Corona Virus How To Treat

managing

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Dr. Raoult--the French doctor in Marseilles whose research kicked off the hydroxychloroquine madness thinks everybody is doing it wrong. He insists that it should only be used early on in treatment. It works then do to its effects on iron metabolism. But everybody using it is using it only when patients get serious. And he insists that is a bad idea, due to its potential cardiovascular harm and immunosuppression.
 

Kray

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**** **** **** **** ****! Medium censored a good piece again. **** **** ****!
Your description of the runaway trucks and releasing prisoners is a great picture of the liberal state of mind, in places like California and New York!
 

Kray

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Interestingly, when I was sick this year with a lingering cough, I upped my use of vitamin C, methylene blue (making DHAA similar to apatone), and doxycycline. The cough did hang around for a few weeks, but there was only about 4 days or so where I felt really bad.

How do you know which of the 3 to attributed to your recovery? And has anyone determined that vitamin C supplementation is a good or bad thing with COVID?
 

tankasnowgod

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How do you know which of the 3 to attributed to your recovery? And has anyone determined that vitamin C supplementation is a good or bad thing with COVID?

Um, I don't. I've had success with Vitamin C in the past. It might have been that. It might have been the others. Might have been the combination. Might not have been any of them and it just passed on its own. I tend to think they all might have helped somewhat, however.
 

yerrag

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Your description of the runaway trucks and releasing prisoners is a great picture of the liberal state of mind, in places like California and New York!
Nice! But I was talking like the character of Jack Nicholson when the evil nurse put him in a straitjacket (in One Flew).
 

md_a

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The high mortality of old age is associated with a high concentration of iron in the tissues, just as the high mortality of young infants is associated with a high concentration of iron. As the infant's iron is diluted by growth, mortality decreases.
Infectious disease and leukemia, which have been associated with excess iron, are highest in childhood and old age. June Goodfield's book gives a nice summing up of the early research on the relation of iron metabolism to cancer and immunodeficiency:

"... in essence the immunological system has evolved with the ability to survey, and recognize, and utilize -I don't know exactly what. But this ability is expressed as a capacity to survey metals and, in particular, iron. It goes in as ferrous iron, and is then rapidly oxidized into ferric iron. This is then bound to a protein, transferrin, and so is carried into the bone marrow and thus given to the early red blood cells, which need it for the blood cycles. But Iron is also bound to a second protein, ferritin, which is a storage protein .... When red cells get old they break down in the spleen and are eaten up by the macrophages, which then make ferritin. (It enters the storage pool again.) Then there is the third protein, lactoferrin, which Is synthesized by polymorphs, the white cells, and is present in milk and in our secretions. The amount we excrete per day is absolutely minimal. You can only shove it in; you can't push It out. Now if, for some reason or other, there is too much iron around, the macrophages go and mop it up. And as far as I'm concerned, in the diseases we've been studying - Hodgkin's. leukemias - there is an abnormality in the lymph nodes and the macrophages in regard to the intake, or the handling, of the iron... I have a simple scheme, again probably too simple.
Lymphocytes go and are caught where there is an excess of iron. A malignant cell, like a virulent cell, behaves like a virulent bacterium. It becomes capable of sucking up iron avidly and utilizing it... if the tumor cells eat up the signal - iron – the lymphocytes won't go there. The tumor will grow undisturbed because the lymphocytes have not had a signal to move toward it.”

As I mentioned above, I think some of the excess iron accumulates in the form of age-pigment, and that this material serves to keep glycolysis running as an emergency energy source. Glycolysis produces lactic acid, which is characteristic of tumor metabolism even in the presence of oxygen, and lactic acid has its own direct effects on immunity. – Ray Peat ‘Mortality Again’
 

RealNeat

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The high mortality of old age is associated with a high concentration of iron in the tissues, just as the high mortality of young infants is associated with a high concentration of iron. As the infant's iron is diluted by growth, mortality decreases.
Infectious disease and leukemia, which have been associated with excess iron, are highest in childhood and old age. June Goodfield's book gives a nice summing up of the early research on the relation of iron metabolism to cancer and immunodeficiency:

"... in essence the immunological system has evolved with the ability to survey, and recognize, and utilize -I don't know exactly what. But this ability is expressed as a capacity to survey metals and, in particular, iron. It goes in as ferrous iron, and is then rapidly oxidized into ferric iron. This is then bound to a protein, transferrin, and so is carried into the bone marrow and thus given to the early red blood cells, which need it for the blood cycles. But Iron is also bound to a second protein, ferritin, which is a storage protein .... When red cells get old they break down in the spleen and are eaten up by the macrophages, which then make ferritin. (It enters the storage pool again.) Then there is the third protein, lactoferrin, which Is synthesized by polymorphs, the white cells, and is present in milk and in our secretions. The amount we excrete per day is absolutely minimal. You can only shove it in; you can't push It out. Now if, for some reason or other, there is too much iron around, the macrophages go and mop it up. And as far as I'm concerned, in the diseases we've been studying - Hodgkin's. leukemias - there is an abnormality in the lymph nodes and the macrophages in regard to the intake, or the handling, of the iron... I have a simple scheme, again probably too simple.
Lymphocytes go and are caught where there is an excess of iron. A malignant cell, like a virulent cell, behaves like a virulent bacterium. It becomes capable of sucking up iron avidly and utilizing it... if the tumor cells eat up the signal - iron – the lymphocytes won't go there. The tumor will grow undisturbed because the lymphocytes have not had a signal to move toward it.”

As I mentioned above, I think some of the excess iron accumulates in the form of age-pigment, and that this material serves to keep glycolysis running as an emergency energy source. Glycolysis produces lactic acid, which is characteristic of tumor metabolism even in the presence of oxygen, and lactic acid has its own direct effects on immunity. – Ray Peat ‘Mortality Again’

curious of your input on this thread. Coronavirus Infection – ACE2, UV, Tryptophan, And Hemoglobin Oxygen Binding
 

LeeLemonoil

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yomama

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[...]June Goodfield's book gives a nice summing up of the early research on the relation of iron metabolism to cancer and immunodeficiency[...]

Hello, what book if you do not mind? I would like to read more about that, thanks.
 

managing

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Ah, let it be so. Would’nt that be a Dream come true for us Peaters? Salicylates and Vitamin C protect you from Corona? And Vitamin D. And, Travis forbids, Bromelain
THe author has not been able to test any of them for C19. But statistically speaking, there should be dozens of them. Maybe more considering that many of them have visited hospitals where C19 patients are treated in recent months. When serological testing is available, I hope he will try to follow through on testing all 522. Presumably salicylates wouldn't prevent them from forming antibodies, even if it did prevent any symptoms from developing. I'd also like to see details on the salicylate therapies. Anybody know what/how they are used in IBD treatment?
 

kafkaz

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THe author has not been able to test any of them for C19. But statistically speaking, there should be dozens of them. Maybe more considering that many of them have visited hospitals where C19 patients are treated in recent months. When serological testing is available, I hope he will try to follow through on testing all 522. Presumably salicylates wouldn't prevent them from forming antibodies, even if it did prevent any symptoms from developing. I'd also like to see details on the salicylate therapies. Anybody know what/how they are used in IBD treatment?

E. g. Mesalamine (5-aminosalicylic acid/5-ASA): oral tablet/capsule delayed realase. Other dosage forms: rectal enema or suppository.
 

Kyle Bigman

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I've posted about two different hypotheses which are both about a bacterial/mycobacterial infection hiding behind COVID19 :
  1. The first one is about the fact that the virus could be able to infect both human cells and bacteria, making them more virulent. It seems like the spike protein of SARS-COV-2 has been found to have a mean of entry into bacteria like phages IIRC. He also think that it's weird that the test provide such high false negative rates which it should not. It's not really a secondary infection but more like a coinfection. He says that antibiotics seems to be more efficient than antivirals in this disease.
  2. The second one is from a doctor who finds "interesting" similarities between COVID19 and tuberculosis. China apparently has a big tuberculosis epidemy. There was also one discovered in Italy recently (but not at the same level than in China I guess). He also think that tuberculosis is behind the flu. He states that there exist fast-acting forms of tuberculosis (otherwise I think tuberculosis has a rather slow development). Tuberculosis spares young people juste like SARS-COV-2. There exist different form of mycobacteria (cell-wall deficient forms) which can't be seen/observed like regular bacteria (and that may be resistant to antibiotics which target bacteria "common" membranes) that's why we could be missing them. Finally, tuberculosis mycobacteria seems to harbor RNA-virus so that what could be the source of these "passenger" viruses. I may be missing some other facts as I write from memory.
Would doxycycline have any effect on mycobacteria? I have some lying around that wouldn't require me to go to the doctor for a prescription.
 
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I don't know what virus I had, but I was taking quite a lot of aspirin, cyproheptadine and vitamin C. It didn't stop me from being sick. Just one single data point, not worth much, but there it is. I was taking 2g - 3g aspirin per day.
 

Ledo

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Regarding the article
Ray Peat:
The article sounds to me like the ideas of students who have taken a pharmacology course in computer modeling of molecules; without an anchor to experiment, it’s perfectly useless. Iron and particulate pollution cause lung damage similar to the inflammation produced by the virus. Ventilating patients decreases their antiinflammatory CO2, making the inflammation worse. Acetaminophen, often given to patients, increases lung nitric oxide and damages red blood cells, adding to the harm done by treatment. The suggested treatments could aggravate the damage; for example, chloroquine increases nitric oxide. The angiotensin produced in response to the virus increases nitric oxide, and blocking that protects from the virus.
J Clin Invest. 1998 Aug 1; 102(3): 595–605.
Chloroquine stimulates nitric oxide synthesis in murine, porcine, and human endothelial cells.
D Ghigo, E Aldieri, R Todde, C Costamagna, G Garbarino, G Pescarmona, and A Bosia
Abstract
Nitric oxide (NO) is a free radical involved in the regulation of many cell functions and in the expression of several diseases. We have found that the antimalarial and antiinflammatory drug, chloroquine, is able to stimulate NO synthase (NOS) activity in murine, porcine, and human endothelial cells in vitro: the increase of enzyme activity is dependent on a de novo synthesis of some regulatory protein, as it is inhibited by cycloheximide but is not accompanied by an increased expression of inducible or constitutive NOS isoforms. Increased NO synthesis is, at least partly, responsible for chloroquine-induced inhibition of cell proliferation: indeed, NOS inhibitors revert the drug-evoked blockage of mitogenesis and ornithine decarboxylase activity in murine and porcine endothelial cells. The NOS-activating effect of chloroquine is dependent on its weak base properties, as it is exerted also by ammonium chloride, another lysosomotropic agent. Both compounds activate NOS by limiting the availability of iron: their stimulating effects on NO synthesis and inhibiting action on cell proliferation are reverted by iron supplementation with ferric nitrilotriacetate, and are mimicked by incubation with desferrioxamine. Our results suggest that NO synthesis can be stimulated in endothelial cells by chloroquine via an impairment of iron metabolism.
Sorry if already posted.

Here is an excellent rebuttal to the removed article.
Covid-19: Debunking the Hemoglobin Story
 

Kyle Bigman

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RealNeat

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I don't know what virus I had, but I was taking quite a lot of aspirin, cyproheptadine and vitamin C. It didn't stop me from being sick. Just one single data point, not worth much, but there it is. I was taking 2g - 3g aspirin per day.
Have you spoken to Ray about this?
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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