Another Reason to Add Quercetin to Your Daily Supplements

I’ve previously reviewed the similarities between the flavonoid quercetin and the drug hydroxychloroquine, discussing the possibility of using quercetin in lieu of the drug against COVID-19. We’re now also starting to see quercetin mentioned more often in the scientific literature on COVID-19. Quercetin Highlighted in COVID-19 Medical Literature For example, a review article1 published in the June 19, 2020, issue of Frontiers in Immunology highlights quercetin’s usefulness as a COVID-19 treatment, especially in conjunction with vitamin C. Quercetin is also featured in a review2 of emerging COVID-19 research published in the Integrative Medicine journal. As reported by MedPage Today:3 “Quercetin … promotes SIRT2, which then inhibits the NLRP3 inflammasome assembly involved with COVID-19 infection, said Samuel F. Yanuck, DC, of the Program on Integrative Medicine at the University of North Carolina Chapel Hill School of Medicine, who co-authored a review4 of emerging research on the subject. It also plays a role in facilitating zinc transportation across lipid membranes, Yanuck said. ‘It's not a bizarre or experimental substance and given it has these potential important biological roles, I think it's worth being considered as part of an overall strategy,’ Yanuck told MedPage Today, adding that quercetin would need to be one part of a multifactorial treatment regimen … COVID-19 has been associated with high levels of interleukin-6, depleted levels of interferons, and a cytokine storm that damages the body and is related to respiratory failure, said Ruben Colunga Biancatelli, MD, of Old Dominion University in Norfolk, Virginia, and first author of a paper on quercetin and vitamin C as a potential therapy for treating SARS-CoV-2 in Frontiers in Immunology.5 Using this rationale, researchers are postulating that vitamin C should be administered with quercetin because it can recycle oxidized quercetin, producing a synergistic effect and enhancing quercetin's antiviral capability, Biancatelli added.” Why Quercetin May Offer Hope Against COVID-19 There are solid reasons to suspect quercetin can be effective against SARS-CoV-2, the virus that causes COVID-19 disease. For example, quercetin has been shown to: Bind to the spike protein of SARS-CoV (the virus responsible for severe acute respiratory syndrome or SARS), thereby inhibiting its ability to infect host cells.6 Using the supercomputer SUMMIT, researchers at Oak Ridge National Lab also identified quercetin as one of the molecules that might inhibit the SARS-CoV-2 spike protein from interacting with human cells.7,8 Inhibit lipopolysaccharide (LPS)-induced tumor necrosis factor α (TNF-α) production in macrophages.9 (TNF-α is a cytokine involved in systemic inflammation, secreted by activated macrophages, a type of immune cell that digests foreign substances, microbes and other harmful or damaged components.) Inhibit the release of proinflammatory cytokines and histamine by modulating calcium influx into the cell.10 Stabilize mast cells and regulate the basic functional properties of immune cells, thereby allowing it to inhibit “a huge panoply of molecular targets in the micromolar concentration range, either by down-regulating or suppressing many inflammatory pathways and functions.”11 Act as a zinc ionophore, i.e., a compound that shuttles zinc into your cells.12 This is one of the mechanisms that can account for the effectiveness seen with hydroxychloroquine, which is also a zinc ionophore. Boost interferon response to viruses, including SARS-CoV-2, by inhibiting the expression of casein kinase II (CK2)13 — CK2 is an enzyme that is fundamental to controlling homeostasis at the cellular level. There is evidence that it down-regulates the ability a cell has to generate Type 1 interferon when attacked by a virus. It does this by inhibiting retinoic acid-inducible gene I (RIG-I),14 which has protein sensors that signal genetic expression of type 1 interferon by identifying the replication of RNA viruses, such as SARS-CoV-2. Quercetin inhibits the expression of CK2, which slows the replication of RNA viruses.15 Interferons are a subset of cytokines discovered in 1957.16 These cells are often the initial defense against viruses. There are two types and three forms of interferon. Within Type 1 interferon, there are alpha and beta. Type 2 interferon has the gamma form.17 The different types are based on the function of the cytokine. Type 1 interferons help cells resist viruses. Type 2 aids in responding to infections and cancer growth. The name "interferon" came from the ability of Type 1 to interfere with the virus's ability to duplicate. A cell secretes interferons when a foreign substance, like a virus, is detected. However, the interferon does not function by attacking the vir

Another Reason to Add Quercetin to Your Daily Supplements

I’ve previously reviewed the similarities between the flavonoid quercetin and the drug hydroxychloroquine, discussing the possibility of using quercetin in lieu of the drug against COVID-19. We’re now also starting to see quercetin mentioned more often in the scientific literature on COVID-19.

Quercetin Highlighted in COVID-19 Medical Literature

For example, a review article1 published in the June 19, 2020, issue of Frontiers in Immunology highlights quercetin’s usefulness as a COVID-19 treatment, especially in conjunction with vitamin C. Quercetin is also featured in a review2 of emerging COVID-19 research published in the Integrative Medicine journal. As reported by MedPage Today:3

“Quercetin … promotes SIRT2, which then inhibits the NLRP3 inflammasome assembly involved with COVID-19 infection, said Samuel F. Yanuck, DC, of the Program on Integrative Medicine at the University of North Carolina Chapel Hill School of Medicine, who co-authored a review4 of emerging research on the subject. It also plays a role in facilitating zinc transportation across lipid membranes, Yanuck said.

‘It's not a bizarre or experimental substance and given it has these potential important biological roles, I think it's worth being considered as part of an overall strategy,’ Yanuck told MedPage Today, adding that quercetin would need to be one part of a multifactorial treatment regimen …

COVID-19 has been associated with high levels of interleukin-6, depleted levels of interferons, and a cytokine storm that damages the body and is related to respiratory failure, said Ruben Colunga Biancatelli, MD, of Old Dominion University in Norfolk, Virginia, and first author of a paper on quercetin and vitamin C as a potential therapy for treating SARS-CoV-2 in Frontiers in Immunology.5

Using this rationale, researchers are postulating that vitamin C should be administered with quercetin because it can recycle oxidized quercetin, producing a synergistic effect and enhancing quercetin's antiviral capability, Biancatelli added.”

Why Quercetin May Offer Hope Against COVID-19

There are solid reasons to suspect quercetin can be effective against SARS-CoV-2, the virus that causes COVID-19 disease. For example, quercetin has been shown to:

Bind to the spike protein of SARS-CoV (the virus responsible for severe acute respiratory syndrome or SARS), thereby inhibiting its ability to infect host cells.6 Using the supercomputer SUMMIT, researchers at Oak Ridge National Lab also identified quercetin as one of the molecules that might inhibit the SARS-CoV-2 spike protein from interacting with human cells.7,8

Inhibit lipopolysaccharide (LPS)-induced tumor necrosis factor α (TNF-α) production in macrophages.9 (TNF-α is a cytokine involved in systemic inflammation, secreted by activated macrophages, a type of immune cell that digests foreign substances, microbes and other harmful or damaged components.)

Inhibit the release of proinflammatory cytokines and histamine by modulating calcium influx into the cell.10

Stabilize mast cells and regulate the basic functional properties of immune cells, thereby allowing it to inhibit “a huge panoply of molecular targets in the micromolar concentration range, either by down-regulating or suppressing many inflammatory pathways and functions.”11

Act as a zinc ionophore, i.e., a compound that shuttles zinc into your cells.12 This is one of the mechanisms that can account for the effectiveness seen with hydroxychloroquine, which is also a zinc ionophore.

Boost interferon response to viruses, including SARS-CoV-2, by inhibiting the expression of casein kinase II (CK2)13 — CK2 is an enzyme that is fundamental to controlling homeostasis at the cellular level. There is evidence that it down-regulates the ability a cell has to generate Type 1 interferon when attacked by a virus.

It does this by inhibiting retinoic acid-inducible gene I (RIG-I),14 which has protein sensors that signal genetic expression of type 1 interferon by identifying the replication of RNA viruses, such as SARS-CoV-2. Quercetin inhibits the expression of CK2, which slows the replication of RNA viruses.15

Interferons are a subset of cytokines discovered in 1957.16 These cells are often the initial defense against viruses. There are two types and three forms of interferon. Within Type 1 interferon, there are alpha and beta. Type 2 interferon has the gamma form.17

The different types are based on the function of the cytokine. Type 1 interferons help cells resist viruses. Type 2 aids in responding to infections and cancer growth. The name "interferon" came from the ability of Type 1 to interfere with the virus's ability to duplicate. A cell secretes interferons when a foreign substance, like a virus, is detected.

However, the interferon does not function by attacking the virus. Instead, it tells the infected cell and the cells that surround the infected cell to make proteins that stop viral replication. In a nutshell, quercetin stops CK2 from interfering with the action of Type 1 interferon so cells receive the signal to stop viral replication.

Modulate the NLRP3 inflammasome, an immune system component involved in the uncontrolled release of proinflammatory cytokines that occurs during a cytokine storm.18

Prevent a wide variety of dangerous viruses from entering cells, including Ebola.19

Exert a direct antiviral activity against SARS-CoV20,21,22 — Quercetin’s general antiviral capacity has been attributed to three primary mechanisms of action:

  1. Inhibiting the virus’ ability to infect cells
  2. Inhibiting replication of already infected cells
  3. Reducing infected cells’ resistance to treatment with antiviral medication

Inhibit the SARS-CoV-2 main protease.23

Quercetin Studied as COVID-19 Treatment and Prophylaxis

As reported by MedPage Today,24 Dr. Hasan Önal is currently conducting an open-label nonrandomized trial25 on quercetin in Turkey. COVID-19 patients are given 1,000 milligram (mg) of quercetin per day as an active treatment, while front-line health care workers are receiving 500-mg doses as a prophylaxis. As noted by the researchers:26

“Quercetin is reported to be effective on treatment and prophylaxis of other SARS like coronavirus infections, as a strong antioxidant and scavenger flavonoid without any adverse events. Upon this data, the investigators hypothesize that quercetin can be effective on both prophylaxis and treatment of COVID-19 cases. Therefore, the aim of this study to evaluate the possible role of quercetin on prophylaxis and treatment of COVID-19.”

Vitamin C Enhances Quercetin’s Efficacy

Vitamin C has been shown to enhance plasma quercetin levels,27,28 and the duo is the subject of the Frontiers in Immunology review article,29 “Quercetin and Vitamin C: An Experimental, Synergistic Therapy for the Prevention and Treatment of SARS-CoV-2 Related Disease (COVID-19),” mentioned earlier.

vitamin C-based sepsis treatment. In “Quercetin and Vitamin C,” Marik and co-authors point out that:30

“Ascorbic acid is a crucial vitamin necessary for the correct functioning of the immune system. It plays a role in stress response and has shown promising results when administered to the critically ill.

Quercetin is a well-known flavonoid whose antiviral properties have been investigated in numerous studies. There is evidence that vitamin C and quercetin co-administration exerts a synergistic antiviral action due to overlapping antiviral and immunomodulatory properties and the capacity of ascorbate to recycle quercetin, increasing its efficacy.

Safe, cheap interventions which have a sound biological rationale should be prioritized for experimental use in the current context of a global health pandemic.

We present the current evidence for the use of vitamin C and quercetin both for prophylaxis in high-risk populations and for the treatment of COVID-19 patients as an adjunct to promising pharmacological agents such as Remdesivir or convalescent plasma.”

Vitamin C and Quercetin Both Provide Antiviral Protection

In summary, aside from having direct viricidal effects, vitamin C:31

Supports lymphocyte activity

Increases interferon-alpha production

Modulates cytokines

Reduces inflammation

Improves endothelial dysfunction

Restores mitochondrial function

All of these effects contribute to vitamin C’s antiviral effects. Like vitamin C, quercetin also has antioxidant, anti-inflammatory, antiviral, immunoprotective and immunomodulatory properties. According to Marik’s review paper, many of quercetin’s antiviral effects are attributable to its inhibition of:32

  • Polymerases
  • Proteases
  • Reverse transcriptase
  • DNA gyrase
  • Viral capsid proteins

Quercetin also inhibits platelet aggregation,33 which is pertinent with regard to COVID-19, seeing how many patients suffer abnormal blood clotting. It also has powerful anti-inflammatory effects, inhibiting lipid peroxidation and proinflammatory mediators.34

Quercetin and Vitamin C Work Synergistically

Marik’s paper goes on to explain the synergistic antiviral action of the two compounds together:35

“Quercetin spontaneously oxidizes to form O-semiquinone and O-quinone/quinone methide (QQ), which can bind protein thiols forming toxic compounds. This process of both anti- and pro-oxidant effects has been named the “quercetin paradox.”

However, QQ can be recycled into quercetin by electron donors like NADPH or ascorbate, or form together, with glutathione either 6-glutathionyl-quercetin or 8-glutathionyl-quercetin (GSQs).

Importantly, if ascorbate or glutathione levels are insufficient, quercetin may be shunted to QQ and exert prooxidant effects. Therefore, we stress the importance for its co-administration with vitamin C …

Even though QQ exhibits a higher affinity for glutathione than for vitamin C, the methylated metabolites of quercetin show a higher preference for ascorbate than for thiols, suggesting a cycling of activity which will exert anti-oxidant effects …

The supraphysiological concentrations of ascorbate achieved with intravenous administration (i.v. 3 gr q6) are capable of free radical scavenging and electron donation, preventing either quercetin or glutathione oxidation.

In this scenario, ascorbate may exert antioxidant and immunoprotective effects, quercetin and its metabolites exert a concurrent antiviral response and, if quercetin-oxidized compounds are formed, they can be partially recycled by ascorbate and transported by glutathione, thus preventing their possible toxicity.

A multi-drug approach with quercetin and vitamin C may disrupt virus entry, replication, enzyme activity and assembly, and concurrently fortify the immune response promoting early IFNs production, modulating interleukins, promoting T cell maturation, and phagocytic activity.

Quercetin and ascorbic acid co-administration represents an experimental strategy for prophylaxis and treatment of several respiratory viruses, such as SARS-CoV-2.”

Optimal Dosing

According to “Quercetin and Vitamin C,”36 both vitamin C and quercetin have excellent safety profiles, and oral supplementation with quercetin at doses up to 1 gram (1,000 mg) per day for three months has not resulted in any significant side effects.

“Only higher intravenously administered doses up to 51.3 mg/Kg (around 3,591 mg per individual) were associated with renal toxicity,” the paper notes. The following table shows the proposed dosages for concurrent use of vitamin C and quercetin, either as a prophylactic for high-risk groups, and/or treatment for mild to severe COVID-19 disease.

Source: Frontiers in Immunology June 19, 2020, Table 1

The Importance of Zinc

While Marik’s paper does not address the use of zinc, it seems reasonable to recommend oral zinc supplementation as well, especially if you’re older. In fact, two oft-noted early symptoms of COVID-19 — the loss of taste and smell — are both symptoms of zinc deficiency.

As noted in the Integrative Medicine journal’s review37 of emerging COVID-19 research, “Zinc plays a crucial role in the function of essentially all immune cells,” and “Deficiency of this critical element has a profound impact on immune response, increasing susceptibility to a variety of infections.” Like quercetin and vitamin C, zinc also has well-known antiviral properties in its own right. As noted in the Integrative Medicine journal’s review:38

“Increasing intracellular zinc concentrations in cell culture impairs the replication of a variety of RNA viruses including SARS-CoV-1 … In vivo evidence for zinc's antiviral role comes from a Cochrane review that found zinc intake was associated with a significant reduction in the duration of the common cold.

Many of the studies showing benefit when taken during the course of an infection were in the form of a zinc lozenge. It makes sense to utilize this mode of delivery during the acute infection phase …

Anosmia (loss of smell) and dysgeusia (distorted sense of taste) are commonly being reported in patients at every phase of COVID-19. These are also classic symptoms of zinc deficiency.

It is too early in the discovery process to determine if this is cause or effect, nonetheless zinc deficiency greatly impairs immune function, especially resistance to viral infections. Notably, inadequate dietary consumption of zinc is found in almost half the older population.”

My Personal Take on This and Strong Recommendations

I am a huge fan of zinc, quercetin and vitamin C, but it is important to understand some very basic principles before using them. It is clear in my mind that quercetin is far less expensive, is safer and is likely equally effective to hydroxychloroquine at driving zinc into the cell, where it does its job of inhibiting viral replication, and unlike hydroxychloroquine, it reduces inflammatory cytokines and also increases interferon.

However, it is important to understand that if this excellent strategy is going to be optimally effective it needs to be administered early in the disease phase — the earlier the better. Using quercetin and zinc would be best done if you were recently exposed to the virus. This way you can inhibit viral replication and keep the viral load low while your innate immune system does its work in clearing the virus.

With respect to vitamin C, it is my perception that there is major confusion in this area. It can be used in low doses of several hundred milligrams to meet nutritional requirements and support your immune system in the early phase of the illness.

However, if you’re really sick and have shortness of breath, and are considering being hospitalized or are already in the hospital, then you need very high doses of vitamin C in the 10 gram to 100 gram-dose per day, either through liposomal or IV administration.

I don’t recommend taking high doses of vitamin C unless you are acutely sick. The bulk of the literature reviewed here is promoting the use of vitamin C to regenerate quercetin, but I believe there are far more powerful approaches. What might that be?

It seems obvious to me that quercetin is best taken at night (with zinc) before you go to bed and you haven’t eaten for at least three to four hours. You will sleep for eight hours, and if you are metabolically flexible, this is the time that you will dive into nutritional ketosis. Ketosis will increase your NADPH levels, which is FAR superior to vitamin C at recycling antioxidants like quercetin.

The other benefit of taking quercetin at night is to take advantage of its senolytic action to remove senescent cells, which are similar to nonreplicating cancer cells that secrete powerful proinflammatory cytokines that destroy your health. You can optimize quercetin’s senolytic properties if you take it while you are fasting.

Source : Mercola More   

What's Your Reaction?

like
0
dislike
0
love
0
funny
0
angry
0
sad
0
wow
0

Next Article

Remdesivir Treatment Stopped Due to Side Effects

The global pandemic has spurred several arms of science into action, with researchers seeking to discover how the virus works and to uncover the best testing, vaccinations and treatments. The biomedical community has been working on antiviral interventions, including remdesivir. A precursor to the drug was initially evaluated during the Ebola outbreak several years ago. Remdesivir was developed using taxpayer money that Public Citizen estimates reached at least $70.5 million, based on publicly available data.1 They also believe the number is likely higher. A 2017 report noted that the Department of Defense “is cost sharing with Gilead Biosciences for continued development of this product.”2 At the time it was labeled GS-5734.3 Public Citizen reports the DOD granted Gilead Biosciences $34.5 million.4 Additionally, the NIH led the Ebola trials using remdesivir, which opened the door for research into the use with COVID-19. The NIH granted nearly $700 million to groups for coronavirus research, including $6 million to the University of North Carolina to move the development of the drug forward. Despite the large amount of taxpayer money poured into research and development from sources other than itself, the company has set a price of more than $3,100 for a single course of treatment.5 While most see this as one example of how Big Pharma is again fleecing the public, NPR justified the pricing process by commenting that the price was determined only: “after months of speculation as the company tried to figure out how to balance profit and public health needs in the middle of a pandemic.” Gilead claims this to be a fair price that will give everyone access:6 "At the level we have priced remdesivir and with government programs in place, along with additional Gilead assistance as needed, we believe all patients will have access.” Remdesivir Lowers Viral Load at an Enormous Health Cost Yet, this curiously high price tag is on a drug that has not produced adequate results and has not been proven to reduce the potential for death in those with severe disease. Worse, the so-called “clear-cut, significant, positive effect in diminishing the time to recovery”7 of remdesivir with COVID-19 comes with an additional price tag that may include renal failure requiring a kidney transplant. In a paper published in the International Journal of Infectious Diseases, scientists reported on five of the first patients treated in France with remdesivir.8 French authorities allowed for the “compassionate-use” treatment of the drug, which is still being studied. In the paper, the authors describe the outcome for the first five patients admitted with severe pneumonia to the University Hospital of Bichat, Paris, France. Following the administration and encouraging results of a recent clinical study and two case reports, five patients admitted to the hospital were treated with the drug. Criteria included signs of severe illness and clinical aggravation of a patient's symptoms. All patients received a loading dose of 200 mg and a planned daily maintenance of 100 mg for 14 days, unless the drug was otherwise stopped for side effects. The team also collected nasopharyngeal and lung samples, which were tested for viral and bacterial growth. These were the results: • Case 1 — A 31-year-old man from Wuhan, China, started on the drug on illness Day 11. It was stopped four days later because of liver alterations and a maculopapular rash. The liver abnormalities improved after discontinuing the treatment. • Case 2 — An 80-year-old man from China was given remdesivir for two days. It was discontinued when his kidneys failed. The gentleman received the drug again as the disease severity persisted and progressed. He died nine days later. • Case 3 — A 39-year-old man with obesity and obstructive sleep apnea received eight doses of remdesivir, which was stopped because of liver enzyme alterations and the same kind of rash as was seen in Case 1. This resolved after the drug was discontinued. The gentleman was discharged on day 20. • Case 4 — A 76-year-old man from France with a history of chronic kidney injury received remdesivir for nine days without side effects. He was discharged on illness day 23. • Case 5 — A 70-year-old man with a history of chronic obstructive bronchopneumopathy was admitted with acute respiratory distress syndrome. Remdesivir was given for two days and discontinued because he suffered acute kidney injury, requiring a kidney transplant. His disease progressed and he died. The team recorded four of the five patients with major side effects, including kidney failure that would have required a transplant had the patients lived. A second study included 53 patients who were also treated under the compassionate use, funded by Gilead Sciences.9 The company recorded 36, or 68%, demonstrated clinical improvement. This was measured by improvement in oxygen transport, extubation from mechanical ventilation or

Remdesivir Treatment Stopped Due to Side Effects

The global pandemic has spurred several arms of science into action, with researchers seeking to discover how the virus works and to uncover the best testing, vaccinations and treatments. The biomedical community has been working on antiviral interventions, including remdesivir.

A precursor to the drug was initially evaluated during the Ebola outbreak several years ago. Remdesivir was developed using taxpayer money that Public Citizen estimates reached at least $70.5 million, based on publicly available data.1 They also believe the number is likely higher.

A 2017 report noted that the Department of Defense “is cost sharing with Gilead Biosciences for continued development of this product.”2 At the time it was labeled GS-5734.3

Public Citizen reports the DOD granted Gilead Biosciences $34.5 million.4 Additionally, the NIH led the Ebola trials using remdesivir, which opened the door for research into the use with COVID-19. The NIH granted nearly $700 million to groups for coronavirus research, including $6 million to the University of North Carolina to move the development of the drug forward.

Despite the large amount of taxpayer money poured into research and development from sources other than itself, the company has set a price of more than $3,100 for a single course of treatment.5

While most see this as one example of how Big Pharma is again fleecing the public, NPR justified the pricing process by commenting that the price was determined only: “after months of speculation as the company tried to figure out how to balance profit and public health needs in the middle of a pandemic.” Gilead claims this to be a fair price that will give everyone access:6

"At the level we have priced remdesivir and with government programs in place, along with additional Gilead assistance as needed, we believe all patients will have access.”

Remdesivir Lowers Viral Load at an Enormous Health Cost

Yet, this curiously high price tag is on a drug that has not produced adequate results and has not been proven to reduce the potential for death in those with severe disease. Worse, the so-called “clear-cut, significant, positive effect in diminishing the time to recovery”7 of remdesivir with COVID-19 comes with an additional price tag that may include renal failure requiring a kidney transplant.

In a paper published in the International Journal of Infectious Diseases, scientists reported on five of the first patients treated in France with remdesivir.8 French authorities allowed for the “compassionate-use” treatment of the drug, which is still being studied.

In the paper, the authors describe the outcome for the first five patients admitted with severe pneumonia to the University Hospital of Bichat, Paris, France. Following the administration and encouraging results of a recent clinical study and two case reports, five patients admitted to the hospital were treated with the drug.

Criteria included signs of severe illness and clinical aggravation of a patient's symptoms. All patients received a loading dose of 200 mg and a planned daily maintenance of 100 mg for 14 days, unless the drug was otherwise stopped for side effects. The team also collected nasopharyngeal and lung samples, which were tested for viral and bacterial growth. These were the results:

Case 1 — A 31-year-old man from Wuhan, China, started on the drug on illness Day 11. It was stopped four days later because of liver alterations and a maculopapular rash. The liver abnormalities improved after discontinuing the treatment.

Case 2 — An 80-year-old man from China was given remdesivir for two days. It was discontinued when his kidneys failed. The gentleman received the drug again as the disease severity persisted and progressed. He died nine days later.

Case 3 — A 39-year-old man with obesity and obstructive sleep apnea received eight doses of remdesivir, which was stopped because of liver enzyme alterations and the same kind of rash as was seen in Case 1. This resolved after the drug was discontinued. The gentleman was discharged on day 20.

Case 4 — A 76-year-old man from France with a history of chronic kidney injury received remdesivir for nine days without side effects. He was discharged on illness day 23.

Case 5 — A 70-year-old man with a history of chronic obstructive bronchopneumopathy was admitted with acute respiratory distress syndrome. Remdesivir was given for two days and discontinued because he suffered acute kidney injury, requiring a kidney transplant. His disease progressed and he died.

The team recorded four of the five patients with major side effects, including kidney failure that would have required a transplant had the patients lived. A second study included 53 patients who were also treated under the compassionate use, funded by Gilead Sciences.9

The company recorded 36, or 68%, demonstrated clinical improvement. This was measured by improvement in oxygen transport, extubation from mechanical ventilation or discharge. During the study period, although 36 showed clinical improvement, only 25 were discharged.

As an added note, the authors of the International Journal of Infectious Diseases studies10 mentioned that they had “waived the need for informed consent from individual patients” — which implies that the patients had no idea they were being given an experimental drug. Also intriguing is that the authors casually noted that “12% of the patients in the remdesivir group discontinued remdesivir due to adverse events, versus 5% in the placebo group.”

In other words, more than twice as many patients in the remdesivir group stopped their treatments due to adverse events than those receiving placebos. The authors ended with the comment, “A particular attention should be given to hepatic and kidney function when administrating this treatment.”

NIH Treatment Guidelines Produced by Experts?

The NIH brought together a panel of experts, including doctors and statisticians, to develop guidelines to treat coronavirus in the U.S.11 The guidelines are intended to be based on published, peer-reviewed data and to incorporate preliminary data from pre-published studies and the panelists’ clinical expertise.

The panel is charged with looking at two categories of therapies. The first are antivirals intended to target the virus directly. The second are immune-based options and host modifiers, which affect the natural immune response.

The panel's conclusions are published online at a website supported by the NIH, which is considered a living document intended for information from panel discussions and conclusions, including clinical data and ongoing trials for therapies.12

The members of this highly influential panel had to disclose financial conflicts they may have.13 Those disclosures are published by the NIH and reveal interesting information. There are 53 experts on the panel, eight of whom declared financial benefits from research support or consulting fees originating from Gilead Biosciences, the manufacturer of remdesivir.

However, the links to pharmaceutical and biotech companies whose bottom lines are impacted by the pandemic don’t stop there. In the group, 40 did not declare any financial support, while 13 did. All 13 had ties to at least one pharmaceutical, while three had ties to three or more companies. The various types of businesses included biotechnology organizations, a blood research laboratory and a flu vaccine company. The types of jobs that garnered the financial support included:

  • Research Support — 10
  • Consultant — 7
  • Advisory board or stockholder — 7
  • Honoraria — 1
  • Employee or Spouse an Employee — 2

Remdesivir Studies Lack Positive Results

Although Gilead Biosciences continues to move forward in their distribution of remdesivir, the scientific evidence has not supported its use. In this video, Del Bigtree from Highwire Talk and CEO of Informed Consent Action Network, outlines the problems with three published studies evaluating the effectiveness of the drug.

In one study published in the New England Journal of Medicine, the scientists changed the end point measurements for the study,14 moving all to secondary outcome measures except the number of days to recovery, which was the single primary outcome measure at the conclusion of the study.15 The trial was also funded by the National Institute of Allergy and Infectious Diseases (NIAID), of which Dr. Anthony Fauci is director.16

There were significant problems with the research design, and consequently the data, that I discuss in “The New COVID-19 Medication Isn't Backed by Results.” The release of the study generated enthusiasm and triggered immediate action across many countries, including the U.S.

The U.S. Food and Drug Administration issued an emergency use authorization on May 1, 2020, since the drug had not yet been approved for use in the U.S. This opened the door for compassionate use of the drug. In the statement the FDA said:17

"While there is limited information known about the safety and effectiveness of using remdesivir to treat people in the hospital with COVID-19, the investigational drug was shown in a clinical trial to shorten the time to recovery in some patients."

One team evaluated the use of the drug in those with severe disease enrolling patients who were 18 years and older with lab-confirmed infection. The study was published in The Lancet and concluded the drug was “not associated with statistically significant clinical benefits.”18

The links between the NIH, Fauci and Gilead Biosciences is a demonstration of the importance of financial ties in scientific research and the development of public policy. As mentioned above, the NIH, NIAID, Department of Defense, and countries around the world funded the study published in the New England Journal of Medicine, essentially declaring remdesivir a success.

When you consider that Fauci, by virtue of being NIAID’s director, has a vested interest in the development of remdesivir, and that it was he who declared the results to be "highly significant,” it certainly suggests that he, too, should be declaring a conflict of interest in remdesivir’s fate.19 When he was asked about the results of the study published in The Lancet, which had to be stopped because of serious adverse events, Fauci disregarded the evidence as "not adequate."

Health Choices That Make a Difference

Some health experts and the media are crying out over the number of new cases of COVID-19 being diagnosed each day, encouraging citizens to stay in place and wait for a vaccination. However, I recommend that you proactively work to support your immune system in ways that research has demonstrated reduce your risk of severe disease.

You can find a number of simple, yet significant strategies on my Coronavirus Resource Page, including proper hand-washing, getting adequate sleep and staying hydrated. However, it has become more apparent with every passing week that optimizing your vitamin D level will be the easiest, least expensive and most beneficial strategy you can use to minimize the risk of severe disease.

Health authorities have been warning of a second wave of the disease that is expected in the fall. This means the best time to start addressing your vitamin D level is right now. You can read more about the importance of Vitamin D and how the body uses it to combat coronavirus and other infectious diseases in “The Most Important Paper Dr. Mercola Has Ever Written.”

It is my hope that you spread the word about the significance of this to your friends and family. An important part of the strategy is to share the information with influencers in the Black community, as this group historically as had low levels of vitamin D — therefore putting them at greater risk of acquiring the coronavirus.

People in nursing homes and skilled nursing facilities, along with the elderly also have notoriously low levels of vitamin D that put them at greater risk of severe COVID-19 and flu, as well. Within my report I go into detail about how to raise your levels between 60 ng/mL and 80 ng/mL by fall.

You'll find a quick summary of the key steps in the article linked above including how to get tested, why you should get tested and how to assess your individualized vitamin D dose to raise your level. With this data you can help significantly reduce your risk of severe disease.

Source : Mercola More   

This site uses cookies. By continuing to browse the site you are agreeing to our use of cookies.