PUFA metabolites (prostaglandins) drive "flu" pathology

haidut

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A highly relevant study in light of the recent (and apparently, still ongoing) COVID-19 pandemic, which not only casts doubt on the official story about how infectious disease develops, but also its treatments and public health response. The study below demonstrated that prostaglandins - the PUFA metabolites through the cyclooxygenase (COX) pathway - are the main signal through which the brain recognizes the presence of a viral respiratory infection. The study used the influenza virus for its experiments, but states that its findings are likely applicable to all other respiratory infection viruses, including SARS-CoV-2. The more prostaglandins synthesized, the more severe the immune response of the host, up to the point of developing the (in)famous cytokine storm, multi-organ failure and even death. Conversely, blocking prostaglandin effects at the receptor or reducing their synthesis greatly reduced symptoms of a viral infection, as well as risk for organ damage and mortality. In other words, what we call the "flu" may be nothing more than a symptom of PUFA overload, and the degree of that overload determines the course of the viral infection. This finding matches the common observation that children - who have much lower PUFA stores than adults - get the flu (and other viral infections) much less often than adults and when they do get sick their disease course is almost always milder, which translates to lower mortality as well. Thus, the study directly suggests that the focus of public health authorities should not be on any specific viral pathogen or a vaccine for it, but on the food supply chain and availability of cheap, safe drugs that reduce prostaglandin synthesis. The classic example of such a prostaglandin-reducing (COX inhibitor) agent is, of course, aspirin. The study used the HED of 1.5 mg/kg bw daily dosage and that increased survival from 30% (control group) to 70% (aspirin group) in influenza-infected animals. The findings of this study also contradict the common medical warning to not use aspirin in viral infections (especially in flu cases) due to risks of developing so-called Reye syndrome. That warning has never been backed by actual evidence, yet it remains widely known among health practitioners and most adults have probably heard it from their doctor(s) either in regards to their own disease or flu infections in their children. As has become customary over the last 2-3 decades such warnings turn out to be nothing more than fear-mongering due to either incompetence or, worse, malicious intent to smear aspirin (as has been the case for its use in heart disease, stroke, dementia, etc). As far as food - the study suggests that limiting PUFA intake and/or administering anti-lipolysis drugs would be another important step towards limiting the impact of viral pandemics on the population, and their combination with aspirin would be even more effective than either agent alone. Luckily, aspirin also happens to reduce excess lipolysis! Finally, the study also throws into question the very concept of "infectious" disease, since older studies with PUFA-depleted animals demonstrate the near-impossibility to get them infected with any virus (and especially the influenza family), and even when infected they were near-impossible to kill regardless of the viral load they got injected with. In other words, it is not the virus that kills, but the host's reaction to it, and PUFA is a core component of that (negative) reaction that is responsible for the totality of symptoms/pathology we know as the "flu".

An airway-to-brain sensory pathway mediates influenza-induced sickness - Nature
How the Brain Senses Infection

"...Importantly, he found that these neurons are necessary to signal to the brain that a flu infection is present and have receptors for lipids called prostaglandins. These lipids are made by both mice and humans during an infection, and they are targeted by drugs such as ibuprofen and aspirin. Cutting the glossopharyngeal nerve, eliminating the neurons, blocking the prostaglandin receptors in those neurons, or treating the mice with ibuprofen similarly reduced influenza symptoms and increased survival. Together, the findings suggest that these airway neurons detect the prostaglandins made during a flu infection and become a communication conduit from the upper part of the throat to the brain. “We think that these neurons relay the information that there’s a pathogen there and initiate neural circuits that control the sickness response,” Liberles said. The results provide an explanation for how drugs like ibuprofen and aspirin work to reduce flu symptoms — and suggest that these drugs may even boost survival. "
 

PopSocket

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Interesting study that puts a dent in the germ theory of disease and shows how important the terrain is.

Could the flu be just a detoxification strategy of the body to get rid of PUFA and other stored toxins ? Maybe sometimes the process gets of out control due to tissues being too unstable and a chain reaction occurs leading to severe organ damage and death rather than a virus actually attacking the organism ?

Same goes for autoimmune issues that seem to be caused by PUFA and their metabolites release. Corticosteroids seem to be cox inhibitos while drugs like methotraxate are indirect cox inhibitors by killing the B cells that activate COX thus keeping the organism in "remission" while eventually too much PUFA is stored which leads to cancer and other complications ?

Wonder what your thoughts are on this.
 

AlaskaJono

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@haidut Très Bien! Wow, what a find. Thank you for your scrolling service to humanity, in all seriousness. My impatience as well as lack of science background allows me to get a general understanding of the article, and appreciate your 'quick translation' into more plain speak with light science-ee words. :): Also they mention the PCR used with the virus proteins in the study, makes me wonder if the "v" proteins are the virus?, something to that effect.

I was just wondering the last few days how Australians got so fat, and obese too, in just the last 20 years. In general there is no corn syrup aspect to the diet, but most other 'bad' ingredients are present. GMO grains, pufa oils for cooking, and fast food is quite prevalent. Again, the most popular oil for deep fried foods - supa popular here - is cottonseed oil. I have been coming to Australia on and off for 30 years, and lived here for the last 8 years. So I have noticed the differences in overweight people from the USA, and Australia, and how they are catching up in the HEAVINESS factor. I just can't eat that sh*te.

From the internet: “Throughout Australia, farmers work year-round to grow the crops that produce nutritious, easy-to-use cooking oils. In summer, sunflower seeds, cottonseed and soy beans are harvested in Queensland and northern New South Wales. Canola – our winter bounty – is grown throughout Western Australia, South Australia, Victoria and New South Wales."

It is not out of economics, but appears to be by design. Organic GMO seed oils anyone?
 
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Regina

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A highly relevant study in light of the recent (and apparently, still ongoing) COVID-19 pandemic, which not only casts doubt on the official story about how infectious disease develops, but also its treatments and public health response. The study below demonstrated that prostaglandins - the PUFA metabolites through the cyclooxygenase (COX) pathway - are the main signal through which the brain recognizes the presence of a viral respiratory infection. The study used the influenza virus for its experiments, but states that its findings are likely applicable to all other respiratory infection viruses, including SARS-CoV-2. The more prostaglandins synthesized, the more severe the immune response of the host, up to the point of developing the (in)famous cytokine storm, multi-organ failure and even death. Conversely, blocking prostaglandin effects at the receptor or reducing their synthesis greatly reduced symptoms of a viral infection, as well as risk for organ damage and mortality. In other words, what we call the "flu" may be nothing more than a symptom of PUFA overload, and the degree of that overload determines the course of the viral infection. This finding matches the common observation that children - who have much lower PUFA stores than adults - get the flu (and other viral infections) much less often than adults and when they do get sick their disease course is almost always milder, which translates to lower mortality as well. Thus, the study directly suggests that the focus of public health authorities should not be on any specific viral pathogen or a vaccine for it, but on the food supply chain and availability of cheap, safe drugs that reduce prostaglandin synthesis. The classic example of such a prostaglandin-reducing (COX inhibitor) agent is, of course, aspirin. The study used the HED of 1.5 mg/kg bw daily dosage and that increased survival from 30% (control group) to 70% (aspirin group) in influenza-infected animals. The findings of this study also contradict the common medical warning to not use aspirin in viral infections (especially in flu cases) due to risks of developing so-called Reye syndrome. That warning has never been backed by actual evidence, yet it remains widely known among health practitioners and most adults have probably heard it from their doctor(s) either in regards to their own disease or flu infections in their children. As has become customary over the last 2-3 decades such warnings turn out to be nothing more than fear-mongering due to either incompetence or, worse, malicious intent to smear aspirin (as has been the case for its use in heart disease, stroke, dementia, etc). As far as food - the study suggests that limiting PUFA intake and/or administering anti-lipolysis drugs would be another important step towards limiting the impact of viral pandemics on the population, and their combination with aspirin would be even more effective than either agent alone. Luckily, aspirin also happens to reduce excess lipolysis! Finally, the study also throws into question the very concept of "infectious" disease, since older studies with PUFA-depleted animals demonstrate the near-impossibility to get them infected with any virus (and especially the influenza family), and even when infected they were near-impossible to kill regardless of the viral load they got injected with. In other words, it is not the virus that kills, but the host's reaction to it, and PUFA is a core component of that (negative) reaction that is responsible for the totality of symptoms/pathology we know as the "flu".

An airway-to-brain sensory pathway mediates influenza-induced sickness - Nature
How the Brain Senses Infection

"...Importantly, he found that these neurons are necessary to signal to the brain that a flu infection is present and have receptors for lipids called prostaglandins. These lipids are made by both mice and humans during an infection, and they are targeted by drugs such as ibuprofen and aspirin. Cutting the glossopharyngeal nerve, eliminating the neurons, blocking the prostaglandin receptors in those neurons, or treating the mice with ibuprofen similarly reduced influenza symptoms and increased survival. Together, the findings suggest that these airway neurons detect the prostaglandins made during a flu infection and become a communication conduit from the upper part of the throat to the brain. “We think that these neurons relay the information that there’s a pathogen there and initiate neural circuits that control the sickness response,” Liberles said. The results provide an explanation for how drugs like ibuprofen and aspirin work to reduce flu symptoms — and suggest that these drugs may even boost survival. "
Awesome findings!! Thx!
 

GTW

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Hormesis: too much and too little can be harmful.
Also, Omega 3 and Omega 6 prostaglandins have different effects.
Furthermore, specific Omega 3 and Omega 6 PUFA are essential\necessary for cell membrane function.
 
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haidut

haidut

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Could the flu be just a detoxification strategy of the body to get rid of PUFA and other stored toxins ?

Yep, this has been a hypothesis for a long time, and of course rabidly rejected by mainstream medicine. I think the main hypothesis is that viral infections take hold when there is a bacterial build up, which matches well with the endotoxin (TLR receptors) presented in this article. There is also Phage-Therapy, which is basically using viruses to destroys bacteria. I think a PUFA clearance mechanism is also plausible but that is probably what "autoimmune" conditions are - the body keeps trying to get rid of specific oran/tissue b/c it is probably very inflamed and stuffed with PUFA/prostaglandins. There is also the possibility that viruses may act in some cases like oxidizing agents (similar to quinones) so a sick organism (in reductive stress) would be more likely to get a viral "infection" as a form of trying to get rid itself of the excess electrons.
The glucocorticoids are really a Trojan horse, as they set up the organism for much higher inflammation upon stopping them, so that means either lifelong use (bad) or higher inflammation than before using them (also bad). There is no reason to use them considering a combination of pregnenolone or progesterone and aspirin would probably be better at controlling inflammation while also having reparative effect on the organ/tissue and the organism as a whole.
 
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haidut

haidut

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cottonseed oil

That oil is probably the most nefarious and explains a lot of the obesity epidemic. It is not only full of PUFA but also contains a substance that has direct sterilizing effects on males and female by suppressing their gonadal function, and hypogonadism (similarly to hypothyroidism) is a well-known cause of obesity even in people eating quality food.
 

DennisX

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That oil is probably the most nefarious and explains a lot of the obesity epidemic. It is not only full of PUFA but also contains a substance that has direct sterilizing effects on males and female by suppressing their gonadal function, and hypogonadism (similarly to hypothyroidism) is a well-known cause of obesity even in people eating quality food.
The quoted article also said
“The researchers discovered evidence of another potential sickness pathway, this one traveling from the lungs to the brain. They found that it appears to become active in the second phase of infection as the virus infiltrates deeper into the respiratory system.

This additional pathway doesn’t involve prostaglandins, the team was surprised to find. Mice in the second phase of infection didn’t respond to ibuprofen.”

which says if the flu virus gets into your lungs aspirin is of no help and puffs is not involved.
 
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haidut

haidut

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The quoted article also said
“The researchers discovered evidence of another potential sickness pathway, this one traveling from the lungs to the brain. They found that it appears to become active in the second phase of infection as the virus infiltrates deeper into the respiratory system.

This additional pathway doesn’t involve prostaglandins, the team was surprised to find. Mice in the second phase of infection didn’t respond to ibuprofen.”

which says if the flu virus gets into your lungs aspirin is of no help and puffs is not involved.

True, but in order for the virus to reach this second stage, the first stage is required, so the PUFA/aspirin angle are still key for prevention and early treatment. Also, once the virus reaches the lungs then the person develops bacterial pneumonia, so the virus becomes irrelevant and antibiotics are needed. Not sure how the initial viral infection enables the subsequent bacterial pneumonia, but this is what happened with many people having COVID-19 and why antibiotics eventually became part of the protocol against severe COVID-19.
 

DennisX

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True, but in order for the virus to reach this second stage, the first stage is required, so the PUFA/aspirin angle are still key for prevention and early treatment. Also, once the virus reaches the lungs then the person develops bacterial pneumonia, so the virus becomes irrelevant and antibiotics are needed. Not sure how the initial viral infection enables the subsequent bacterial pneumonia, but this is what happened with many people having COVID-19 and why antibiotics eventually became part of the protocol against severe COVID-19.
True but if the virus is covid then ivermectin and/or Hydroxychloroquine are more effective in phase 1 and perhaps effective in phase 2.
 

aliml

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GABRA1 neurons provide an airway–brain communication route.
Gamma-aminobutyric acid receptor subunit alpha-1 is a protein that in humans is encoded by the GABRA1 gene. The GABRA1 receptor is the specific target of the z-drug class of nonbenzodiazepine hypnotic agents and is responsible for their hypnotic and hallucinogenic effects.
Benzodiazepines increase vulnerability to infection through alpha-1 subunit dependent gamma-amino-butyric-type-A (GABAA) signalling.
Here, we assessed whether clinically applicable GABA-R agonists could be repurposed for the treatment of a lethal coronavirus (murine hepatitis virus 1, MHV-1) infection in mice. We found that oral GABA administration before, or after the appearance of symptoms, very effectively limited MHV-1-induced pneumonitis, severe illness, and death. GABA treatment also reduced viral load in the lungs, suggesting that GABA-Rs may provide a new druggable target to limit coronavirus replication.
 
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