MORTALITY FROM COVID-19 INCREASES WITH UNSATURATED FAT

Jam

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MORTALITY FROM COVID-19 INCREASES WITH UNSATURATED FAT, AND MAY BE REDUCED BY EARLY CALCIUM AND ALBUMIN SUPPLEMENTATION

- Hypocalcemia, hypoalbuminemia occur early during severe COVID-19

- UFAs cause MSOF, inflammation resembling severe COVID-19

- Mortality from COVID-19 correlates with dietary unsaturated fat intake, while saturated fat is protective.

- SFAs in triglycerides impede interaction with ATGL

- UFAs injure and impede cell functions; albumin binding prevents but does not reverse injury

- Thus early supplementation with albumin and calcium maybe better than correcting deficiencies later
during severe COVID-19 infection or sepsis, which may be too little too late.
 

LLight

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Unexpected free fatty acid binding pocket in the cryo-EM structure of SARS-CoV-2 spike protein

"The present study reveals that SARS-CoV-2 comprises a FFA-binding pocket that specifically accretes LA, and suggests that this could be a feature shared with SARS-CoV and MERS-CoV.
The high affinity, high specificity LA scavenger function conveyed by our results could confer a tissue-independent mechanism by which pathogenic coronavirus infection drives immune dysregulation and inflammation."​
 

orewashin

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Unexpected free fatty acid binding pocket in the cryo-EM structure of SARS-CoV-2 spike protein

"The present study reveals that SARS-CoV-2 comprises a FFA-binding pocket that specifically accretes LA, and suggests that this could be a feature shared with SARS-CoV and MERS-CoV.
The high affinity, high specificity LA scavenger function conveyed by our results could confer a tissue-independent mechanism by which pathogenic coronavirus infection drives immune dysregulation and inflammation."​
So that means when LA takes up the same binding spot as the virus, it's released as an unbound form and causes replication and damage?
 

LLight

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So that means when LA takes up the same binding spot as the virus, it's released as an unbound form and causes replication and damage?

I'm not sure how to interpret that.

Is Covid virus protecting cells from LA by scavenging it?
 

michael94

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I'm not sure how to interpret that.

Is Covid virus protecting cells from LA by scavenging it?
Very interesting so the Sars Covid virus has pockets to bind for LA ( 3 I think they said ), and the researchers make note that the binding is highly specific for LA.

I'm not really clear what they are saying the virus uses the LA for, they say lipid metabolome remodeling, and that it was LA -> AA (Arachidonic Acid) as the main pathway. So maybe the virus uses LA to alter cell membranes and other bodily structures/functions by creating AA? The researchers say significant changes in cell signaling are expected from altering LA to AA which I'm sure is true.
 

maillol

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Good find. I've just came across this. Looks like the root problem/danger may just be excessive fatty acid metabolism like almost everything else. It's not surprising diabetics are at greater risk. They have had success treating covid with BTK inhibitors recently.

Study identifies potential approach to treat severe respiratory distress in patients with COVID-19
Early data from a clinical study suggest that blocking the Bruton tyrosine kinase (BTK) protein provided clinical benefit to a small group of patients with severe COVID-19.

They used a drug called acalabrutinib in the study above but ibrutinib is another BTK inhibitor and I found the following study about it.

Bruton’s tyrosine kinase is at the crossroads of metabolic adaptation in primary malignant human lymphocytes | Scientific Reports
Recently, the inhibition of free fatty acid synthesis induced by ibrutinib was reported. Notably, ibrutinib-resistant CLL lymphocytes were re-sensitized to ibrutinib by the combination of a fatty acid metabolism inhibitor and ibrutinib in vitro, confirming the connection of BTK signaling and fatty acid metabolism regulation.

The fatty acid metabolism inhibitor mentioned in the above study was etomoxir which is similar to mildronate. I would guess niacinamide could substitute.
 

Fred

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Since the PCR test used to diagnose Covid-19 has never been demonstrated to be even remotely accurate, how do the researchers know that they were studying actual covid-19 patients (if they even exist)?
Science is dead.
 

maillol

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Since the PCR test used to diagnose Covid-19 has never been demonstrated to be even remotely accurate, how do the researchers know that they were studying actual covid-19 patients (if they even exist)?
Science is dead.
I'm not quite confident enough to commit to the theory that they don't exist but I would agree that inhibiting fatty acid metabolism would help almost anything.
 

Fred

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I'm not quite confident enough to commit to the theory that they don't exist but I would agree that inhibiting fatty acid metabolism would help almost anything.

False positives could be 80% or more, for all we know. Ray talked about how the DNA/RNA from exosomes (which we all have), or stray viruses, etc. could trigger the test in his interview with Patrick Timpone a few days ago.
 

Fred

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Severe SAR-CoV-2 infection in humans is defined by a shift in the serum lipidome resulting in dysregulation of eicosanoid immune mediators

https://www.researchhub.com/paper/818044/summary

The opening line of the paper ... "The COVID-19 pandemic has affected more than 10 million people worldwide with mortality exceeding 3 half a million patients" is KNOWN to be unsubstantiated poppycock. The test has not been shown to be even remotely accurate, and there are no specific symptoms allowing for clinical diagnosis. I would dismiss this paper on those grounds, as they obviously made no attempt to ensure that they were studying patients with the same condition.
 
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