Revive Therapeutics Ltd (RVVTF)

[Ecomike]

In answer to your question let me make one thing clear first.

Too little active Vitamin in the blood and the Covid19 death rate was confirmed in the summer up in the NY area outbreak to be a 100% death rate.

People living up north in the winter, and with dark or black skin are chronically low in Vitamin D because of too too little sunlight on the skin, and due to the larger amounts of melanin in their skin that block the sun's UV light from being able to convert cholesterol in the skin into Vitamin D-3.

The point being if you have too little Vitamin D, and you get Covid19, you die.

But, that said, Vitamin D will NOT do what RVVTF's Bucillamine will do.

We know Bucillamine's benefits, that is why the FDA invited RVVTF to a phase III EUA trial to determine the best dosing, etc. for Covid19 infected people. They already know it is safe.

Vitamin D is available Over the counter as Vit D-2 or Vit D-3

Every one seems to agree D-3 is the way better version.

It is not the simple subject one might want to claim.

https://en.wikipedia.org/wiki/Category:Vitamin_D

In total, there are 5 different forms, D1 to D5. The most common ones are D2 and D3 (see images).

D3 (also called cholecalciferol) is the kind produced by the body. It is also found naturally in marine oils and in lanolin (oil from sheep's wool), the most common source for supplements.

D2 (also called ergocalciferol) is produced by fungi. It is similar to D3, but not exactly the same.
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Getting enough

D3 is made in the skin from cholesterol, and changed into a more active form by the liver. However, the skin will not make it unless enough ultraviolet light shines on it. As sunlight contains ultraviolet light, getting enough sun is one way of getting enough D3.

Many things can keep the skin from making enough D3. Winter sunlight may be too weak.

Melanin, which protects skin from damage, also keeps it from making D3, which is why people with darker skin are more prone to deficiency. Older people are also prone, because aging skin makes less D3, even with enough sunlight. Clothing, glass, sunscreens and sunblocks also shield the skin from getting enough ultraviolet light to make D3.
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Most of the medical profession is using >>50 year old BS data on Vit D, they have been vomiting out for >50 years as gospel.

But some of them are finally waking up. Every time I said to take 50 mg of Zinc and 5,000 to 10,000 IU of Vitamin D-3 pre and during Covid19 infections some university professor or self proclaimed expert would pick a futile battle me. My answer was:

For instance this year:
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"To reduce the risk of infection, it is recommended that people at risk of influenza and/or COVID-19 consider taking 10,000 IU/d of vitamin D3 for a few weeks to rapidly raise 25(OH)D concentrations, followed by 5000 IU/d. The goal should be to raise 25(OH)D concentrations above 40–60 ng/mL (100–150 nmol/L).Apr 2, 2020"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7231123/
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and in 2018:

This is the 2018 evidence I was sharing everywhere daily in March, before April article was published.
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6121423/

"Vitamin D generates many extraskeletal effects due to the vitamin D receptor (VDR) which is present in most tissues throughout the body. The possible role of vitamin D in infections is implied from its impact on the innate and adaptive immune responses.

A significant effect is also the suppression of inflammatory processes.

Because vitamin D could be acknowledged as a “seasonal stimulus”, as defined by R. Edgar Hope-Simpson, it would be crucial to prove it from a potential easy and cheap prophylaxis or therapy support perspective as far as influenza infections are concerned.

The survey of the literature data generates some controversies and doubts about the possible role of vitamin D in the prevention of influenza virus.

The most important point is to realise that the broad spectrum of this vitamin’s activity does not exclude such a possibility.

According to most of the authors, more randomized controlled trials with effective, large populations are needed to explore the preventive effect of vitamin D supplementation on viral influenza infections."



"Vitamin D comes from two sources: skin synthesis from the precursor—7-dehydrocholesterol—to cholecalciferol upon UVB radiation, and from the diet as cholecalciferol (D3) or ergocalciferol (D2).

Metabolic pathways (Figure 1), common for both forms, include: 25-hydroxylation to calcidiol (25(OH)D), which is carried by the liver enzymes CYP2R1 and CYP27A1 (cytochrome P450-associated 25-hydroxylases),

followed by 1a-hydroxylation to the active metabolite 1a,25–dihydroxyvitamin D3 (calcitriol, 1a,25(OH)2D),

catalysed by cytochrome P450-associated 25(OH)D(3)-1a-hydroxylase (CYP27B1), the enzyme present in the kidney but also in other extrarenal tissues, including immune cells [2,3,4].

Due to a developed feedback loop system, the metabolic activation of chole- and ergocalciferol and catabolic reactions are strictly regulated.

The positive regulators of 1a,25(OH)2D production are parathormone (PTH), secreted by parathyroid glands, and calcium level,

and the negative ones are phosphate level and fibroblast growth factor-23 (FGF-23).

All of them affect the activity of 1a-hydroxylase"

"Unlike the renal form, CYP27B1 present in the immune cells is not regulated by PTH, FGF-23, calcium, or phosphate signaling,

but is stimulated by cytokines such as tumour necrosis factor a (TNF a) and interferon (IFN?) [4,6].

In turn, CYP27B1 in keratinocytes is upregulated in response to injury and Toll-like receptor (TLR) activation [4].

Extrarenal expression of that enzyme may also be promoted by alternate pathogen recognition receptors (PRRs) [7].

Regulation of extrarenal 1a-hydroxylase is strongly dependent on the concentration of the circulating 25(OH)D"

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Please say all that three times real fast LOL.

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"As was found in recent years, polymorphism in some enzymes and proteins related to vitamin D, such as DBP, CYP28B1, CYP2R1, CYP24A1, or VDR (especially polymorphs FokI, TaqI, ApaI, and BsmI), [color=red]can affect the individual’s response to anti-infectious treatment, such as interferon/ribavirin therapy in chronic hepatitis C [13,14], susceptibility of the individuals to cancer, tuberculosis, ulcerative colitis, and Crohn’s disease, or the increased risk of type 1 diabetes,[/color] as was noted in European people"