Covid 19: adjuvant approaches etc,

[WillBrink]

Just updated my article on the anti viral effects of lactoferrin:

https://brinkzone.com/lactoferrin-a-...um-anti-viral/

[P2Vaircrewman]

I keep acyclovir for cold sore treatment which is a form of the herpes virus. It is also used to treat shingles. No harm starting it at the first sign of covid.

[WillBrink]

All, another important paper that discusses iron dysregulation as a key aspect of the pathogensis of the tissue damage and death from covid, which I have been discussing since this all started (1) and continue to do so. While iron homeostasis may or may not be the key driver of the hyper immune cascade, ROS clearly is, and a year + into this, and papers piling up, not addressing that aspect is a huge blind spot in treatment. This paper does suggest “…iron chelators, ferroptosis inhibitors, hepcidin modulators and erythropoietin” as “promising therapeutic approach can be associated with drugs that specifically target extra and intracellular mitochondria dysfunction or even the reactive species interactome production and ferroptosis.”

However, per my (recently updated) article linked below (1), I strongly suspect ROS formation can mitigated via use of GSH, LF, NAC, etc. and that info needs to be disseminated.

Iron: Innocent bystander or vicious culprit in COVID-19 pathogenesis?

Int J Infect Dis. 2020 Aug; 97: 303–305.

Abstract
The coronavirus 2 (SARS-CoV-2) pandemic is viciously spreading through the continents with rapidly increasing mortality rates. Current management of COVID-19 is based on the premise that respiratory failure is the leading cause of mortality. However, mounting evidence links accelerated pathogenesis in gravely ill COVID-19 patients to a hyper-inflammatory state involving a cytokine storm. Several components of the heightened inflammatory state were addressed as therapeutic targets. Another key component of the heightened inflammatory state is hyper-ferritinemia which reportedly identifies patients with increased mortality risk. In spite of its strong association with mortality, it is not yet clear if hyper-ferritinemia in COVID-19 patients is merely a systemic marker of disease progression, or a key modulator in disease pathogenesis. Here we address implications of a possible role for hyper-ferritinemia, and altered iron homeostasis in COVID-19 pathogenesis, and potential therapeutic targets in this regard.

Full paper:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7264936/

(1) https://brinkzone.com/life-saving-st...complications/

[P2Vaircrewman]

As luck would have it I am taking both a statin and PCSK9. My TC is 90

https://pubmed.ncbi.nlm.nih.gov/33333472/

I also take Losartan an angiotensin II antagonist.

https://pubmed.ncbi.nlm.nih.gov/32645228/

[WillBrink]

As luck would have it I am taking both a statin and PCSK9. My TC is 90

https://pubmed.ncbi.nlm.nih.gov/33333472/

I also take Losartan an angiotensin II antagonist.

https://pubmed.ncbi.nlm.nih.gov/32645228/

Interesting papers. I knew about angiotensin II antagonists, didn't read much on statins in that application.

[WillBrink]

Great vid from Dr. John Campbell on recent study on vite D levels rates of hospitalizations. His is one a handful of channels I recommend of science based objective info on all things covid related:



For those who say it's correlational, here's a recent RCT of interest:

https://www.sciencedirect.com/scienc...764?via%3Dihub

[Arik]

Great vid from Dr. John Campbell on recent study on vite D levels rates of hospitalizations. His is one a handful of channels I recommend of science based objective info on all things covid related:



For those who say it's correlational, here's a recent RCT of interest:

https://www.sciencedirect.com/scienc...764?via%3Dihub

Had mine checked back in May. Was at 55

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[WillBrink]

Had mine checked back in May. Was at 55

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Good deal. Amazing how few even get that checked.

[Arik]

Good deal. Amazing how few even get that checked.

It was just coincidence that started a few years ago. My doctor noticed I had low D, like 12 nmol. So had me take supplements, I think it was only like 2000 IU. The next year it went up 23 nmol or so. I started taking 3500 IU without recommendations and by next year I was in the mid 30s nmol. Then covid hit and I did some research and found out that it's really really hard to OD on vD so I started taking more. Right now I take 8000 IU and have been for about a 6 months.

I know somewhere I'm getting my IU wrong because originally I was buying 1000 IU bottles then switched to 2000 but since about Christmas time I've been taking 4x2000 IU daily.

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[WillBrink]

It was just coincidence that started a few years ago. My doctor noticed I had low D, like 12 nmol. So had me take supplements, I think it was only like 2000 IU. The next year it went up 23 nmol or so. I started taking 3500 IU without recommendations and by next year I was in the mid 30s nmol. Then covid hit and I did some research and found out that it's really really hard to OD on vD so I started taking more. Right now I take 8000 IU and have been for about a 6 months.

I know somewhere I'm getting my IU wrong because originally I was buying 1000 IU bottles then switched to 2000 but since about Christmas time I've been taking 4x2000 IU daily.

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5k IU seems to be the starting dose for most, 10 even 20k IU, not uncommon to get levels where needed, and there's racial differences there also. Best way to dose, always, is via labs, or it's all a WAG. Best article on that topic:

https://brinkzone.com/vitamin-d-what...to-achieve-it/