Health & Fitness

From the beginning, researchers and scientists have been scrambling to find answers to a multitude of questions that affect patients with SARS-CoV-2. Scientists want to know how the virus infects human cells, how it is spread and what might be done to effectively treat a population that does not respond consistently.

In other words, there are some people who are either asymptomatic or have a mild illness and others who develop significant disease and die from the virus. Experts are asking what causes one person’s immune system to go out of control and not others’?

Interferon Plays a Critical Role Controlling Cytokines

The body uses type 1 interferon in response to many viral infections.¹ As scientists have gotten a clearer understanding of how the virus affects the human immune system early in the disease, they have begun to theorize that interferons may be able to counter the process and prevent the development of severe illness.²

Interferons are a family of proteins produced by the immune system. Human-type interferons have also been commercially produced using recombinant DNA for treatment against viral infections, some cancers and multiple sclerosis.³ The objective is to change the immune system’s response to bacteria, cancer and viruses.

Natural interferon regulates the action of genetic material that secretes cellular proteins affecting growth.^4,5 The theory is that building a stronger immune system will result in directing a strong defense against the virus and alleviating the cytokine storm.

In the 1990s interferon was used to treat hepatitis C. However, the cure rate was 30% or less and the side effects were significant, including psychiatric issues, liver problems and depression that sometimes led to suicide.⁶ Other side effects included fever, muscle aches, headaches and other flu-like symptoms.⁷

Dr. Anthony Fauci, director of NIH’s National Institute of Allergy and Infectious Diseases (NIAID), calls interferon “the best soldiers, as it were, of the innate immune system."⁸

Several trials are currently underway to evaluate the effectiveness of interferon in patients with COVID-19. These trials are the result of studies demonstrating that individuals with the worst cases of coronavirus have the weakest interferon response.

People With Severe Disease Have Impaired Interferon Response

One team conducted an immune analysis on 50 patients who presented in various stages of the disease. They found that those with severe and critical illness had an impaired interferon type 1 response.⁹ Another group from New York's Mount Sinai Hospital reported similar results in the journal Cell after studying the virus in infected cells in the lab, humans and ferrets.¹⁰ Their data showed low levels of interferon types 1 and 3 were associated with higher levels of chemokines.

One team used immune cells from the blood of individuals who had severe disease. Using mass cytometry, they assessed the immune response in patients with confirmed disease.¹¹

As reported in the Washington Post, when the immune cells were challenged with bacteria and viruses the normal reaction of producing defense of molecules, including interferons, did not occur.¹²

British company Synairgen published In a July 2020 press release, British company Synairgen suggested results from a randomized clinical trial using inhaled interferons could be used to reduce the potential risk of developing severe disease.¹³ While these results are promising, it's important to note that the trial was limited and the results have not yet been peer-reviewed or published.

One month later, the NIAID announced they were sponsoring a clinical trial to test interferon in hospitalized patients.¹⁴ Scientists are currently recruiting for the trial and hope to evaluate data from 1,000 patients across 100 hospitals worldwide.

The patients in the study will be getting remdesivir, the antiviral approved by the FDA in spring 2020. Fauci commented on the combination:

“What you’re likely going to see, as more antivirals come along and then the monoclonal antibodies come along, will be a propensity to treating as early as you possibly can to prevent people from getting into the hospital.”

New Trial Couples Interferon With Remdesivir

Researchers are seeking answers as to whether interferon will give added value to the antiviral agent remdesivir. However, not all scientists think there may be positive results. Marta Gaglia is a microbiologist at Tufts University. She spoke with a reporter from The Washington Post, saying, “In principle, you could think, why don’t we just give it to everybody who has a viral infection ever. But in reality, it has proven less effective than we would like.”¹⁵

The results from remdesivir studies have not been positive, either. For instance, in one study published in the New England Journal of Medicine, the endpoint measurements were changed throughout the study.¹⁶ At the conclusion the single primary outcome measure was the number of days to recovery.¹⁷ All other criteria were moved to secondary outcome measurements.

This trial was also funded by the NIAID, which Fauci directs. Although the release generated enthusiasm, there were significant issues with the design and consequently the data, which I discussed in “The New COVID-19 Medication Isn't Backed by Results.”

A second study published in The Lancet concluded the drug was “not associated with statistically significant clinical benefits.”¹⁸ As the head of NIAID, Fauci has a vested interest in the development of the antiviral drug remdesivir. As it was, when he declared the results of the NEJM study to be “highly significant,”¹⁹ it suggests he should have also declared a conflict of interest in the use of the drug in the U.S.

When he was asked about the results of the study, which was stopped because of serious adverse events related to the drug, Fauci disregarded the evidence as “not adequate.”²⁰ 

Despite scientists' concerns over the veracity of the studies, the U.S. FDA issued an emergency use authorization for it May 1, 2020, which opened the door for compassionate use of the questionable drug.²¹

Retroviruses May Play a Role in COVID-19 Illness

One reason interferon may have a more positive result in the treatment of COVID-19 than they had with SARS or MERS is the potential that the SARS-CoV-2 virus is not completely responsible for the severe disease that affects a small percentage of the population.

In my interview with cellular and molecular biologist Judy Mikovits, Ph.D., she discusses the potential that the SARS-CoV-2 virus activates a retrovirus in the body. You can see the interview in my article, “Judy Mikovits Suggests Retroviruses Play a Role in COVID-19.”

The genetic code for a retrovirus is in ribonucleic acid (RNA), rather than in deoxyribonucleic acid (DNA). The virus uses an enzyme, reverse transcriptase, to transform the single strand of RNA into a double strand of DNA.²² The enzyme is in the host cell where the virus replicates and then spreads throughout the body. As Mikovits describes, the key to health is to keep these viruses silent.²³

She believes her data show that the SARS-CoV-2 virus is not the cause of COVID-19 but rather the catalyst to its expression, as it activates a dormant XMRV retrovirus found in some people. XMRV stands for “xenotropic murine leukemia virus-related virus.” Xenotrophic refers to viruses that only replicate in cells other than those of the host species.

So, XMRVs are viruses that infect human cells yet are not human viruses.²⁴ In my interview with her, Mikovits describes how many of the current vaccines may be contaminated with this retrovirus.

As some vaccine viruses are grown in contaminated animal cell cultures, the retroviruses are then transferred to the genetic material of the vaccine virus. This may well explain the varying effect the virus has, creating severe disease in some and asymptomatic or mild illness in others.

Consider These Options to Reduce the Severity of Disease

In addition to hand-washing and maintaining overall health, there are further strategies to consider. These are approaches you can use to help reduce the risk you'll get sick or reduce the severity of the illness if you do get sick, without depending on prescribed medications.

As I've written before, optimizing your vitamin D level is probably the easiest, least expensive and most beneficial strategy you can use to minimize your risk of COVID-19 and other infections. Unfortunately, there's a pandemic of vitamin D deficiency across all age groups.^25,26,27

The report I wrote on vitamin D and the prevention of COVID-19 is a resource to help you understand the importance of optimizing it for healthy immune function. Evidence continues to be published demonstrating that vitamin D levels are an independent indicator of the risk for infection and hospitalization.²⁸

There are many health experts who are getting significantly positive results using hydroxychloroquine in combination with zinc and azithromycin.²⁹ However, you have access to a similar combination at home using quercetin and zinc. Quercetin is a natural antihistamine and anti-inflammatory³⁰ that also functions as a zinc ionophore.³¹

In other words, it helps zinc to enter the cells and stem the tide of viral replication. This works not only in lung tissue but also in endothelial cells, which affect symptoms outside the pulmonary system.³²

Zinc deficiencies are commonly found in older adults and in those who are obese, have diabetes or atherosclerosis.³³ Likely not by coincidence, these are some of the same populations who have a higher risk of severe disease.³⁴

I recently interviewed Dr. David Brownstein, who has a clinic outside of Detroit. He has successfully treated more than 100 patients with COVID-19 using nebulized hydrogen peroxide. You can see the interview in “How Nebulized Peroxide Helps Against Respiratory Infections.”

I first wrote about using nebulized hydrogen peroxide in April 2020 and since then have received some impressive testimonials of its effectiveness from friends and acquaintances who got severely ill and used it. Brownstein was an early adopter of both vitamin D optimization and nebulized peroxide.

He's been using nebulized peroxide in the clinical setting for 25 years and with each revision of his protocol, his patients have appeared to fare better than those before them. For a couple of months, Brownstein posted some video interviews with his patients in which they told their story.

However, he removed them after receiving a warning letter from the Federal Trade Commission in which they stated that since there was no established prevention, treatment or cure for COVID-19, any mention thereof is in violation of FTC law.

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Over the past few months, several investigations have highlighted the apparent influence of vitamin D in COVID-19 incidence, severity and mortality. Interestingly, recent genetic analysis has produced a novel hypothesis¹ that helps explain the unusual disease progression of COVID-19.

The hypothesis,² published in the journal eLife in July 2020, specifically identifies bradykinin, a blood pressure regulating chemical controlled by your renin-angiotensin system (RAS), as a primary culprit.

As reviewed in greater depth in "Bradykinin Hypothesis Explains COVID-19 Complexities," the lethality of COVID-19 may be due to the virus' ability to induce a bradykinin storm. The effects of the virus on your RAS also adds further support to the recommendation to optimize your vitamin D.

In fact, the researchers who came up with the novel bradykinin hypothesis stress the usefulness of vitamin D, as it plays an important role in the RAS system^3,4,5,6 and suppresses the biosynthesis of a compound called renin (REN), thereby preventing a deadly bradykinin storm.

Conversely, if you are vitamin D deficient, your renin expression is stimulated, and based on the latest data, that may render you more prone to bradykinin storm. Other studies have also emerged in recent weeks, showing that raising patients' vitamin D levels has a dramatic and beneficial effect on COVID-19 outcomes.

Vitamin D Massively Reduces ICU Admissions

Among them is a pilot randomized clinical study^7,8,9 published online August 29, 2020, which found hospitalized COVID-19 patients in Spain who were given supplemental calcifediol (a vitamin D3 analog also known as 25-hydroxycholecalciferol or 25-hydroxyvitamin D) in addition to standard of care — which included the use of hydroxychloroquine and azithromycin — had significantly lower intensive care unit admissions.

Patients in the vitamin D arm received 532 micrograms of calcifediol on the day of admission (equivalent to 106,400 IUs of vitamin D¹⁰) followed by 266 mcg on Days 3 and 7 (equivalent to 53,200 IUs¹¹). After that, they received 266 mcg once a week until discharge, ICU admission or death.

Of those receiving calcifediol, only 2% required ICU admission, compared to 50% of those who did not get calcifediol. None of those given vitamin D supplementation died, and all were discharged without complications.

CDC Warns of Second Wave of COVID-19

In the video above, NBC News interviews Michael Osterholm, virologist and director of the Center for Infectious Disease Research and Policy at the University of Minnesota in Minneapolis, about the prospect of a second wave of COVID-19.

According to Osterholm, we likely have another 12 to 14 months of "a really hard road ahead of us." While Swedish statistics suggest the virus can and is dying off naturally, Osterholm believes cases will again rise as we move into fall and winter. Even if a vaccine does become available, it will take months to vaccinate the population, he notes.

Chief epidemiologist in charge of Sweden's coronavirus response, Anders Tegnell, has stated¹² he does not believe Sweden will see a second wave with widespread contagion as the country is seeing a rapid decline in positive tests, indicating herd immunity is being achieved.¹³

That said, there are still open questions as to how long natural immunity might last.¹⁴ Some evidence points to months,¹⁵ while other data point to several years.¹⁶ Then there are the data suggesting herd immunity for COVID-19 occurs at much lower rates than normal.

As reported¹⁷ by Dr. James Hamblin in The Atlantic, infectious disease modeling by Gabriela Gomes, who specializes in nonlinear chaos dynamics, "selective depletion" of individuals susceptible to infection can rapidly reduce viral spread, and in the case of SARS-CoV-2, models suggest the threshold for herd immunity may occur below 20% of the population.

Yet other data^18,19,20,21 suggest certain antibodies against other coronaviruses, such as the common cold, appear to provide some protection against SARS-CoV-2 as well, such that a majority of people may already have some level of immunity. So, there's a variety of "moving parts" that still need to be nailed down before we can come to any firm conclusions about future risks.

Vitamin D Versus Vaccine

While Osterholm²² and other health officials are still focused on getting people onboard with vaccination, both against influenza and COVID-19, no one at the federal level has as of yet addressed the elephant in the room, which is vitamin D deficiency and its impact on these infections.

Importantly, influenza vaccination has been shown^23,24 — by the Department of Defense, no less — to increase the risk of subsequent coronavirus infections by 36%. If we are to follow the science, as Osterholm says, then we should not be so quick to overlook such findings.

Then, of course, there's the issue of whether a safe and effective COVID-19 vaccine is achievable. I've discussed the reasons for why I believe COVID-19 vaccines will fail in several previous articles. Vitamin D optimization, in contrast, is already known to be both safe and effective against not only influenza but also COVID-19^25,26,27 and other respiratory infections.²⁸

According to a 2017 systematic review^29,30,31 published in The BMJ, vitamin D supplementation protected against acute respiratory tract infection. The number needed to treat (NNT) was 33, meaning 33 people had to take the supplement in order to prevent a single case of infection. Among those with severe vitamin D deficiency at baseline, the NNT was 4.

Meanwhile, a systematic review³² by the Cochrane Database of Systematic Reviews found that to prevent one case of influenza-like illness (defined³³ by the World Health Organization as an acute respiratory infection), the NNT for inactivated vaccines was 40. To prevent a single case of confirmed influenza, the number needed to vaccinate (NNV) was 71.

Vitamin D Is an Important Modifier of COVID-19 Risk

In a November 1, 2020, commentary³⁴ in the journal Metabolism Clinical and Experimental, JoAnn Manson and Shari Bassuk call for the elimination of vitamin D deficiency to effectively squelch the COVID-19 pandemic, noting that 23.3% of the total U.S. population have insufficient or deficient vitamin D levels, with people of color having disproportionately lower levels than non-Hispanic whites.

They list several types of studies showing vitamin D deficiency is "an important modifiable risk factor for COVID-19," including:³⁵

Vitamin D Protects Your Lungs

A 2020 GrassrootsHealth study published in the journal Nutrients⁴⁴ describes how vitamin D can reduce the risk of both influenza and SARS-CoV-2 infection by lowering the viral replication rate and reducing the pro-inflammatory cytokines that damage the lungs, leading to pneumonia.

Vitamin D also helps increase concentrations of anti-inflammatory cytokines that may help protect your lungs. The researchers recommended those at risk for COVID-19 take:

"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)."

Vitamin D and COVID-19 Comorbidities

Vitamin D may also help protect against COVID-19 by beneficially impacting many of the comorbidities associated with poor COVID-19 prognosis. In an August 2020 paper⁴⁵ published in the NSF Journal, the authors review the "fatal relationship" between vitamin D deficiency in combination with comorbidities in COVID-19 patients, noting that:

" … low vitamin D status is common in Europe with the exception of the Scandinavian countries. The calculated COVID-19 mortality rate from 12 European countries shows a significant inverse correlation with the mean 25(OH)D plasma concentration.

This raises the question whether insufficient vitamin D supply has an influence on the course of COVID-19 disease? An analysis of the distribution of COVID-19 infections showed a correlation between geographical location (30–50° N+), mean temperature between 5–11 °C and low humidity.

In a retrospective cohort study (1,382 hospitalized patients) 326 died … The mortality of COVID-19 (cases/ million population) shows a clear dependence on latitude. Below latitude 35, mortality decreases markedly. Indeed, there are exceptions … however, the management of the pandemic may increase infection risk …

Older age and comorbidities are linked to an insufficient vitamin D supply. Over 60 years of age, a reduction in the synthesis of vitamin D in the skin becomes apparent, which further increases getting older …

Based on a meta-analysis including 30 studies with 53,000 COVID-19 patients, co-morbidities are risk factors for disease severity … Comorbidities and old age show a relationship with Renin-Angiotensin-Aldosteron-System (RAS), vitamin D status and COVID-19 infection."

How Vitamin D Helps Modulate SARS-CoV-2 Infection 

This brings us back to where I started. While this NSF Journal study does not make reference to bradykinin storm being part of the disease progression and lethality of COVID-19, it does review how vitamin D impacts your RAS (which regulates bradykinin), and how your RAS in turn plays a role in the progression of SARS-CoV-2 infection:⁴⁶

"Infection with SARS-CoV-2 causes the virus spike protein to come into contact with ACE2 on the cell surface and thus to be transported into the cell. This endocytosis causes upregulation of a metallopeptidase (ADAM17), which releases ACE2 from the membrane, resulting in a loss of the counter regulatory activity to RAS.

As a result, proinflammatory cytokines are released extensively into the circulation. This leads to a series of vascular changes, especially in the case of preexisting lesions, which can promote further progression of cardiovascular pathologies.

SARS-CoV-2 not only reduces the ACE2 expression, but also leads to further limitation of the ACE2/Ang 1–7/Mas axis via ADAM17 activation, which in turn promotes the absorption of the virus. This results in an increase in Ang II, which further upregulates ADAM 17.

Thus a vicious circle is established turning into a constantly self-generating and progressive process. This process may contribute not only to lung damage (Acute respiratory distress syndrome - ARDS), but also to heart injury and vessels damage, observed in COVID-19 patients …

Several studies have shown increased plasma renin activity, higher Ang II concentrations and higher RAS activity as a consequence of low vitamin D status. The same applies to the decreasing Renin activity with increasing vitamin D levels. There is an inverse relationship between circulating 25(OH)D and renin, which is explained by the fact that vitamin D is a negative regulator of renin expression …"

The NSF Journal paper goes on to review the connections found between the RAS, vitamin D levels and a list of comorbidities shown to worsen COVID-19 outcomes, including high blood pressure, cardiovascular diseases, obesity, Type 2 diabetes and ARDS. It also reviews how vitamin D levels, RAS function and cytokine storms are interconnected. The authors state, in conclusion:⁴⁷

"There is ample evidence that various non-communicable diseases (hypertension, diabetes, CVD, metabolic syndrome) are associated with low vitamin D plasma levels. These comorbidities, together with the often concomitant vitamin D deficiency, increase the risk of severe COVID-19 events.

Much more attention should be paid to the importance of vitamin D status for the development and course of the disease. Particularly in the methods used to control the pandemic (lockdown), the skin's natural vitamin D synthesis is reduced when people have few opportunities to be exposed to the sun.

The short half-lives of the vitamin therefore make an increasing vitamin D deficiency more likely. Specific dietary advice, moderate supplementation or fortified foods can help prevent this deficiency. In the event of hospitalization, the status should be urgently reviewed and, if possible, improved."

Summary

To summarize what the NSF and eLife journals tell us, when your vitamin D is low, your risk of COVID-19 complications and death increases because your renin expression is stimulated.

High renin increases both cytokines and bradykinin, placing you at risk for increased inflammation and oxidative stress resulting in both cytokine storm (as discussed in the NSF paper⁴⁸) and bradykinin storm (as discussed in the eLife paper⁴⁹).

Considering cytokine and/or bradykinin storms are key factors in COVID-19 mortality, it seems reasonable to conclude that anything that can help modulate and prevent these devastating storms would be of significant value. As of right now, the one thing we know can do that is vitamin D.

In addition to that, vitamin D lowers viral replication,⁵⁰ boosts your overall immune function by modulating both innate and adaptive immune responses, reduces respiratory distress,⁵¹ improves overall lung function and helps produce surfactants in your lungs that aid in fluid clearance.⁵²

Vitamin D also lowers your risk of comorbidities associated with poor COVID-19 prognosis, including obesity,⁵³ Type 2 diabetes,⁵⁴ high blood pressure⁵⁵ and heart disease.⁵⁶ In my view, there's every reason to believe vitamin D optimization will help lower your risk of COVID-19 complications and death, and no reason to dismiss this strategy. 

Optimize Your Vitamin D Level Now

My #StopCOVIDCold campaign seeks to raise awareness about the importance of vitamin D optimization to prevent a resurgence of COVID-19 hospitalizations and deaths.

As temperatures and humidity levels drop — two factors that influence the viability of the virus in air and on surfaces — it's quite likely we'll see a reemergence. But a surge in positive tests, by itself, should not be cause for panic.

Remember, a vast majority of so-called "cases," meaning positive tests, remain asymptomatic. I believe raising vitamin D levels among the general public can go a long way toward increasing the number of people who have no symptoms or only mild illness.

Now is the time to check your vitamin D level and start taking action to raise it if you're below 40 ng/mL. An easy and cost-effective way of measuring your vitamin D level is to order GrassrootsHealth's vitamin D testing kit and learn more about vitamin D and its impact on your health.

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