by liver. It produces an inactive peptide: Angiotensin I (AngI).

    Then, ACE mediate the conversion of AngI to AngII, a major RAS effector. ACE is a protein with high expression on membranes of vascular endothelial cells, predominantly in lung tissue. The most of the RAS associated physiologic effects are run by interacting of AngII with a G-protein coupled AngII type 1 (AT1) receptor. This activates a physiologic pathway in different tracts, such as kidney, liver, central nervous system, respiratory, and cardiovascular system. Some crucial events are regulated via active AT1 receptors including arterial pressure, fluid and sodium balance, fibrosis, and cellular growth and migration.

    In some pathological conditions, overactivation of AT1 may lead to damaging events like fibrosis in different organs such as liver and lungs, perhaps through increasing TGFβ expression.

    Some studies indicate that ACE2 has a protective effect on the fibrogenesis and inflammation of different organs as well as liver and lung. Altogether given the several studies, the ACE-AngII-AT1 axis in the RAS system shows a predominant role in the organ fibrosis, particularly in lung and liver.

    According to some recent studies, ACE2 has a regulatory effect on innate immunity and gut microbiota composition. Moreover, ACE2 has a determinant antifibrotic role in the lung injury induced by sepsis, acid aspiration, SARS, and lethal avian influenza A H5N1 virus.

    The most common complication leading to the CoV-induced mortality is respiratory failure due to an extensive, accelerating lung fibrogenesis. Rather than PCRbased testing to detect CoV infection, a radiologic lung infiltration pattern in chest X ray could have a diagnostic value to screen the suspicious patients. It seems the cytopathic effects of virus resulted from its massive replication in infected cells need more time than what happens to cause acute manifestation of the disease. So, the acute accelerating lung fibrosis induced by COVID19 infection can be justified through ACE-AngII-AT1 overactivation caused by the virus.

    Coronavirus is more severe and deadly in the aged, hypertensive, and diabetic.

    It is also of note that ATR-1 Receptors increase with age and are increased in diabetes, hypertension, COPD. All of which are the populations at high risk for COVID-19. They are less in children, which is one reason hypertension is rare in children. As the SARS-COV2 virus attaches to the ACE2 it causes a decrease in ACE2 availability/activity. This would lead to a higher AngII and in patients with more AT-1, we would expect the effects would be worse, which is what we see in COVID-19. Another factor playing a role is that hypoxia causes cells to produce more AT-1. So the localized edema in the lungs decreases oxygen, which increased AT-1, which further leads to edema.

    Old people have a decreased expression of ACE2 (Angiotensin-converting enzyme 2), and increased expression of AT-1 receptors compared to the young.

    If young people have higher ACE2, and that was the factor allowing faster viral inoculation, then it would be worse in the young, but it is not.

    Cancer, hypertension, diabetes, chronic obstructive pulmonary disease are all conditions that are associated with higher levels of the AT-1 receptor (Angiotensin II receptor type 1), with greater age or severity related to higher levels.

    In patients with low ACE2 by age, sickness or virus binding to ACE2 means that it leaves the ACE1 which produces angiotensin.

    ACE2 is capable in inactivating angiotensin breaking down to the first seven amino acids, they call it angiotensin 1-7, and this is a defensive anti-inflammatory peptide, so if your ACE2 is knocked out, angiotensin has a free range to cause damage, so the virus increases the inflammatory reaction by sticking to the defensive enzyme ACE2, and that enzyme combined with the virus, than acts to enter the cell by way of the Angiotensin II receptor type 1 which is called the AT1, that are two known receptors by which angiotensin can do damage, with stimulation of the larger population of AT-1 receptors within the local tissue eliciting further edema, leading to hypoxia witch upregulates the expression and function of AT1 receptor, with a whole range of destructive processes, nitric oxide production, pulmonary hypertension, acute lung injury and lung fibrosis.

    Endotoxin (LPS) induced an increase in the AT1 subtype of the angiotensin II receptors.

    Angiotensin-converting enzyme or ACE, is a central component of the renin–angiotensin system (RAS), which controls blood pressure by regulating the volume of fluids in the body. It converts the hormone angiotensin I to the active vasoconstrictor angiotensin II

    ACE is also part of the kinin-kallikrein system where it degrades bradykinin, a potent vasodilator, and other vasoactive peptides.

    Other less known functions of ACE are degradation of bradykinin and amyloid beta-protein.

    Bradykinin is an inflammatory mediator. It is a peptide that causes blood vessels to dilate (enlarge) via the release of prostacyclin, nitric oxide, and Endothelium-Derived Hyperpolarizing Factor.

    Bradykinin is a potent endothelium-dependent vasodilator and mild diuretic, which may cause a lowering of the blood pressure. It also causes contraction of non-vascular smooth muscle in the bronchus and gut, increases vascular permeability and is also involved in the mechanism of pain.

    During inflammation, it is released locally from mast cells and basophils during tissue damage. Specifically, in relation to pain, bradykinin has been shown to sensitize TRPV1 receptors, thus lowering the temperature threshold at which they activate, thus presumably contributing to allodynia.

    Bradykinin is also thought to be the cause of the dry cough in some patients on widely prescribed angiotensin-converting enzyme (ACE) inhibitor drugs.

    ACE inhibitors - lower your blood pressure by reducing Angiotensin II in the body.

    I understand that, the large number of deaths in Italy are old people with hypertension, heart disease and diabetes and probably have used ACE inhibitors drugs.

    ACE inhibitors inhibit ACE competitively. That results in the decreased formation of angiotensin II and decreased metabolism of bradykinin, which leads to systematic dilation of the arteries and veins and a decrease in arterial blood pressure. In addition, inhibiting angiotensin II formation diminishes angiotensin II-mediated aldosterone secretion from the adrenal cortex, leading to a decrease in water and sodium reabsorption and a reduction in extracellular volume.

    Therefore, ACE inhibitors, by blocking the breakdown of bradykinin, increase bradykinin levels, which can contribute to the vasodilator action of ACE inhibitors.

    Angiotensin converting enzyme 2 (ACE2) - is a protein that sits on the lining cells within alveoli of the lung. It acts as an enzyme, being an exopeptidase that catalyses the conversion of Angiotensin II to angiotensin 1–7, which acts as a vasodilator. It also converts angiotensin I to nanopeptide angiotensin[1–9] It is a single-pass type I membrane protein expressed on the surface of epithelial cells of the pulmonary alveolus, and on small intestine enterocytes and other cell types.

    ACE2 has been shown to be the entry point into human cells for some coronaviruses, including SARS-CoV, the virus that causes SARS. A number of studies have identified that the entry point is the same for SARS-CoV-2, the virus that causes COVID-19.

    This might lead some to believe that decreasing the levels of ACE2, in cells, might help in fighting the infection. On the other hand, ACE2 has been shown to have a protective effect against virus-induced lung injury by increasing the production of the vasodilator angiotensin 1–7.

    In fact, the interaction of the spike protein of the virus with the ACE2 induces a drop in the levels of ACE2 in cells. (A Crucial Role of Angiotensin Converting Enzyme 2 (ACE2) in SARS Coronavirus-Induced Lung Injury - PubMed)

    Acute respiratory distress syndrome (ARDS) is a devastating inflammatory lung disorder that is frequently associated with multiple organ dysfunction leading to high mortality. The mechanisms underlying ARDS are multi-factorial, and are thought to include the renin-angiotensin system (RAS).

    The RAS is a coordinated complex hormonal cascade that is composed of angiotensinogen, angiotensin-converting enzyme (ACE) and its homolog angiotensin converting enzyme 2 (ACE2), and angiotensin II (Ang II) type 1 and type 2 receptors (AT1, AT2). ACE cleaves the decapeptide Ang I into the octapeptide Ang II, while ACE2 cleaves a single residue from Ang II to generate Ang 1-7, which in turn blocks Ang II and inhibits ACE. Thus, the ACE2 axis negatively regulates the ACE axis.

    Conversion of Ang I to Ang II can readily occur in the lung by abundant ACE in pulmonary vessels. This may contribute to rapid responses of vasoconstriction in the pulmonary circulation and low blood flow, leading to ventilation/perfusion mismatch in conditions such as tissue hypoxia. On the other hand, ACE2 is primarily produced in Clara cells and type II alveolar epithelial cells and epithelial injury is a critical event in the development of ARDS in humans; thus, the ability to produce ACE2 is severely impaired, resulting in dominant ACE activities during ARDS and/or ventilator-induced lung injury.

    The RAS—specifically Ang II via AT1 and AT2 receptors—has a number of effects: induction of pulmonary vasoconstriction and vascular permeability in response to hypoxia resulting in pulmonary edema; stimulation of the lung production of inflammatory cytokines directly and indirectly by targeting bradykinin; acceleration of the Fas-induced apoptosis in alveolar epithelial cells; and promotion of extracellular matrix synthesis and human lung fibroproliferation. These effects of the RAS highlight the crucial role of Ang II in ACE/ACE2-regulated ARDS. Indeed, enhanced ACE activity and decreased ACE2 activity contribute to lung injury during cyclic stretch of human lung epithelial cells and to VILI in animal models. In models of ARDS, the use of ACE2 gene knockout mice demonstrated that ACE2 and Ang 1-7 are protective.

    The use of Ang II receptor blockers or ACE inhibitors has been effective in decreasing lung injury in animal models, but this approach could have potential side effects, including systemic hypotension in humans. Since ACE2 protected the lung from developing ARDS and functioned as a coronavirus receptor for severe acute respiratory syndrome, the recombinant ACE2 (rACE2) protein may have an important place in protecting ARDS patients and as a potential therapeutic approach in the management of emerging lung diseases such as avian influenza A infections. ([https://pubmed.ncbi.nlm.nih.gov/16007097/]. Acute respiratory distress syndrome, also known as ARDS, is a common killer among critically ill patients hospitalized with COVID-19.
     
  22. @md_a, thank you so much for taking the time to write out an extremely detailed explanation. :hattip
     
  23. Ray Peat humor...

    Lothar Wieler, head of Robert Koch Instute (the German CDC) and adviser to WHO is among the biggest fear mongerers in Germany, and he is big in pushing vaccines. In interviews he comes across as if he was personally offended that so few elderly get the flu shot. Yesterday he warned: We are in the beginning of an epidemic and the numbers are increasing!

    Below are the numbers that the Robert Koch Institute reports. It's the weekly report of influenza-like illnesses. This is such a clown show!

    2020-w20 - flu-like cases in Germany.GIF


    https://influenza.rki.de/Wochenberichte/2019_2020/2020-12.pdf
     
  24. [This is a reply to a post in another thread. I think it fit better here.]

    Thanks for sharing. He completely demolishes influenza vaccines.

     
  25. I fear, based on that interview you posted, that the direction this will go is to add additional viruses to the yearly vaccination schedule.

    I could see them also pushing (hopefully not by law) the vaccinations on young adults as a way to keep old people safe. The assumption being that if young people are vaccinated they will not get sick during flu season and spread the virus to old people.

    That's how I'd argue it if I were on the their side anyway.
     
  26. btw: the interview with David Icke that Dr Peat cited is here.
    For the forum members that do not think talk of financial implications belongs on this forum, the polictics and financial dynamics are part of the perceive, think, act.
    btw: I just got a blasting EMERGENCY ALERT to my phone: Lakefronts and parks are shutdown. Stay Home or be arrested.
     
  27. That’s insane.
     
  28. This is my fear, too. The rhetoric they use now, 'It's all to protect the elderly and weak, and you act selfish and irresponsible if you just go on with your life'... The same rhetoric is used to push vaccines: 'We need 95% vaccine coverage to acchieve herd immunity, otherwise the vaccine fails. And you must want to protect the vulnerable who are too weak to get vaccinated.' Many biolabs are now working on mRNA vaccine for SARS-CoV-2. To me this sounds like some kind of gene therapy. I don't believe that this is save.
     
  29. [​IMG]
     
  30. That sucks. Thankfully I live on 10 acres with 60 acres of forest behind me that I can walk through. I can't imagine being quarantined in an apartment... with kids...
     
  31. Me too. Thank God I’ve got access to 65 acres out my back door. I’d love to never go back to work but to be honest so far it doesn’t seem like anything much is going on.
     
  32. I live in an apartment with my 2 kids. I have to homeschool them now also. They have friends around
    so they go hang out with their friends for a few hours of the day. Everything here is shutdown
    except necessities and going to the park and trails for exercise is listed as a necessity, thank
    goodness. So I will take them there weekends. They dont miss school other than
    my daughter is bummed because she is in theater and a lot of her plays are cancelled.
    They are enjoying themselves, unlike myself working all day then homeschooling in the evening leaves
    me little free time anymore, but hopefully not for too much longer.
     
  33. I hope so too. Hang in there.
     
  34. I don't really believe that david icke is safe anymore he lives in the country where the elites live too wouldn't it be weird to see him making talking chatting writing conspiracies about them.. but atleast what we have to know is The elites are doing this stuff. 100% sure they want to depopulate first and claim the power over everything.
     
  35. What is this gif all about? him drinking a soda.
     
  36. I really wasn't too worried till recently. I just survived a severe and lengthy illness, so thought I was good, but now I have intestinal inflammation flaring up again and can't really eat much. Ray Peat's suggestions are what I believe got me through that illness and possibly saved my life. But I definitely have a serious underlying disease, plus I'm oldish (41 years). RPs suggestions to avoid getting respiratory failure from this is to already be healthy, but frankly, most of us are not well yet despite our trying. Some of us here are close but not there yet. So when RP says there's nothing unusual going on yet he's right but it seems to be growing extremely quickly. Or is it not and I'm just not getting the right information? Like, why are they getting freezer trucks in NY to ship out dead bodies? Is this normal for flu season, or is it bunk? Or is it because they are giving them too much oxygen like in Italy? According to some reports the age group in NY is much younger than in Italy.
    Below is a video currently circulating... I don't know what to make of it. Is it the treatment that's causing these deaths too?


    I know the economy needs to get back on track and there's politicians and corporations that could make out great by all this. But for people like me it is going to be unsettling when things get back to normal. I don't want to be the crazy one who thinks it's all worse than it really is, I definitely don't want to add to hysteria. I want to understand what is going on but I can't seem to get all the correct info.
     
  37. I didn't know this. After reading @Regina 's bleak description of Chicago and now this imagery, combined with this negative aatmosphere in my city (also got an emergency extreme alert like Chicago) I'm scared of getting nightmares. Doesn't help that I've gotten dark supernatural images in my head lately. Sounds childish I know but I think I'm going to try to sleep as little as I can tonight...

    I think all this is starting to mess with my head...
     
  38. I‘m not sure if „they“ want to or can push a.vaccination agenda with covid.
    It seems now huge Antigen-Testing is about to start, and when it becomes clear that 50-80% of any population was infected already they can’t at least force it on all.
    Surely the elderly and sick will be told to take a shot for prevention just like with influenza, but it’s only a relatively small part of the populace that actually takes it.
    It’s still bad, but not as worse as a mandatory shot for all
     
  39. Sorry Lamp. You're such a treasure here.
    I'm looking at a weird view here. I.e., No people. But officials calling for draconian removal the (no) people.
    Maybe I just need a good night's sleep.

    :praying:
     
  40. Tennent's Extra. He realises that the food pyramid is Illuminati in plain sight.
     
  41. I came across a couple of tweets/videos pushing back on the panic. Something to think about.

    This Youtuber has been walking around New York, observing, and asking questions:


    Here's his Twitter feed, which you can skim for a sense of his take:
    CrowdsourcetheTruth (@csthetruth) | Twitter
     
  42. Probably hospitals are getting overwhelmed, but how much so because everybody thinks every little illness now is COVID-19? If anyone remember AIDS in the 80s, everything was a symptom and everyone was scared to death. Similarly with Anorexia Nervosa, I remember reading how it spread like wildfire in Japan, after a few newspaper articles came out detailing cases in America. Of course it is impossible in modeling to separate the anxiety driven hypochondria from the real thing, perhaps especially when dealing with a coronavirus that no one really know how long it has been around. For example, a few weeks ago a respected epidemiologist in MN said the virus was already 4 generations deep in MN society and MN is just getting around to going on lockdown today.
     
  43. Lol
     
  44. I was out walking and somebody yelled at me. Righto.

    Went to a medical centre. Receptionist snaps at me to leave and use hand sanitizer and come back in. Don't touch the counter, stand behind the tape on the carpet. Do you have a cough? Where have you been?

    Ffs they've all gone nuts. Everybody has germophobia and feels the right to police others.

    Tonnes of people walking around the shops in those ridiculous masks, regardless of how many times doctors have appeared in the media telling them they are absolutely pointless.

    Still shortages of basic items in the supermarkets due to idiotic panic buying. It's tiring.
     
  45. who is the epidemiologist im in MN?
     
  46. Today’s census shows the three hospitals have 292 fewer patients than they did three weeks ago.

    The hospitals currently have 447 patients in medical-surgical beds used for routine care and 75 patients in intensive care and critical care beds, according to the Hospital Executive Council. Three weeks ago, the three hospitals had 704 patients in medical surgical beds and 110 in intensive care and critical care beds.​

    Syracuse hospitals have 300 empty beds, despite coronavirus surge



    Four days after its opening, the larger Leishenshan hospital had only 90 patients, on wards designed for 1,600, but was reporting no spare beds, Wuhan city health data, first reported by the Chinese magazine Caixin, showed. The other facility, Huoshenshan, had not yet filled its 1,000 beds a week after opening.​

    What China’s empty new coronavirus hospitals say about its secretive system

    Which hospitals? I keep reading people claiming the hospitals are overrun. All I find is normal utilization.
     
  47. This.

    You can never underestimate the power of psychology and unconscious motivations. The whole thing actually reminds me of the Dancing Plague of 1518. Society has always been much more superstitious and vulernable to hysteria than it lets on. All the more so during this age of apparent rationality and science.

    When this is all over (and god I'm praying it doesn't end in forced vaccinations, cos I'll have to upend my life and go on the lam, or to jail), people will marvel at the mass hysteria and pick over its bones for decades.
     
  48. Michael Osterholm There are some good youtube vids with him.
     
  49. Aint that the truth. People are absolutely losing their ***t these days. Turning on each other. I got yelled at by a woman at the shop because I walked too close to her. It must be horrible to live in fear like that. I’d rather get any virus than live a life in fear.. as a danish citizen I really hope the forced vaccinations do not become a reality. I am absolutely astonished that they even got that law passed. Making my preparations to disappear into the woods incase they ever try to force that ***t on everyone.. shitty times indeed..
     
  50. Exactly explains why you got yelled at. Those are the ones who wants to avoid getting sick . And when pandemic is over feminism will rise again.
     
  51. IMG_20200402_172752.jpg
     
  52. Suicides are going to go through the roof.

    Once the extent of the economic damage is apparent, many will shift from fear and anxiety to hopelessness.
     
  53. He really said that? I just listened to his latest podcast with Peter Attia and he says 1,000,000 people could die and just keeps emphasizing the shortages of everything and the supply chains.

     
  54. I don't remember what video it was- he's done a ton, but he said this March 10 in an interview for CNN
    Look at the situation in Seattle. There was a case that was detected in January when upon return from China an individual became ill. This person was put in isolation, but not before he had been in the community. Nonetheless our response to this case this largely considered a great success in terms of stopping ongoing transmission. As we now know, at least one of the patients who was tested in Seattle, another individual six weeks later, was infected with the same strain. It’s likely that original virus introduction into the Seattle area did occur with this January case, meaning that there had to be at least six or seven generations of transmission between the time that the individual first arrived in the United States from China back in January and this new case. So, we’ve had ongoing transmission in this country for weeks.
    He's interesting, I haven't seen him being in favor of total lockdown, even as he may be too high in his death estimates.
     
  55. Is Peat exercising his sense of humour here? He said something like "usually I think David Icke is a bit crazy but here I agree with pretty much everything apart from the anti sugar stuff".

    I kinda took this to mean that Icke is sort of *figuratively* right in this interview. Do forum members think Peat thinks that the world is really run by a cult and everything here is being done on purpose?
     
  56. I was leaving my condo building this afternoon and a woman was speaking with the concierge at a 9 foot distance in the lobby while blocking the entrance/exit door. Me and my girl just continued walking towards the door hoping she would use her common sense and move out of the way, especially if she was concerned about contracting airborne HIV .....yet she didn’t move. Instead she stood in position and had to inquire if we were going that way.... She then proceeded to say how we weren’t following the guidelines. At that point I was very close to losing it on her. It blows my mind how insane/full retard people have become. Who stands in front of a door to begin with?????!

    I wish the nut jobs would just hunker down for the remainder of this “pandemic” and not interact with anybody but the television and their pets. Hopefully the have enough food to get them through this nuclear fallout
     
  57. :hilarious:
    I'm still working and in NYC almost every day. You described almost everyone I encounter!
     
  58. He mentioned the Icke video in two different interviews.
     
  59. The new executive orders on health care workers are similar to Nazi germanys labor laws of precariously placing workers anywhere and paying them whatever wage, taking away vacation time and paid time off, violating basic rights
     
  60. This was discussed on another thread:

    Ray Peat Interview - 03/30/2020 - COVID-19, Losartan, Sugar, Methylene Blue & More, Q&A - Dr Ray Peat
     
  61. Chicagoans aren't giving each other lip. But that's just it. They aren't interacting at all.
    Everyone has autism.
     
  62. lol all we can do for now is at least laugh.
     
  63. it was brought up before in a different thread but I think the northern Italy deaths are highly correlated to previous vaccinations, ie meningitis and influenza.

    Also found it funny that apparently Bill Gates refused to vax his own children. Thanks for sharing whoever did so. Maybe the vaccine agenda is shown for what it is when this corona nonsense proves to be hoax
     
  64. I listened to the first of these interviews and I wasn’t very impressed by some of what Peat had to say. For instance he claimed that coronaviruses typically cause about 10% of the seasonal flu deaths, so he would expect 3,000-4,000 deaths for the season from this Coronavirus.

    I wonder what he’s got to say now that the toll is already up over 8,400?
     
  65. HUGE! From CDC Website: Hospitals to List COVID-19 as Cause of Death Even if It's "Assumed to Have Caused Or Contributed to Death" - Lab Tests Not Required

    :rightagain
     
  66. I think 10% is a bit conservative. I've seen it listed usually at 15% and sometimes with a range of 15-30% like in the paper below.

    The effects of coronavirus on human nasal ciliated respiratory epithelium
    "Human coronavirus (HCoV) accounts for 15–30% of common colds..."

    Edit: Just realized it specifically says deaths. I will leave what I wrote though.

    Edit 2: It's early okay, and I have 3 kids! Lol
     
  67. Whats role of LPS ( produced by anaerobe bacteria ) in Corona virus infection
     
  68. Viruses don't produce LPS, but LPS will increase inflammation, fibrosis and suppress your immune system.

    Basically, if you have a lot of endotoxin, you will be in a worse position to fight Covid19 if you do get infected.
     
  69. https://www.medrxiv.org/content/med...20.04.08.20058578.full.pdf?mod=article_inline

    The Role of Vitamin D in Suppressing Cytokine Storm in COVID-19 Patients and Associated Mortality
    Ali Daneshkhah1 , Adam Eshein1 , Hariharan Subramanian1 , Hemant K. Roy 2 , and Vadim Backman1 1 Department of Biomedical Engineering, Northwestern University 2 Boston Medical Center Abstract
    Background Statistical analysis of data obtained from hospitals and clinics across the world has been analyzed to illuminate new insights into characteristics of COVID-19 and to discern whether a link exists between severe cases of COVID-19 that feature cytokine storm and vitamin D (Vit D) deficiency.
    Method Daily admission, recovery and deceased rate data for patients with COVID-19 from countries with over 5,000 confirmed cases through March 21, 2020, were selected. A potential association between severe Vit D deficiency and age-specific case fatality (CFR) was investigated. Reported medical characteristics of 793 COVID-19 patients were used to evaluate the intensity of cytokine storm in severe COVID-19 using C-reactive protein (CRP) levels. Medical data reported from a national study of 3,848 participants in 2007- 2008 was used to investigate the association between Vit D status and CRP. Odds ratio and risk factors from these conditions were used to predict the potential impact of Vit D on the reduction of cytokine storm and severe COVID-19. Findings Age-specific CFR in Italy, Spain, and France (70 yo ≤ age < 80 yo) was substantially higher (>1.9 times) than other countries (Germany, South Korea, China); for the elderly (age ≥70 yo), Italy and Spain present the highest CFR (>1.7 times that of other countries). The age-specific ratio of confirmed cases in Italy, Spain, and France has also been substantially higher than in other countries. A more severe deficiency of Vit D (mean 25- hydroxyvitamin D (25OHD) concentration <0.25 ng/L) is reported in Italy and Spain compared to other countries. Our analysis of the reported clinical data (25OHD, CRP) from multiple studies suggests that elimination of severe Vit D deficiency reduces the risk of high CRP levels (odds ratio of 2) which may be used as a surrogate marker of cytokine storm which was estimated to a potential reduction in severe COVID-19 cases of up to 15%. All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: The Role of Vitamin D in Suppressing Cytokine Storm in COVID-19 Patients and Associated Mortality. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. medRxiv preprint doi: https://doi.org/10.1101/2020.04.08.20058578. The copyright holder for this preprint (which was not peer-reviewed) is the Interpretation The substantially higher age-specific CFR and the age-specific ratio of confirmed cases in Italy and Spain (countries with low mean 25OHD level) suggest a potential link between severe Vit D deficiency and severe COVID-19, which can lead to a higher CFR. No direct link between the performance of health care systems, the age distribution of the nation, or Vitamin A deficiency and the CFR of COVID-19 were observed. Our analysis of the published data on the status of Vit D and CRP levels (in the US) and laboratory data (CRP levels) reported from 792 patients in China suggests that a proper supplementation of Vit D across populations may reduce the number of severe COVID-19 cases by up to 15 percentage points by lowering the risk factors related to cytokine storm. Our analysis did not eliminate the possibility of the circulation of different sub-genera of COVID-19 across the globe or other factors.
     
  70. Sun light (vitamin D) and Fresh air are medicinal

    The Open-Air Treatment of PANDEMIC INFLUENZA
    Richard A. Hobday, PhD[​IMG] and John W. Cason, PhD
    Author information Article notes Copyright and License information Disclaimer
    This article has been cited by other articles in PMC.

    Go to:
    Abstract
    The H1N1 “Spanish flu” outbreak of 1918–1919 was the most devastating pandemic on record, killing between 50 million and 100 million people. Should the next influenza pandemic prove equally virulent, there could be more than 300 million deaths globally. The conventional view is that little could have been done to prevent the H1N1 virus from spreading or to treat those infected; however, there is evidence to the contrary. Records from an “open-air” hospital in Boston, Massachusetts, suggest that some patients and staff were spared the worst of the outbreak. A combination of fresh air, sunlight, scrupulous standards of hygiene, and reusable face masks appears to have substantially reduced deaths among some patients and infections among medical staff. We argue that temporary hospitals should be a priority in emergency planning. Equally, other measures adopted during the 1918 pandemic merit more attention than they currently receive.

    THREE INFLUENZA PANDEMICS occurred during the last century: in 1918, 1957, and 1968. Each was caused by a novel type A influenza virus of avian origin. The H1N1 influenza pandemic of 1918–1919 is notorious because of the infectivity of the virus and the number of lives it claimed. Although the fatality rate was relatively low, the incidence of infection was so great that the number of deaths was high. No other pandemic in history killed so many in such a short time.1

    Global mortality from the pandemic is not known, because there are large areas of the world for which there is little information. In the 1920s, it was estimated that the disease had killed 21 million people. In 1991, this figure was revised to between 24.7 million and 39.3 million, and more-recent scholarship suggests 50 million to 100 million people may have died.2 Morbidity was high, at anywhere from 25% to 90%, and the fatality rate was between 1% to 3%.3 However, some regions reported mortality rates for the entire population as high as 5% to 10%.2 Most deaths occurred between mid-September and mid-December of 1918.4 Unusually, many of those who died were young adults, who normally have a low death rate from influenza. Another striking feature was the discoloration of the seriously ill, who often exhibited “heliotrope cyanosis,” which is characterized by a blue-gray tinge to the face and other parts of the body.3,5 Many victims died of pneumonia caused by secondary bacterial infections. Others succumbed to a condition similar to acute respiratory distress syndrome that could kill within days or hours.5,6 Pleurisy, hemorrhage, edema, inflammation of the middle ear, meningitis, nephritis, and pericarditis were among the many complications reported.6,7

    There were 3 waves of infection between 1918 and 1919. The first, in the spring of 1918, spread through parts of the United States, Europe, and Asia. This was a fairly mild form of influenza and caused relatively few fatalities. The second wave, which spread around the world in a few months, was disastrous. In less than a year, 220 000 influenza-related deaths occurred in Britain, and between September 1918 and June 1919 it proved fatal to at least half a million US citizens.1,3 Death rates in Africa were comparable to or higher than those in North America and Europe.8 Figures suggest that China was spared the worst of the pandemic, although this may simply reflect a lack of accurate records. The mortality in India alone has been estimated at 18 million.9,10 According to one estimate of the period, 800 of every 1000 people who showed symptoms suffered from uncomplicated influenza. This was more severe than the so-called “three-day fever” of the spring of 1918, but no worse than ordinary influenza. The remaining 200 suffered pulmonary complications; of these, the mortality rate for those developing heliotrope cyanosis was 95%.7

    With so many infected, and so many dying within a few weeks, the burden on medical staff and the funerary industry were immense, as was the accompanying economic and social disruption.1,3 There was much debate about the origins of the illness and whether it was indeed influenza. The symptoms were so severe that there was speculation that it was some other disease such as “trench fever,” dengue, anthrax, cholera, or even plague.1,3,11 Mortality reached alarming levels. The pandemic arrived in Boston, Massachusetts, early in September and by October 19 had claimed 4000 lives out of a total population of less than 800 000.12 At the peak of the outbreak, more than 25% of patients at an emergency hospital in Philadelphia died each night, many without seeing a nurse or doctor. The bodies of those who succumbed were stored in the cellar of the building, from where they were tossed onto trucks and taken away. Attempts at therapy for those still alive were described as “exercises in futility.”13(p139)

    The demands of wartime meant that many doctors had been called into military service; those not in uniform were caring for the wounded in hospitals at home or inspecting potential recruits at medical boards. The shortage of nurses was even more acute: as they and other medical staff fell ill, patient care rapidly deteriorated.1,3,14 Hospitals were turning patients away; mortuaries were overflowing, some handling 10 times their normal capacity. Gravediggers, many of whom were ill, could not keep up with the demand for burials.1,3,15 Early in October 1918, a delegate from a health department in the US Midwest went east to find out how best to combat the infection. Officials there offered the following advice:

    When you get back home, hunt up your wood-workers and cabinet-makers and set them to making coffins. Then take your street laborers and set them to digging graves. If you do this you will not have your dead accumulating faster than you can dispose of them.12(p787)



    This was not meant to cause undue alarm; it was merely a practical solution to a problem that had to be addressed once the pandemic arrived.12 In an attempt to prevent the infection from spreading, many cities banned public assembly, closed their schools, isolated those infected, and mandated the wearing of surgical face masks.1,3,6 Recent studies suggest that when such measures were introduced quickly—before the pandemic was fully established—and then sustained, death rates were reduced.1619 Yet for those who contracted the disease and went on to develop pneumonia, the prospects were poor. Anyone fortunate enough to gain admission to an “open-air” hospital, however, may have improved their chances of survival.

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    THE ORIGINS OF THE OPEN-AIR REGIMEN
    By the time of the 1918–1919 pandemic, it was common practice to put the sick outside in tents or in specially designed open wards. Among the first advocates of what was later to become known as the “open-air method” was the English physician John Coakley Lettsom (1744–1815), who exposed children suffering from tuberculosis to sea air and sunshine at the Royal Sea Bathing Hospital in Kent, England, in 1791.20,21 Lettsom's enthusiasm for fresh air attracted little support at the time, and the next doctor to recommend it met with fierce opposition. George Bodington (1799–1882) was the proprietor of the first institution that could be described as a tuberculosis sanatorium, at Sutton Coldfield near Birmingham, England. He treated pulmonary tuberculosis with a combination of fresh air, gentle exercise in the open, a nutritious, varied diet, and the minimum of medicines.

    In 1840, Bodington published the results of his work in An Essay on the Treatment and Cure of Pulmonary Consumption, On Principles Natural, Rational and Successful.22 Bodington's essay includes accounts of six cases; one patient died, as he acknowledged, but the others were either cured or greatly improved. This was at a time when, he estimated, one in five people in England were dying of the disease and little was being done to prevent it. Tuberculosis was generally regarded as hereditary, noninfectious, and incurable. Bodington argued otherwise, objecting strongly to the use of blistering, bleeding, and the popular purgative drugs of the day as well as the practice of confining patients in warm, badly ventilated rooms to protect them from the supposedly harmful effects of cold air, “thus forcing them to breathe over and over again the same foul air contaminated with the diseased effluvia of their own persons.”22(p2)

    Bodington had noticed that people who spent their time indoors were susceptible to tuberculosis, whereas those who worked outdoors, such as farmers, shepherds, and plowmen, were usually free of the disease. He reasoned that patients should copy the lifestyles of those who appeared immune to tuberculosis. They should live in well-ventilated houses in the country and spend much of their time outside breathing fresh air. According to Bodington,

    The application of cold pure air to the interior surface of the lungs is the most powerful sedative that can be applied, and does more to promote the healing of cavities and ulcers of the lungs than any other means that can be employed.22(p17)



    It is not known when Bodington started treating tuberculosis in this way, but there is evidence that he was doing so by 1833. By 1840, he had taken the tenancy of the “White House” at Maney, Sutton Coldfield, to provide suitable accommodation for his tubercular patients. Bodington's tenancy of this seminal building was brief—only three to four years. The Lancet published a sarcastic review of his essay and methods, and he abandoned the White House to devote himself to the care of the mentally ill.23,24

    George Bodington had anticipated the principles of sanatorium treatment that were to become the main line of defense against the disease.25 By the 1850s, Florence Nightingale (1820–1910) was writing about the importance of sunlight and copious amounts of fresh air in the recovery of hospital patients,26,27 but her ideas were slow to gain acceptance. And so it was in Germany that the open-air regimen reemerged, most notably at the Nordrach-Kolonie in the Black Forest, a sanatorium established in 1888 by Otto Walter (1853–1919). It was so well known that “Nordrach” became the term for open-air sanatoria. By 1908, there were at least 90 of them in Britain, many of which were enthusiastic imitations of Nordrach.28 An open-air recovery school for tubercular children, founded in 1904 at Charlottenburg, a suburb of Berlin, was the first of its type and, as with Germany's open-air sanatoria, was widely imitated.29 In 1884, Edward Livingston Trudeau (1848–1915) opened America's first sanatorium at Saranac Lake in New York State.30 The first open-air orthopedic hospital was set up in the Shropshire village of Baschurch in England in 1907.31 In the two decades before World War I, charitable associations, leagues, and societies dedicated to preventing and eliminating tuberculosis among the poor flourished, as did sanatoria.32

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    THE OPEN-AIR TREATMENT OF THE WOUNDED
    There is evidence that the open-air regimen may have improved the health of some tuberculosis patients. Records for the Dreadnought Hospital in Greenwich, one of the first British hospitals in which such methods were adopted, appear to show that there were benefits to this approach. From 1900 to 1905, the overall mortality of consumptive patients in open-air wards was less than half that of those who received the orthodox treatment of the day. An improvement in their state of “well-being” was also reported.33 Later, during World War I, the use of open-air therapy extended to nontubercular conditions, and on a large scale. Temporary open-air hospitals were built to take casualties from the Western Front.

    An early example stood on one of Cambridge University's best cricket pitches at the King's and Clare Athletic Ground. The First Eastern General Hospital, which was mobilized in August 1914, was originally designed to provide 520 beds and to be erected in 4 weeks. It proved so popular with the authorities, however, that within 8 weeks its complement of beds more than doubled to 1240. The hospital's wards were completely open to the south except for some low railings and adjustable sun blinds.34,35

    In June 1915, the eminent scientist and Master of Christ's College, A. E. Shipley (1861–1927), judged the open-air treatment of sick and wounded soldiers at the First Eastern a success, particularly for those with pneumonia. Some 6600 patients had passed through the hospital, with a death rate of 4.6 per 1000. Sixty patients with pneumonia had been treated, and 95% of them recovered. Critics ascribed the low mortality at the hospital to the absence of “bad cases,” but according to Shipley, some convoys arrived from the trenches almost entirely made up of them. In his opinion, the open wards produced much better results than closed ones. Instead of patients losing their bodily health and strength during the period of recovery from infections or wounds, they maintained their vigor and even improved it. The only people who felt the cold at the hospital were apparently the nurses, the patients having comfortable beds with plenty of blankets and hot-water bottles.35 Nearer the front, the British Army put its casualties in tents. As the military surgeon Lieutenant Colonel Sir Berkeley Moynihan observed in 1916,

    In the treatment of all gunshot wounds where the septic processes are raging, and the temperature varies through several degrees, an immense advantage will accrue from placing patients out of doors. While in France I developed a great affection for the tented hospitals. There is great movement of air, warmth and comfort; when a sunny day comes the side of the tent may be lifted and the patient enjoys the advantage of open-air treatment.”36(p337)



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    INFLUENZA AT THE CAMP BROOKS OPEN-AIR HOSPITAL
    When the influenza virus pandemic took hold in the United States in 1918, emergency hospitals were started in schools, halls, and large private houses, and open-air hospitals were being “thrown up” all over the country.1 In the harbor of East Boston, 1200 out of 5100 merchant sailors onboard training ships had contracted influenza. The seriously ill were too numerous for local hospitals to accommodate. The Massachusetts State Guard responded by building the Camp Brooks Open Air Hospital at Corey Hill in Brookline, near Boston.37,38 The hospital comprised 13 tents, 12 of which were occupied by one or two patients each and the other by the head nurse. The State Guard took seven hours to erect the tents, make sure the site was properly drained, and provide running water, latrines, and sewerage. Portable buildings were then set up for the medical staff and nurses. From the time the camp opened on September 9, 1918, until its closure a month later on October 12, a total of 351 victims of the pandemic were admitted, one third of whom were diagnosed with pneumonia. In total, 36 of the 351 sailors received at the hospital died.37

    The treatment at Camp Brooks Hospital took place outdoors, with “a maximum of sunshine and of fresh air day and night.”37(p1747) The medical officer in charge, Major Thomas F. Harrington, had studied the history of his patients and found that the worst cases of pneumonia came from the parts of ships that were most badly ventilated. In good weather, patients were taken out of their tents and put in the open. They were kept warm in their beds at night with hot-water bottles and extra blankets and were fed every few hours throughout the course of the fever. Anyone in contact with them had to wear an improvised facemask, which comprised five layers of gauze on a wire frame covering the nose and mouth. The frame was made out of an ordinary gravy strainer, shaped to fit the face of the wearer and to prevent the gauze filter from touching the nostrils or mouth. Nurses and orderlies were instructed to keep their hands away from the outside of the masks as much as possible. A superintendent made sure the masks were replaced every two hours, were properly sterilized, and contained fresh gauze.38

    Other measures to prevent infection included the wearing of gloves and gowns, including a head covering. Doctors, nurses, and orderlies had to wash their hands in disinfectant after contact with patients and before eating. The use of common drinking cups, towels, and other items was strictly forbidden. Patients’ dishes and utensils were kept separate and put in boiling water after each use. Pneumonia and meningitis patients used paper plates, drinking cups, and napkins; paper bags with gauze were pinned to pillowcases for sputum. Extensive use was made of mouthwash and gargle, and twice daily, the proprietary silver-based antimicrobial ointment Argyrol was applied to nasal mucous membranes to prevent ear infection.37

    Of the camp's medical staff—15 doctors, 45 nurses and aids, 20 sanitary corps men, and 74 sailors acting as orderlies—only six nurses and two orderlies developed influenza. In five of these cases, exposure to the virus was reported to have taken place outside the camp. A few medicines were used to relieve the patients’ symptoms and aid their recovery, but these were considered less important than were regular meals, warmth, and plenty of fresh air and sunlight.37

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    VENTILATION AND SUNLIGHT
    The curative effects of fresh air were investigated at length by the physiologist Sir Leonard Hill (1866–1952) in the years following World War I. He reported favorably on the effects of sun and air when judiciously applied, particularly for tuberculosis.39,40 In 1919, Hill wrote in the British Medical Journal that the best way to combat influenza infection was deep breathing of cool air and sleeping in the open.41 Whether the patients at Camp Brooks or other temporary hospitals were spared the worst of the influenza pandemic because they slept in the open is uncertain. The apparent success in reducing the number of infections and deaths reported at this open-air hospital may simply have been caused by patients and staff experiencing levels of natural ventilation far higher than in a conventional hospital ward. Significantly, the minimum amount of ventilation needed to prevent the spread of infectious diseases such as severe acute respiratory syndrome (SARS) and tuberculosis is unknown. Much more fresh air may be needed than is currently specified for hospitals, schools, offices, homes, and isolation rooms.4244

    The patients at Camp Brooks recovered in direct sunlight when available. This may have kept infection rates down, because laboratory experiments have shown that ultraviolet radiation inactivates influenza virus and other viral pathogens and that sunlight kills bacteria.4550 In addition, exposure to the sun's rays may have aided patients’ recovery, because sunlight is known to promote healing in other conditions such as septic war wounds.35 There is evidence that heart attack victims stand a better chance of recovery if they are in sunlit wards.51 Depressed psychiatric patients fare better if they get some sun while hospitalized, as do premature babies with jaundice.5255 In one study, patients in hospital wards exposed to an increased intensity of sunlight experienced less perceived stress and less pain and took 22% less analgesic medication per hour.56 One advantage of placing patients outside in the sun is that they can synthesize vitamin D in their skin, which they cannot do indoors behind glass. Rickets, the classic childhood disease of vitamin D deficiency, has long been associated with respiratory infections; it has been hypothesized that low levels of vitamin D may increase susceptibility to influenza.57,58

    The surgeon general of the Massachusetts State Guard, William A. Brooks, had no doubt that open-air methods were effective at the hospital, despite much opposition to the therapy. Many doctors felt that patients would get the same benefits if the windows of a conventional ward were open or the patients were put in a hospital “sun parlor.” Brooks, however, held that patients did not do as well in an ordinary hospital, no matter how well ventilated, as they did outdoors. Patients in indoor sun parlors were not exposed to direct sunlight all day as they were when outdoors. He reported that in one general hospital with 76 cases, 20 patients died within three days and 17 nurses fell ill.38 By contrast, according to one estimate, the regimen adopted at the camp reduced the fatality of hospital cases from 40% to about 13%.12 Brooks wrote that “The efficacy of open air treatment has been absolutely proven, and one has only to try it to discover its value.”38(p750)

    Coincidentally, in 1918 a British soldier, Patrick Collins, reached a similar conclusion. When Collins developed the first signs of influenza, he dragged himself and his tent up a hill away from his regiment. There he sweated, shivered, and was delirious for several days, sustained only by his rum ration. He was one of the few survivors of his regiment.59

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    DISCUSSION
    The seeming success of the medical team who confronted pandemic influenza on Corey Hill in 1918 was in stark contrast to others’ experience of the infection. The high standard of personal and environmental hygiene upheld by staff at the camp may have played a large part in the relatively low rates of infection and mortality there compared with other hospitals. Significantly, the outbreak of SARS in Hong Kong in 2003 showed that basic infection controls, such as those employed at Camp Brooks Hospital, can help to contain the spread of a virulent respiratory infection.60,61

    Of the measures introduced to combat pandemic influenza at the hospital, the use of improvised facemasks—including their design and the frequency with which they were changed—is noteworthy. Another is the fresh air the patients enjoyed. When Major Harrington, the medical officer at Camp Brooks, discovered that sailors from the most poorly ventilated areas of the ships in East Boston also had the worst cases of pneumonia, he put his patients outdoors. Sailors, such as those on board the ships at East Boston, were particularly vulnerable to influenza infection, because the influenza virus is readily transmitted in confined quarters. In 1977, for example, an influenza outbreak on board a commercial airliner with deficient ventilation resulted in an infection rate of 72%. The aircraft was grounded for over four hours with the passengers on board and the ventilation system turned off.62

    There is still much uncertainty surrounding the transmission and epidemiology of influenza. As yet, the proportion of influenza infections that occur by the airborne route is not known,63 nor is there any evidence to support the idea that fresh air helps those infected to recover. Given the threat to public health posed by the avian influenza virus, both merit further study. So too does the part played by sunlight in preventing the spread of the virus. Solar radiation may retard its transmission by directly inactivating virions and by increasing immunity to them. A combination of outdoor air and sunlight could also reduce the likelihood of secondary respiratory infections.

    The current H5N1 avian influenza virus has high virulence and lethality but as yet is not readily transmitted from person to person.64 We do not know how virulent the next type A pandemic will be, but should it prove to be as pathogenic as that of 1918, there could be 180 million to 360 million deaths globally.65 Vaccines, antiviral drugs, and antibiotics may be effective in controlling avian influenza and dealing with secondary infection; however, for much of the world's population, access to them will be limited. In many countries, the only viable strategy would be to disrupt the transmission of the virus by banning public gatherings, closing schools, isolating infected people, and wearing surgical masks, as was the case during the 1918–1919 pandemic.66,67

    Epidemiological studies show that the wearing of masks in public places in Hong Kong and Beijing during the SARS outbreak was associated with a lower incidence of infection.68,69 However, no controlled studies have been undertaken to assess the effectiveness of surgical masks in preventing influenza from passing from one host to the next.70 In addition, it is uncertain whether transmission of the influenza virus from person to person is chiefly by large droplets or aerosols. If droplets are the main mode of transmission, the isolation of patients in private rooms and the use of ordinary surgical face masks may suffice.63 If airborne transmission is significant, reusable respirators could be pivotal in preventing infection, because surgical masks do not offer reliable protection from aerosols.71,72 Also, measures that prevent the influenza virus from spreading through buildings would assume greater importance. Improvements in air-handling equipment, portable filtration units, and the introduction of physical barriers in the form of partitions or doors may offer some protection.73

    However, more might be gained by introducing high levels of natural ventilation or, indeed, by encouraging the public to spend as much time outdoors as possible. It might also be prudent to stockpile tents and beds, because hospitals in the United Kingdom, the United States, and elsewhere are not prepared for a severe pandemic.7480 Temporary accommodation would be required to deal with the most seriously ill, just as it was in 1918. The Camp Brooks Open Air Hospital might serve as a useful model.

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    References
    1. Crosby AW. America's Forgotten Pandemic: The Influenza of 1918. 2nd ed Cambridge, England: Cambridge University Press; 2003. [Google Scholar]
    2. Johnson NP, Mueller J. Updating the accounts: global mortality of the 1918–1920 “Spanish” influenza pandemic. Bull Hist Med. 2002;76:105–115. [PubMed] [Google Scholar]
    3. Johnson N. Britain and the 1918–19 Influenza Pandemic. A Dark Epilogue. Oxford, England: Routledge; 2006. [Google Scholar]
    4. Barry JM. The site of origin of the 1918 influenza pandemic and its public health implications. J Transl Med. 2004;2:3. [PMC free article] [PubMed] [Google Scholar]
    5. Morens DM, Fauci AS. The 1918 influenza pandemic: insights for the 21st Century. J Infect Dis. 2007;195:1018–1028. [PubMed] [Google Scholar]
    6. Barry JM. The Great Influenza: The Epic Story of the Greatest Pandemic in History. London, England: Penguin; 2005. [Google Scholar]
    7. French H. The clinical features of the influenza epidemic of 1918–19. : Great Britain Ministry of Health. Reports on Public Health and Medical Subjects No. 4: Report on the Pandemic of Influenza, 1918–19. London, England: His Majesty's Stationery Office; 1920: 66–109. [Google Scholar]
    8. Patterson KD. The influenza pandemic of 1918–19 in the Gold Coast. J Afr Hist. 1983;24:485–502. [PubMed] [Google Scholar]
    9. Mills ID. 1918–1919 influenza pandemic: the Indian experience. Indian Econ Soc Hist Rev. 1986;23:1–40. [PubMed] [Google Scholar]
    10. Cheng KF, Leung PC. What happened in China during the 1918 influenza pandemic? Int J Infect Dis. 2007;11:360–364. [PubMed] [Google Scholar]
    11. Tognotti E. Scientific triumphalism and learning from facts: bacteriology and the “Spanish flu” challenge of 1918. Soc Hist Med. 2003;16:97–110. [PubMed] [Google Scholar]
    12. Anon Weapons against influenza. Am J Public Health. 1918;8:787–788. [PMC free article] [PubMed] [Google Scholar]
    13. Starr I. Influenza in 1918: recollections of the epidemic in Philadelphia. 1976. Ann Intern Med. 2006;145: 138–140. [PubMed] [Google Scholar]
    14. Carnwath T. Lessons of the influenza pandemic 1918. J State Med. 1919;27:142–157. [Google Scholar]
    15. Schoch-Spana M. “Hospital's full-up”: the 1918 influenza pandemic. Public Health Rep. 2001;116(suppl 2): 32–33. [PMC free article] [PubMed] [Google Scholar]
    16. Markel H, Lipman HB, Navarro JA, et al. Nonpharmaceutical interventions implemented by US cities during the 1918–1919 influenza pandemic. JAMA. 2007;298:644–654. [PubMed] [Google Scholar]
    17. Hatchett RJ, Mecher CE, Lipsitch M. Public health interventions and epidemic intensity during the 1918 influenza pandemic. Proc Natl Acad Sci USA. 2007;104:7582–7587. [PMC free article] [PubMed] [Google Scholar]
    18. Bootsma MJ, Ferguson NM. The effect of public health measures on the 1918 influenza pandemic in US cities. Proc Natl Acad Sci USA. 2007;104: 7588–7593. [PMC free article] [PubMed] [Google Scholar]
    19. Halloran ME, Ferguson NM, Eubank S, et al. Modeling targeted layered containment of an influenza pandemic in the United States. Proc Natl Acad Sci USA. 2008;105:4639–4644. [PMC free article] [PubMed] [Google Scholar]
    20. St Clair Strange FG. The History of the Royal Sea Bathing Hospital Margate 1791–1991. Rainham, England: Meresborough Books; 1991. [Google Scholar]
    21. Jones ER. Lettsom and the Royal Sea Bathing Hospital. Trans Med Soc Lond. 1973;89:285–287. [PubMed] [Google Scholar]
    22. Bodington G. An Essay on the Treatment and Cure of Pulmonary Consumption, On Principles Natural, Rational and Successful. London, England: Simpkin, Marshall, Hamilton and Kent; 1906. [Google Scholar]
    23. Cyriax RJ. George Bodington: the pioneer of the sanatorium treatment of pulmonary tuberculosis. Br J Tuberc. 1925;19:1–16. [Google Scholar]
    24. Keers RY. Two forgotten pioneers—James Carson and George Bodington. Thorax. 1980;35:483–489. [PMC free article] [PubMed] [Google Scholar]
    25. McCarthy OR. The key to the sanatoria. J R Soc Med. 2001;94:413–417. [PMC free article] [PubMed] [Google Scholar]
    26. Nightingale F. Notes on Hospitals. 3rd ed London, England: Longman, Green, Longman, Roberts and Green; 1863. [Google Scholar]
    27. Nightingale F. Notes on Nursing; What It Is and What It Is Not. New York, NY: Dover Publications; 1969. [Google Scholar]
    28. Smith FB. The Retreat of Tuberculosis 1850–1950. London, England: Croom Helm; 1988. [Google Scholar]
    29. Connolly C. Pale, poor, and “pretubercular” children: a history of pediatric antituberculosis efforts in France, Germany, and the United States, 1899–1929. Nurs Inq. 2004;11:138–147. [PubMed] [Google Scholar]
    30. Mera FE. History of the sanatorium movement in America. Chest. 1935;1:8–9. [Google Scholar]
    31. Carter AJ. A breath of fresh air. Proc R Coll Physicians Edinb. 1994;24:397–405. [PubMed] [Google Scholar]
    32. Dormandy T. The White Death: A History of Tuberculosis. London, England: Hambledon Press; 1999. [Google Scholar]
    33. Cook GC. Early use of “open-air” treatment for “pulmonary phthisis” at the Dreadnought Hospital, Greenwich, 1900–1905. Postgrad Med J. 1999;75:326–327. [PMC free article] [PubMed] [Google Scholar]
    34. Anon A military open-air hospital. Br Med J. 1915;1:1015–1016. [Google Scholar]
    35. Shipley AE. The Open-Air Treatment of the Wounded (The First Eastern General Hospital). 2nd ed London, England: Country Life Library; 1915. [Google Scholar]
    36. Moynihan B. An address on the treatment of gunshot wounds. Br Med J. 1916;1:333–339. [PMC free article] [PubMed] [Google Scholar]
    37. Anon Influenza at the Camp Brooks Open Air Hospital. JAMA. 1918;71:1746–1747. [Google Scholar]
    38. Brooks WA. The open air treatment of influenza. Am J Public Health. 1918;8:746–750. [PMC free article] [PubMed] [Google Scholar]
    39. Hill AB, Hill B. The life of Sir Leonard Erskine Hill FRS (1866–1952). Proc R Soc Med. 1968;61:307–316. [PMC free article] [PubMed] [Google Scholar]
    40. Hill LE, Campbell A. Health and Environment. London, England: Edward Arnold & Co; 1925. [Google Scholar]
    41. Hill LE. The defence of the respiratory membrane against influenza, etc. Br Med J. 1919;1:238–240. [PMC free article] [PubMed] [Google Scholar]
    42. Li Y, Leung GM, Tang JW, et al. Role of ventilation in airborne transmission of infectious agents in the built environment—a multidisciplinary systematic review. Indoor Air. 2007;17:2–18. [PubMed] [Google Scholar]
    43. Tang JW, Li Y, Eames I, Chan PK, Ridgway GL. Factors involved in the aerosol transmission of infection and control of ventilation in healthcare premises. J Hosp Infect. 2006;64:100–114. [PMC free article] [PubMed] [Google Scholar]
    44. Escombe AR, Oeser CC, Gilman RH, et al. Natural ventilation for the prevention of airborne contagion. PLoS Med. 2007;4:e68. [PMC free article] [PubMed] [Google Scholar]
    45. Hollaender A, Oliphant JW. The inactivating effect of monochromatic ultraviolet radiation on influenza virus. J Bacteriol. 1944;48:447–454. [PMC free article] [PubMed] [Google Scholar]
    46. Tamm I, Fluke DJ. The effect of monochromatic ultraviolet radiation on the infectivity and hemagglutinating ability of the influenza virus type A strain PR-8. J Bacteriol. 1950;59:449–461. [PMC free article] [PubMed] [Google Scholar]
    47. Jensen MM. Inactivation of airborne viruses by ultraviolet irradiation. Appl Microbiol. 1964;12:418–420. [PMC free article] [PubMed] [Google Scholar]
    48. Jakab GJ, Knight ME. Decreased influenza virus pathogenesis by infection with germicidal UV-irradiated airborne virus. Environ Int. 1982;8:415–418. [Google Scholar]
    49. Sagripanti JL, Lytle CD. Inactivation of influenza virus by solar radiation. Photochem Photobiol. 2007;83:1278–1282. [PubMed] [Google Scholar]
    50. Hockberger PE. A history of ultraviolet photobiology for humans, animals and microorganisms. Photochem Photobiol. 2002;76:561–579. [PubMed] [Google Scholar]
    51. Beauchemin KM, Hays P. Dying in the dark: sunshine, gender, and outcomes in myocardial infarction. J R Soc Med. 1998;91:352–354. [PMC free article] [PubMed] [Google Scholar]
    52. Beauchemin KM, Hays P. Sunny rooms expedite recovery from severe and refractory depressions. J Affect Disord. 1996;40:49–51. [PubMed] [Google Scholar]
    53. Benedetti F, Colombo C, Barbini B, Campori E, Smeraldi E. Morning sunlight reduces length of hospitalization in bipolar depression. J Affect Disord. 2001;62:221–223. [PubMed] [Google Scholar]
    54. Dobbs RH, Cremer RJ. Phototherapy. Arch Dis Child. 1975;50:833–836. [PMC free article] [PubMed] [Google Scholar]
    55. Barss P, Comfort K. Ward design and jaundice in the tropics: report of an epidemic. Br Med J (Clin Res Ed). 1985;291:400–401. [PMC free article] [PubMed] [Google Scholar]
    56. Walch JM, Rabin BS, Day R, Williams JN, Choi K, Kang JD. The effect of sunlight on postoperative analgesic medication use: a prospective study of patients undergoing spinal surgery. Psychosom Med. 2005;67:156–163. [PubMed] [Google Scholar]
    57. Hobday RA. The Light Revolution: Health Architecture and the Sun. Forres, Scotland: Findhorn Press; 2006. [Google Scholar]
    58. Cannell JJ, Vieth R, Umhau JC, et al. Epidemic influenza and vitamin D. Epidemiol Infect. 2006;134:1129–1140. [PMC free article] [PubMed] [Google Scholar]
    59. Moriarty KJ. The 1918 influenza pandemic: a survivor's tale. BMJ. 2006;332:889. [Google Scholar]
    60. Chan WF, Wong TK. Preparing for pandemic influenza: revisit the basics. J Clin Nurs. 2007;16:1858–1864. [PubMed] [Google Scholar]
    61. Seto WH, Tsang D, Yung RW, et al. Advisors of Expert SARS Group of Hospital Authority. Effectiveness of precautions against droplets and contact in prevention of nosocomial transmission of severe acute respiratory syndrome (SARS). Lancet. 2003;361:1519–1520. [PMC free article] [PubMed] [Google Scholar]
    62. Moser MR, Bender TR, Margolis HS, Noble GR, Kendal AP, Ritter DG. An outbreak of influenza aboard a commercial airliner. Am J Epidemiol. 1979;110:1–6. [PubMed] [Google Scholar]
    63. Oshitani H. Potential benefits and limitations of various strategies to mitigate the impact of an influenza pandemic. J Infect Chemother. 2006;12:167–171. [PMC free article] [PubMed] [Google Scholar]
    64. Gambotto A, Barratt-Boyes SM, de Jong MD, Neumann G, Kawaoka Y. Human infection with highly pathogenic H5N1 influenza virus. Lancet. 2008;371:1464–1475. [PubMed] [Google Scholar]
    65. Osterholm MT. Preparing for the next pandemic. N Engl J Med. 2005;352:1839–1842. [PubMed] [Google Scholar]
    66. Toner E. Do public health and infection control measures prevent the spread of flu? Biosecur Bioterror. 2006;4:84–86. [PubMed] [Google Scholar]
    67. Low DE. Pandemic planning: non-pharmaceutical interventions. Respirology. 2008;13(suppl 1):S44–S48. [PubMed] [Google Scholar]
    68. Wu J, Xu F, Zhou W, et al. Risk factors for SARS among persons without known contact with SARS patients, Beijing, China. Emerg Infect Dis. 2004;10:210–216. [PMC free article] [PubMed] [Google Scholar]
    69. Lau JT, Tsui H, Lau M, Yang X. SARS transmission, risk factors, and prevention in Hong Kong. Emerg Infect Dis. 2004;10:587–592. [PMC free article] [PubMed] [Google Scholar]
    70. Bell DM, World Health Organization Writing Group. Non-pharmaceutical interventions for pandemic influenza, national and community measures. Emerg Infect Dis. 2006;12:88–94. [PMC free article] [PubMed] [Google Scholar]
    71. Tellier R. Review of aerosol transmission of influenza A virus. Emerg Infect Dis. 2006;12:1657–1662. [PMC free article] [PubMed] [Google Scholar]
    72. Weiss MM, Weiss PD, Weiss DE, Weiss JB. Disrupting the transmission of influenza A: face masks and ultraviolet light as control measures. Am J Public Health. 2007;97(suppl 1):S32–S37. [PMC free article] [PubMed] [Google Scholar]
    73. Morse SS, Garwin RL, Olsiewski PJ. Next flu pandemic: what to do until the vaccine arrives? Science. 2006;314:929. [PubMed] [Google Scholar]
    74. Bartlett JG. Planning for avian influenza. Ann Intern Med. 2006;145:141–144. [PubMed] [Google Scholar]
    75. Toner E, Waldhorn R, Maldin B, et al. Hospital preparedness for pandemic influenza. Biosecur Bioterror. 2006;4:207–217. [PubMed] [Google Scholar]
    76. Menon DK, Taylor BL, Ridley SA. Modelling the impact of an influenza pandemic on critical care services in England. Anaesthesia. 2005;60:952–954. [PubMed] [Google Scholar]
    77. Sobieraj JA, Reyes J, Dunemn KN, et al. Modeling hospital response to mild and severe influenza pandemic scenarios under normal and expanded capacities. Mil Med. 2007;172:486–490. [PubMed] [Google Scholar]
    78. Giacomet V, Tarallo L, De Marco G, Giannattasio A, Barbarino A, Guarino A. Preparing for an influenza pandemic in Italy: resources and procedures in paediatric hospital units. Euro Surveill. 2007;12:E7–E8. [PubMed] [Google Scholar]
    79. De Cauwer HG, Mortelmans LJ, d'Orio V. Are Belgian hospitals prepared for an H5N1-pandemic? Eur J Emerg Med. 2007;14:204–206. [PubMed] [Google Scholar]
    80. Brundage JF. Interactions between influenza and bacterial respiratory pathogens: implications for pandemic preparedness. Lancet Infect Dis. 2006;6:303–312. [PMC free article] [PubMed] [Google Scholar]


    The Open-Air Treatment of PANDEMIC INFLUENZA
     
  71. Very interesting. Thank you
     
  72. I live and work in NYC and my office will probaby reopen before June.

    I hope it will, because I can't afford to not work.

    Niacinamide doesn't pay for itself you know!
     
  73. No it certainly does not pay for itself! :)
    But yes, I have heard as well through my work that the medical offices I deliver for in NYC will start opening up again too.
     
  74. Excellent...had tuberculosis at the end of the WW2 and my grandmother saved my life...she used all these principles...now I understand what she did.
     
  75. I work in a dental office so if we assume that Covid19 is as deadly as they say it is, returning to work right now would not be wise.

    On the other hand, if the epidemic is being blown out of proportion by mass hysteria, I'd be ready to return to work today.

    Lol, when I Was younger my family subjected me to cupping therapy during a bad flu.

    I can't confirm if it worked, since I was too young to remember, but apparently I yelled and screamed because of the pain.
    [​IMG]