Fighting COVID-19 with Melatonin and Ascorbic Acid: An Unlikely Yet Powerful Dual-Arm Treatment

Jay Campbell

By Jay Campbell

July 9th, 2020

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The last time I formally wrote about the coronavirus was two whole months ago, when I recommended the BEST form of Vitamin C for fighting off COVID-19 infections.

An awful lot has happened in the past 60 days… far too many events for me to cover in a single blog post.

But here is a rough picture of where the world stands as of today:

  • 12 million COVID-19 cases, 548,000 deaths, 6.53 million patients recovered (Source: Google.com)
  • Over 100 coronavirus treatments – vaccines, drugs, non-drug therapies – under development, 15 are in preliminary stages of testing (Source: Reuters.com)
  • Several countries are reopening their economy and relaxing their lockdown restrictions, with a few countries opening their borders for international travel (Source: BusinessInsider.com)
  • Countries such as Canada have successfully “flattened the curve” and reduced the number of new coronavirus-induced deaths per day, while the United States continues to see massive spikes every day in new cases (Source: ThinkGlobalHealth.org)

And with the summer season already halfway through, organizations such as the Center for Infectious Disease Research and Policy (CIDRAP) are anticipating possible scenarios in which the world experiences a second wave of the virus:

“(1) A first wave in spring 2020, followed by a series of smaller waves over the following 1-2 years.

(2) A first wave in spring 2020, followed by a larger wave in the fall/winter (similar to the 1918 influenza pandemic). This may be followed by smaller subsequent waves. 

(3) A single wave in spring 2020, followed by ongoing transmission without a clear wave pattern. This remains possible, though it differs from what was observed during previous influenza pandemics.”

I think a second wave is entirely within the realm of likelihood, thanks to brand-new research from independent health wizard Doris Loh showing that SARS-CoV-2 has taken on a “new form”.

We recently did a 2-hour live stream explaining her new findings, which can be found below:

If you don’t have time to watch the entire thing, consider this article as the high-level summary “for dummies”.

The New COVID-19 Mutation The World Is Unaware Of

Before I go on, I STRONGLY recommend reading two prior articles I wrote about the coronavirus in the following order:

They will equip you with the terminology and the background information needed to understand the information presented in this article.

But if you already understand how the coronavirus works on a basic level, continue reading…

Around late February, a brand new mutation of the “spike protein” in the SARS-CoV-2 virus particle was discovered in Europe:

“About 1,300 amino acids serve as building blocks for a protein on the surface of the virus.

In the mutant virus, the genetic instructions for just one of those amino acids — number 614 — switched in the new variant from a “D” (shorthand for aspartic acid) to a “G” (short for glycine).”

This “D614G mutation” is of grave concern because it enhances the virus’ ability to evade antibody detection while becoming far more transmissible.

As of right now, this new variant of SARS-CoV-2 is the dominant form of the coronavirus in several countries around the world (the blue color in the picture below):

And since the D614G mutation occurred in the spike protein, the way in which SARS-CoV-2 enters the human cell has also changed in several ways…

Modified Binding Affinity for the ACE2 Receptor

As discussed many times in my prior articles, the original SARS-CoV-2 binds to the ACE2 receptor:

“ACE2 helps modulate the many activities of a protein called angiotensin II (ANG II) that increases blood pressure and inflammation, increasing damage to blood vessel linings and various types of tissue injury.”

“When the SARS-CoV-2 virus binds to ACE2, it prevents ACE2 from performing its normal function to regulate ANG II signaling…This “decreased braking” likely contributes to injury, especially to the lungs and heart, in COVID-19 patients”

But the D614G mutation works differently.

Even though the receptor-binding domain (RBD) within the spike protein of the mutated SARS-CoV-2 has a high binding affinity for ACE2, the spike protein itself has a lower affinity for ACE2.

(FYI: The RBD can be defined as the part of the spike protein responsible for binding onto cellular receptors)

This is a complete opposite of how SARS-CoV-1 works, which is responsible for causing the SARS virus that broke out in 2003.

Difference in Symptoms

ARDS (acute respiratory distress syndrome) was the most common symptom of SARS-CoV-2, which leads to low oxygen levels despite the lungs working normally.

However, a new symptom has become more pronounced in more severe cases: Thrombotic Microangiopathy (TMA).

Also known as TTP (thrombotic thrombocytopenic purpura) or aHUS (atypical hemolytic uremic syndrome), TMA involves the buildup of microscopic blood clots within smaller-sized arteries and capillaries.

Here are some of the features of TMA you need to know about:

  • Acute kidney injury
  • Organ damage
  • Low platelet count
  • Destruction of red blood cells (a.k.a. hemolytic anemia)
  • Thrombosis (abnormal blood clotting)
  • Myocardial injury (i.e. damage to the heart)
  • Pulmonary embolism (blood clots in the artery of your lung)

If TMA happens in the skin, you’ll find discoloration that arises from damaged small blood vessels and the ensuing leakage of blood.

In more severe cases of TMA, excessive blood flow blockage leads to the formation of lesions known as “Retiform purpora”

This informative YouTube video provides a great overview of TMA in relation to COVID-19:

Drastic Change in the “Type of Disease” Involved

The D614G mutation of SARS-CoV-2 may have re-defined the type of disease we are handling.

While SARS-CoV-1 was primarily a respiratory disease, this new form of SARS-CoV-2 is a dangerous blood vessel disease where abnormal clotting and blockages can have serious life-threatening effects in patients with severe symptoms.

The main area of concern for the mutated form of SARS-CoV-2 then revolves around myocardial injuries and prominent features of TMA.

What is ACTUALLY Essential For SARS-CoV-2 to Enter Your Cells?

While low cellular expression of ACE2 leads to a lower degree of infection in SARS-CoV-1, a higher cellular expression of ACE2 receptors leads to a greater degree of infection by SARS-CoV-1.

However, here’s the head-turning part: Increased ACE2 expression in SARS-CoV-2 expression DOES NOT correlate with increased severity of infection:

“The use of ACE inhibitors and ARBs was not associated with the risk of hospitalization or mortality among those infected with SARS-CoV-2.

However, there was a nearly 40% lower risk of hospitalization with the use of ACE inhibitors in the Medicare population.”

Here’s what this means… when you inject clinical-grade soluble human ACE2 in the EARLY stages of SARS-CoV-2 infections to block the virus from binding to ACE2, you can actually protect the lungs from COVID-19 injuries.

So when you increase the binding of the virus to ACE2 receptors without activating the virus, the virus itself CANNOT replicate.

Which leads us to investigate what mechanisms are critical for the virus to enter the cell.

As we discovered earlier this year, it’s the furin cleavage sites on the spike protein itself that are ESSENTIAL for the virus to enter the cell:

“…the cellular protease furin cleaves the spike protein at the S1/S2 site and that cleavage is essential for S-protein-mediated cell-cell fusion and entry into human lung cells.

…optimizing the S1/S2 site increased cell-cell, but not virus-cell, fusion, suggesting that the corresponding viral variants might exhibit increased cell-cell spread and potentially altered virulence

…acquisition of a S1/S2 multibasic cleavage site was essential for SARS-CoV-2 infection of humans and identify furin as a potential target for therapeutic intervention.”

(FYI: A protease is an enzyme responsible for cleaving bonds within proteins and breaking them down into smaller peptides)

So unless the spike protein is cleaved by furin proteases, SARS-CoV-2 cannot fuse and enter the cells.

And this leads to a further questioning of the role ACE2 plays in this new SARS-CoV-2 mutation, according to Doris Loh:

“No study to date, has ever demonstrated an association between ACE2 and furin protease in SARS-CoV-2 cleavage and activation processes. It is entirely possible that ACE2 is not the major binding receptor that is responsible for viral entry and replication COVID-19.”

Furthermore, ACE2 is NOT known to be involved in the activation – and subsequent replication – of other viruses requiring furin cleavage (viruses such as HIV-1 and HIV-2, measles, and human papillomavirus).

It turns out that the hidden culprit we are looking for is a membrane protein known as CD147 (aka EMMPRIN, Basigin):

“…a multifunctional transmembrane protein involved in neural function, inflammation, and tumor invasion…expressed by various cell types, including epithelial, endothelial, and neuronal cells”

Recent research published in late March found that the binding of the SARS-CoV-2 spike protein to the CD147 receptor in cellular membranes was a novel route for viral invasion.

This is a particularly important finding because CD147 is required for the entry of the other three viruses mentioned a few sentences ago (here, here, and here).

Moreover, it’s been discovered that the spike protein of SARS-CoV-2 predominately binds to CD147 over ACE2, making CD147 the MAIN receptor for the virus to enter your cells.

Once SARS-CoV-2 spike protein binds to CD147, sooner or later, furin protease will cleave and activate the virus to enable fusion, entry, and replication.

The binding of spike protein to CD147 can damage the receptor, lowering CD147 expression in people who may be deficient in CD147.

CD147 is highly expressed in cortical neurons, which turn out to be a VERY preferential target for SARS-CoV-2.

If you’ve ever wondered why COVID-19 patients commonly report phantom pain, high levels of fatigue, difficulty recognizing common odors, and memory loss… now you have your answer.

SARS-CoV-2 + CD147 + Blood Cells = ???

Here is how SARS-CoV-2 starts to become a blood disease…

While ACE2 expression is NOT found in your blood cells, CD147 is widely expressed in your red blood cells (i.e. erythrocytes).

This is important because malaria parasites gain entry into your red blood cells (RBCs) through CD147, causing hemolysis (destruction of red blood cells) and therefore the release of toxic free heme into your bloodstream.

The major complications of hemolysis include:

  • Liver damage
  • Lung injury
  • Acute kidney failure
  • Vascular injury (blood vessel damage)

And as we now know, the mechanism of cellular entry for SARS-CoV-2 is disturbingly similar to malaria as both of them can cause TMA.

So just like malaria, SARS-CoV-2 also uses CD147 to gain entry and fuse with erythrocytes in order to replicate.

What does this mean for the RBC diseases expressed by COVID-19 patients, such as severe inflammation of endothelial cells (located on the interior surface of blood vessels)?

CD147 is expressed in many types of cells, including erythrocytes, platelets, epithelial and endothelial cells… and dysfunction in these cells can result in abnormal blood clots.

Hemolysis activates compounds called “NLRP3 inflammosomes” that can cause dysregulation in platelets (cells that form tiny clots to stop bleeding from blood vessel injuries) and thereby lead to abnormal blood clotting.

How to Stop the Mutated “Blood-Destroying” SARS-CoV-2

The key to counteracting hypercoagulation and thrombosis in COVID-19 infections lies in a bodily process called fibrinolysis:

“Fibrinolysis describes the process of removing (lyzing) the clot formed by activation of hemostatic pathways, either in physiological response to vascular trauma or in pathological thrombosis.”

In plain English, this regulated enzymatic process allows for the breakdown and removal of blood clots.

COVID-19 patients who are critically ill have the process of fibrinolysis shut down, which leads to complications such as renal failure, depletion of platelets, and eventually TMA.

To re-activate fibrinolysis in COVID-19 patients, two inexpensive and easy-to-access supplements may prove to be helpful…

Treatment #1: Ascorbic Acid (a.k.a. Vitamin C)

Remember when I touted the value of Vitamin C in fighting COVID-19?

Well, it turns out that ascorbic acid is 20x more concentrated in platelets than your blood plasma.

In addition to increasing fibrinolysis and improving clotting in patients with coronary artery disease (CAD) at very high doses (2 grams of ascorbic acid per day), ascorbic acid also confers protective effects for your erythrocytes by reducing blood glucose levels.

(NOTE: This is the same reason why COVID-19 patients with diabetes experience increased disease severity!)

Treatment #2: Melatonin

The same over-the-counter supplement used to induce sleep in restless patients can also be an effective way to fight COVID-19:

“Melatonin, a well-known anti-inflammatory and anti-oxidative molecule, is protective against [acute lung injury]/ARDS caused by viral and other pathogens.

Melatonin is effective in critical care patients by reducing vessel permeability, anxiety, sedation use, and improving sleeping quality, which might also be beneficial for better clinical outcomes for COVID-19 patients”

Your RBCs (i.e. erythrocytes) depend on antioxidants to regulate hemolysis that naturally occurs due to auto-oxidation, and melatonin can maintain RBC deformability (i.e. change shapes) in oxidative stress conditions:

“Our results indicate that melatonin is actively taken up into erythrocytes under oxidative stress, and is consumed in the defence of the cell, delaying Hb denaturation and release of hemin.

RBCs are highly exposed to oxygen and can be a site for radical formation, under pathological conditions, which results in their destruction”

Melatonin can also inhibit the activation of NLRP3 inflammasomes and therefore prevent the cytokine storms (i.e. chronic inflammation) often observed in COVID-19 patients.

And here’s another point worth considering: Furin expression is extremely high in pineal glands, and melatonin can increase plasma levels that may counter suppressed production as a result of POSSIBLE INTERFERENCE caused by CD147 binding.

Just to add more information to prove how effective melatonin can be at VERY high doses for fighting COVID-19, here’s a recent study showing how melatonin was for improving patient survival

Ten hospitalized COVID-19 patients in Manila were given 36 to 72 milligrams of melatonin by mouth with no negative effects.

All of the patients treated with high-dose melatonin responded favorably with no other side effects outside of sleepiness, and none of those patients died!

The BEST Way to Use Vitamin C and Melatonin Together for Fighting COVID-19

Doris Loh was kind enough to provide a comprehensive treatment protocol for COVID-19 patients at different stages of disease progression using melatonin and ascorbic acid.

I’ll re-paste them here for your convenience:

Here are Doris’s recommendations for Melatonin and Ascorbic Acid:

While you’re waiting for your supply of both supplements to arrive at your doorstep, I implore you to take the following actions…

1) Share this article WIDELY with your friends and family and educate them on the truth.

The global implications of the first wave of coronavirus have largely come true, according to my earlier predictions.

However, the American economy CANNOT afford a second wave of coronavirus to take place:

“Second wave infection fears have come to the fore, as the seven day moving average of net new reported Covid-19 case counts has hit a new high of 40,000, eclipsing the previous infection peak from early April.”

“…around 44% of economic activity that was lost due to social distancing has come back. But as multiple states begin grappling with a second wave of lockdowns, that number could flatline, or even decline in a worst case scenario”

2) Educate yourself further on the awesome power of melatonin against COVID-19 infections

I HIGHLY recommend reading Doris Loh’s recently published paper on the use of melatonin for fighting SARS-CoV-2, as it explains all of these concepts in far greater detail.

She has also taken the time to explain in further detail how the new mutation of SARS-CoV-2 leads to several forms of blood disease.

Now is not the time for fear, as that is exactly what our demented overlords and politicians want for the world population.

It is only through sound education and a high-level awareness of WHAT IS that we can empower ourselves to end this global pandemic.

As I always say… Raise Your Vibration to Optimize Your Love Creation!

And if you want access to the world’s best health optimization intel before anybody else finds out about it, don’t forget to subscribe to my email list!

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