Downing goes on to cite research and supporting data. Among them is a study from the Philippines, which found that for each standard deviation increase in serum vitamin D, the odds of experiencing only mild disease rather than severe illness was 7.94 times greater, and the odds of having a mild clinical outcome rather than a critical outcome was 19.61 times greater. According to the author:
"The results suggest that an increase in serum 25(OH)D level in the body could either improve clinical outcomes or mitigate worst (severe to critical) outcomes, while a decrease in serum 25(OH)D level in the body could worsen clinical outcomes of COVID-2019 patients."
Another study3 from Indonesia, which looked at data from 780 COVID-19 patients, found those with a vitamin D level between 20 ng/mL (50 nmol/L) and 30 ng/mL (75 nmol/L) had a sevenfold higher risk of death than those with a level above 30 ng/mL. Having a level below 20 ng/mL was associated with a 12 times higher risk of death. As noted by Downing:4
"With a deficient vitamin D status (<50nmol/L) the mortality rate from COVID-19 was 98.8% against 4.1% with adequate vitamin D (>75nmol/L). The Hazard Ratio is 24.1 … A Hazard Ratio of 4 means that in one condition, for instance vitamin D deficiency, you are 4 times more likely to suffer the 'hazard' than in another condition, say vitamin D adequacy."
A third paper,5 which provides data from 20 European countries, also found that "the probability of developing COVID-19, and of dying from it, is negatively correlated with mean population vitamin D status, with both probabilities reaching zero above about 75 nmol/L," (30 ng/mL) Downing notes.6
A vitamin D3 blood level of at least 75 nmol/L (30 ng/ml) is needed for protection against COVID-19.
In their preprint submission of this paper,7 the authors concluded, "We believe that we can advise vitamin D supplementation to protect against SARS-CoV2 infection." Downing created the following graph8 to illustrate the data in that paper.
Downing also addresses the issue of dosage and safety, highlighting how warnings about "excessive vitamin D intakes" being dangerous are very misleading and unwarranted, as toxicity has not been demonstrated until you hit blood levels above 200 ng/mL (500 nmol/L).
The recommended blood level for optimal health is currently between 60 ng/mL (150 nmol/L) and 80 ng/mL (200 nmol/L). In other words, there's a significant margin of safety, even if you manage to exceed the optimal range.
"The three papers9,10 mentioned above show that a vitamin D3 blood level of at least 75 nmol/L (30 ng/ml) is needed for protection against COVID-19," Downing writes.11
"Government recommendations for vitamin D intake — 400 IU/day for the UK and 600 IU/day for the USA (800 IU for >70 years) and the EU — are based primarily on bone health. This is woefully inadequate in the pandemic context.
An adult will need to take 4,000 IU/day of vitamin D3 for three months to reliably achieve a 75 nmol/L level.12 Persons of color may need twice as much.13 These doses can reduce the risk of infection, but are not for treatment of an acute viral infection.
And since vitamin D is fat-soluble and its level in the body rises slowly, for those with a deficiency, taking an initial dose of 5-fold the normal dose (20,000 IU/day) for two weeks can help to raise the level up to an adequate level to lower infection risk."
In addition to vitamin D optimization, quercetin — which acts similarly to the drug hydroxychloroquine — and zinc16 may further lower your risk of COVID-19. Compelling evidence suggests the reason hydroxychloroquine appears so useful in the treatment of COVID-19 is a zinc ionophore, meaning it improves zinc uptake into the cell.
Quercetin has the same effect. In fact, one study17 has suggested the biological actions — which include antiviral effects — of quercetin may in fact be related to its ability to increase cellular zinc uptake.
Zinc is vital for healthy immune function18 and a combination of zinc with a zinc ionophore (zinc transport molecule) was in 2010 shown to inhibit SARS coronavirus in vitro. In cell culture, it also blocked viral replication within minutes.19 Conversely, zinc deficiency has been shown to impair immune function.20 As noted in a 2013 paper on zinc deficiency:21
"Zinc is a second messenger of immune cells, and intracellular free zinc in these cells participate in signaling events. Zinc … is very effective in decreasing the incidence of infection in the elderly. Zinc not only modulates cell-mediated immunity but is also an antioxidant and anti-inflammatory agent."
The problem is that zinc is largely insoluble and cannot easily enter through the fatty wall of your cells. Getting all the way into the cell is crucial, as this is where the viral replication occurs. This is where zinc ionophores such as quercetin come in.
Quercetin is also a potent antiviral in its own right, and has the added advantage of inhibiting the 3CL protease22 — an enzyme used by SARS coronaviruses to infect healthy cells.23 According to one 2020 study,24 the ability of quercetin to inhibit SARS coronaviruses "is presumed to be directly linked to suppress the activity of SARS-CoV 3CLpro in some cases."
To this you could also add pryidoxine (vitamin B6) and selenium, as both play a role in the absorption and bioavailability of zinc in the body. For example, a study25 published in 1991 demonstrated that when young women were on a vitamin B6-deficient diet, their serum zinc declined, suggesting B6 deficiency affected zinc metabolism such that "absorbed zinc was not available for utilization."
A more in-depth exploration and explanation of both niacin and selenium's relationship to zinc is provided in the 2008 paper, "Zinc, Metallothioneins and Longevity: Interrelationships With Niacin and Selenium."