(2 of 2) Chauss et al. studied Th1 cells from the lungs of hospitalised COVID-19 patients.
They found that the cells' intracine signaling system was being activated as it should be, with the 1-hydroxlase enzyme and VDR being produced in the cytosol. However, the whole system did not work, in that the cells remained stuck indefinitely in t…
(2 of 2) Chauss et al. studied Th1 cells from the lungs of hospitalised COVID-19 patients.
They found that the cells' intracine signaling system was being activated as it should be, with the 1-hydroxlase enzyme and VDR being produced in the cytosol. However, the whole system did not work, in that the cells remained stuck indefinitely in their pro-inflamamtory start-up program. They concluded that this was due largely or entirely to the cells not having enough 25-hydroxyvitamin D. There were no observations of these patient's circulating 25-hydroxyvitamin D levels, but it is well established (see research cited at: https://vitamindstopscovid.info/00-evi/) that those who suffer the worst outcomes with COVID-19 are, in general, those with the lowest 25-hydroxyvitamin D levels.
These people were hospitalised due to the virus getting into their lungs, rather than being stopped at the upper respiratory stage, which is what would normally occur if the immune system was working properly. In the lungs, most of the damage follows from the inflammatory immune responses, which damage endothelial cells there (those which line the blood vessels and capillaries, particulary in the oxygen and carbon dioxide exchange air sacs - alveoli). The body responds to the damaged blood vessels as if there was an injury, with loss of blood by making the blood hyper-coagulatory in an effort to plug the leaks. This hyper-coagulatory blood does most of the final harm, by causing micro-embolisms and larger clots in all organs: the lungs, heart, liver, kidneys, brain and spinal cord. The resulting organ damage and/or lack of oxygen, due to impaired exchange in the alveoli, especially due to these being flooded with fluid, is what kills most COVID-19 patients.
This cascade would never occur in most people if they had 50 ng/mL or more circulating 25-hydroxyvitamin D. Without proper vitamin D3 supplementation, most people have only a fraction of this, 1/10th to 1/2. So their immune systems cannot function properly. (There is very little vitamin D3 in food or multivitamins. It can be produced by UV-B irradiation of ideally white skin, but this is impossible for most people to obtain all year round, and it always damages DNA and so raises the risk of skin cancer.)
In clinical emergencies such as this, most doctors have no idea that lack of 25-hydroxyvitamin D is an easily correctable deficiency which must be reversed immediately. This is because they have never heard of 25-hydroxyvitamin D -> calcitriol intracrine signaling in immune cells. (A related paracrine signaling system involves some of the intracellularly produce calcitriol diffusing to nearby cells, where it affects their behaviour.)
No amount of vitamin C or any other treatment can compensate for the patient's 25-hydroxyvitamin D level being far below 50 ng/mL.
Supplementing ordinary healthy quantities of vitamin D3 (see Prof. Sunil Wimalawansa's recommendations: https://vitamindstopscovid.info/00-evi/#00-how-much) such as 0.125 mg (5000 IU) a day will raise 25-hydroxyvitamin D levels to 50 ng/mL, but this takes two months or so.
A loading (bolus = single, very large) dose of vitamin D3 such as 10 mg 400,000 IU for average weight adults will boost the 25-hydroxyvitamin D level over 50 ng/mL over several days. The delay is due to how long it takes the liver to hydroxylate it, with about 1/4 of the supplied vitamin D molecules becoming circulating 25-hydroxyvitamin D.
This treatment could have saved the lives of most of those who died from COVID-19, but there is a still better treatment: oral calcifediol.
For an average weight adult, 1 milligram of oral calcifediol (which _is_ 25-hydroxyvitamin D), raises the level of circulating 25-hydroxyvitamin D safely over 50 ng/mL in 4 hours or less. 25-hydroxyvitamin D is more easily absorbed than vitamin D3 since it has two hydrophilic hydroxyl groups,while vitamin D3 has only one. The calcifediol is well absorbed and goes straight into circulation.
Unfortunately, except in Spain, Italy and a few nearby countries, it is difficult for doctors to obtain calcifediol by the milligram. See the stunning success of this treatment in Castillo et al. 2020, cited and discussed at: https://vitamindstopscovid.info/00-evi/#castillo. Every doctor in the world should have known about this by late 2020.
This would have been an even more effective treatment for COVID-19 than bolus vitamin D3, since some of these hospitalised patients were fighting for their lives, and didn't have a few days to wait for bolus vitamin D3 to boost their circulating 25-hydroxyvitamin D level.
While the FLCCC COVID-19 protocols do recommend this calcifediol treatment (0.014 mg per kg body weight) with bolus vitamin D3 if this is not available, the FLCCC's sepsis protocol does not mention vitamin D.
Low 25-hydroxyvitamin D is the primary avoidable cause of the extreme weakness of desirable immune responses in sepsis and of the dysregulated, self-destructive, very high levels of cell-destroying inflammation which characterises this often deadly condition. Sepsis killed about 11 million people, worldwide, in 2017: https://www.thelancet.com/ journals/lancet/article/PIIS0140-6736(19)32989-7/ .
Please also see the research cited at: https://vitamindstopscovid.info/06-adv/ which shows that most people in developed countries, who are not infested with intestinal worms (helminths) have more intense, likely self-destructive, inflammatory responses, since helminths evolved compounds to downmodulate these responses which target them, and our ancestor's immune systems evolved to have stronger and stronger inflammatory responses, in an effort to counter the effects of ubiquitous infestation with one or more species of helminth.
(2 of 2) Chauss et al. studied Th1 cells from the lungs of hospitalised COVID-19 patients.
They found that the cells' intracine signaling system was being activated as it should be, with the 1-hydroxlase enzyme and VDR being produced in the cytosol. However, the whole system did not work, in that the cells remained stuck indefinitely in their pro-inflamamtory start-up program. They concluded that this was due largely or entirely to the cells not having enough 25-hydroxyvitamin D. There were no observations of these patient's circulating 25-hydroxyvitamin D levels, but it is well established (see research cited at: https://vitamindstopscovid.info/00-evi/) that those who suffer the worst outcomes with COVID-19 are, in general, those with the lowest 25-hydroxyvitamin D levels.
These people were hospitalised due to the virus getting into their lungs, rather than being stopped at the upper respiratory stage, which is what would normally occur if the immune system was working properly. In the lungs, most of the damage follows from the inflammatory immune responses, which damage endothelial cells there (those which line the blood vessels and capillaries, particulary in the oxygen and carbon dioxide exchange air sacs - alveoli). The body responds to the damaged blood vessels as if there was an injury, with loss of blood by making the blood hyper-coagulatory in an effort to plug the leaks. This hyper-coagulatory blood does most of the final harm, by causing micro-embolisms and larger clots in all organs: the lungs, heart, liver, kidneys, brain and spinal cord. The resulting organ damage and/or lack of oxygen, due to impaired exchange in the alveoli, especially due to these being flooded with fluid, is what kills most COVID-19 patients.
This cascade would never occur in most people if they had 50 ng/mL or more circulating 25-hydroxyvitamin D. Without proper vitamin D3 supplementation, most people have only a fraction of this, 1/10th to 1/2. So their immune systems cannot function properly. (There is very little vitamin D3 in food or multivitamins. It can be produced by UV-B irradiation of ideally white skin, but this is impossible for most people to obtain all year round, and it always damages DNA and so raises the risk of skin cancer.)
In clinical emergencies such as this, most doctors have no idea that lack of 25-hydroxyvitamin D is an easily correctable deficiency which must be reversed immediately. This is because they have never heard of 25-hydroxyvitamin D -> calcitriol intracrine signaling in immune cells. (A related paracrine signaling system involves some of the intracellularly produce calcitriol diffusing to nearby cells, where it affects their behaviour.)
No amount of vitamin C or any other treatment can compensate for the patient's 25-hydroxyvitamin D level being far below 50 ng/mL.
Supplementing ordinary healthy quantities of vitamin D3 (see Prof. Sunil Wimalawansa's recommendations: https://vitamindstopscovid.info/00-evi/#00-how-much) such as 0.125 mg (5000 IU) a day will raise 25-hydroxyvitamin D levels to 50 ng/mL, but this takes two months or so.
A loading (bolus = single, very large) dose of vitamin D3 such as 10 mg 400,000 IU for average weight adults will boost the 25-hydroxyvitamin D level over 50 ng/mL over several days. The delay is due to how long it takes the liver to hydroxylate it, with about 1/4 of the supplied vitamin D molecules becoming circulating 25-hydroxyvitamin D.
This treatment could have saved the lives of most of those who died from COVID-19, but there is a still better treatment: oral calcifediol.
For an average weight adult, 1 milligram of oral calcifediol (which _is_ 25-hydroxyvitamin D), raises the level of circulating 25-hydroxyvitamin D safely over 50 ng/mL in 4 hours or less. 25-hydroxyvitamin D is more easily absorbed than vitamin D3 since it has two hydrophilic hydroxyl groups,while vitamin D3 has only one. The calcifediol is well absorbed and goes straight into circulation.
Unfortunately, except in Spain, Italy and a few nearby countries, it is difficult for doctors to obtain calcifediol by the milligram. See the stunning success of this treatment in Castillo et al. 2020, cited and discussed at: https://vitamindstopscovid.info/00-evi/#castillo. Every doctor in the world should have known about this by late 2020.
This would have been an even more effective treatment for COVID-19 than bolus vitamin D3, since some of these hospitalised patients were fighting for their lives, and didn't have a few days to wait for bolus vitamin D3 to boost their circulating 25-hydroxyvitamin D level.
While the FLCCC COVID-19 protocols do recommend this calcifediol treatment (0.014 mg per kg body weight) with bolus vitamin D3 if this is not available, the FLCCC's sepsis protocol does not mention vitamin D.
Low 25-hydroxyvitamin D is the primary avoidable cause of the extreme weakness of desirable immune responses in sepsis and of the dysregulated, self-destructive, very high levels of cell-destroying inflammation which characterises this often deadly condition. Sepsis killed about 11 million people, worldwide, in 2017: https://www.thelancet.com/ journals/lancet/article/PIIS0140-6736(19)32989-7/ .
Please also see the research cited at: https://vitamindstopscovid.info/06-adv/ which shows that most people in developed countries, who are not infested with intestinal worms (helminths) have more intense, likely self-destructive, inflammatory responses, since helminths evolved compounds to downmodulate these responses which target them, and our ancestor's immune systems evolved to have stronger and stronger inflammatory responses, in an effort to counter the effects of ubiquitous infestation with one or more species of helminth.