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Protecting from Coronavirus - Supplements & Therapies

coronavirus flu disease epidemics viruses immunity covid-19

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#1 jroseland

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Posted 28 January 2020 - 08:44 AM

I'm trying to put organize a big list of supplements and drugs that one should take to protect from the Coronavirus. If I'm understanding correctly, Coronavirus is a SARS-like flu, so anything that prevents or treats flu would be smart to use.



Siberian Ginseng (Eleuthero)





Adaptogenic Mushrooms

Cordyceps, Chaga, Red Reishi, and Turkey Tail.


Immuno-Fortifying Vitamins

Vitamin C

Vitamin D3



Immune Biohacks

Immune 26

C60 Olive Oil


N-Acetyl Cysteine (NAC)



What am I missing? Which vitamins, supplements or drugs have are particularly effective against influenza? Which of these would you rank first? Feel free to share any anecdotes or studies you might have in regard to beating flu...

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#2 Hip

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Posted 28 January 2020 - 01:50 PM

Coronavirus is not the same as influenzavirus (the virus which causes flu), and antivirals such as Tamiflu which work for influenzavirus will not work for coronavirus. There are no specific antiviral drugs which work for coronavirus, except possibly for interferon and/or ribavirin, which one paper suggests might be useful against the very similar SARS coronavirus. 


Interferon is very expensive, with a two-week course of subcutaneously-injected interferon alpha or interferon beta costing around $3000. Ribavirin is relatively inexpensive, costing around $130 for 40 x 200 mg capsules at cheap prescription-free overseas pharmacies. Typically dosing is 400 mg twice daily. 



Herbs which boost the interferon response at the mucous membranes of the respiratory tract may be useful, as the interferon response is the first responder arm of the immune system. So by boosting interferon you may be able to kill any virus which lands on your mucous membranes before it gets a chance to enter the rest of the body.


Echinacea is an interferon-booster, and has been shown in studies to reduce the risk of catching a cold when the mucous membranes are exposed to a cold virus. 



One of the best protective measures against viral infection is regular hand washing with soap and water several times a day.




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#3 Dorian Grey

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Posted 30 January 2020 - 06:04 AM

We might also consider how to optimally avoid vector transmission.  I was a surgical technologist for 35 years, & "aseptic technique" is our specialty.   


As a respiratory virus, corona (or flu) can only enter the body by one of two ways.  You may pick up the virus shed from others by touching contaminated surfaces and literally shoving it up your nose (picking/itching) or introducing it to your eyes (rubbing/degrunging), which drain into the nose through the nasolacrimal duct.  Inhalation of infectious droplets created when an infected person sneezes is the other vector.  I say sneezes as from what I understand, "airborne" pathogens are actually "droplet" or "particle" born, and normal respiration from sick individuals should not in itself generate "infectious air".  No sneezing = little risk of airborne transmission.  I don't have data to back this up, but I do not believe respiratory/rhinoviruses are particularly contagious by mouth, provided you are not breathing through your mouth and inhaling droplet born pathogens into your lungs.  These bugs do not colonize the mouth esophagus or survive stomach acid, so don't worry too much about eating food prepared by an infected person.  


When an infected person does sneeze, a great many droplets are introduced into breathable air.  These droplets are heavy enough to fall fairly quickly to the floor or other surface, EXCEPT when introduced into a dry atmosphere, where rapid evaporation can render them light enough to float around, carried by air currents.  This is why viral respiratory infections are considerably more problematic during Winter months when relative humidity is typically much lower than during the Summer when relative humidity is usually higher.  


There is a lot of debate about whether or not surgical masks may be helpful.  Some say the virus is so small, it can easily pass through the pours of a typical paper mask and this is true, but if we consider these virus do not fly on their own, but always "ride" on droplets or particles (which is also true), the benefit of a mask becomes much more plausible.  Even a cheap, disposable paper mask should catch most infectious droplets or particles PROVIDED it is worn properly.  The best masks have a strap/tie at the top & bottom of the mask, and a wire sown into the nose bridge so you can mold the mask to your nose.  Tie the top strap across the crown of your head, and the bottom at the base of the skull, snugly enough so that you are breathing THROUGH the mask, and not around the sides or bottom of the mask.  A cloth bandana worn snugly enough so that you breath THROUGH it will be much more effective than the masks with the rubber bands that go around your ears that rarely fit snugly enough so that you breath through them.


Avoiding itching your nose or eyes can be harder than one might think.  I used to teach Surgical Technology, and the hardest part of being a new student is always being conscious of the fact you must never itch your nose or eyes while you're scrubbed.  I truly believe more people infect themselves by touching contaminated communal surfaces and shoving the pathogens right up their noses or into their eyes, than through droplet born inhalation.  When I'm out and about during cold & flu season, I like to wash my hands, and then give my eyes a good rub every hour or so, which I have found greatly reduces sudden urges for incidental itching & rubbing.  If I absolutely have to itch my eye and I can't wash my hands, I use a knuckle on the back of my finger rather than my finger tip.  My finger tips come in contact with a lot more surfaces than my knuckles do!  


Blowing your nose frequently is also theoretically helpful.  If you do manage to inhale a contaminated droplet, it may well stick in the mucus of your nose.  Blow it out before it starts multiplying or colonizing nasal tissue, and you've dodged a bullet with very little effort.  Never (EVER!) snarf snot into the back of your nose or throat, even to spit it out.  This not only introduces any pathogens deeper into your nose & sinuses, but if mucus is watery, it can actually form aerosols you may snarf right into your LUNGS.  Noses get watery in Winter weather in a desperate effort to flush any pathogens that find their way into nasal tissue out of the body.  Do not sabotage this natural defense mechanism by snarfing watery mucus deep into your respiratory system!  


In surgical technology school, we teach students to develop a "sterile conscience".  Know what is sterile & what is contaminated if you want to keep sterile items from becoming contaminated.  This has served me well in avoiding seasonal virus.  My girlfriend is always amazed when she has a cold & I don't catch it.  My 35 years as a scrub tech have taught me where the germs are, and how to avoid introducing them to my own tissues.  


Stay Healthy My Friends, & Best of Luck!  

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#4 Hip

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Posted 31 January 2020 - 08:39 PM

There is a lot of debate about whether or not surgical masks may be helpful.  Some say the virus is so small, it can easily pass through the pours of a typical paper mask and this is true, but if we consider these virus do not fly on their own, but always "ride" on droplets or particles (which is also true), the benefit of a mask becomes much more plausible.  Even a cheap, disposable paper mask should catch most infectious droplets or particles PROVIDED it is worn properly. 



Great post, @Dorian Grey. 


One other advantage of wearing a face mask I would guess is that it stops you from unconsciously touching your mouth or nose, and thereby introducing the pathogen into your respiratory tract via contaminated hands. If you are in a public place and touching contaminated surfaces, then you may have the virus on your hands. As you pointed out, it can be difficult to avoid unconsciously scratching an itch that appears on your face. But if you wear a mask, this places a physical barrier in front of your mouth and nose. Of course, a regular face mask will not protect your eyes, and there have been reports of the Wuhan coronavirus transmitting by getting into the eyes. But at least it will protect the nose and mouth. 


Once you get home, you can wash your hands, and then take the mask off, as with your hands washed, it should be safe to touch your face.





Note that death is not the only concern with the Wuhan coronavirus. Since it's been reported that the deaths tend to occur in the over 60s, younger people may feel that this virus does not concern them as much. However, with the very similar SARS coronavirus, it was found that 17% of the infected survivors went on to develop a post-viral fatigue syndrome similar to chronic fatigue syndrome / myalgic encephalomyelitis, which was severe enough to prevent them from going to work. The same might happen with Wuhan coronavirus: you may survive the virus, but develop a life-long fatiguing illness which prevents you from working and prevents you from participating in life. So best avoided if possible.

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#5 adamh

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Posted 31 January 2020 - 10:51 PM

Yes many viruses are known to persist for years or forever after the patient has supposedly recovered from it. Chicken pox comes back often as shingles for example. Something like cfs would be a terrible curse

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#6 Kalliste

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Posted 06 February 2020 - 10:18 AM

So what are we doing supplement wise here?

I bought 1000g of AA and going to start a 2g/2 a day and up that by 2g every 4 hours if I get sick.

Bought garlic extract, usually stink too much but I wiill work with open windows.

Upped my UVB exposure to Daily.

1000mg L-Lysine every morning

Starting with daily turmeric roots


Hoping this is something that only affects asians, but in a month this could be a true wordwide pandemic.


Chinese state is very conservative and pragmatic, their massive response scares me.

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#7 xEva

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Posted 06 February 2020 - 12:16 PM

sorry if this has already been posted, but what do you think?
Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCoV) in vitro, 2020


Chloroquine, a widely-used anti-malarial and autoimmune disease drug, has recently been reported as a potential broad-spectrum antiviral drug.8,9 Chloroquine is known to block virus infection by increasing endosomal pH required for virus/cell fusion, as well as interfering with the glycosylation of cellular receptors of SARS-CoV.10 Our time-of-addition assay demonstrated that chloroquine functioned at both entry, and at post-entry stages of the 2019-nCoV infection in Vero E6 cells (Fig. 1c, d). Besides its antiviral activity, chloroquine has an immune-modulating activity, which may synergistically enhance its antiviral effect in vivo. Chloroquine is widely distributed in the whole body, including lung, after oral administration. The EC90 value of chloroquine against the 2019-nCoV in Vero E6 cells was 6.90 μM, which can be clinically achievable as demonstrated in the plasma of rheumatoid arthritis patients who received 500 mg administration.11 Chloroquine is a cheap and a safe drug that has been used for more than 70 years and, therefore, it is potentially clinically applicable against the 2019-nCoV.

Our findings reveal that remdesivir and chloroquine are highly effective in the control of 2019-nCoV infection in vitro. Since these compounds have been used in human patients with a safety track record and shown to be effective against various ailments, we suggest that they should be assessed in human patients suffering from the novel coronavirus disease.


about Remdesivir:


it has not been approved anywhere globally and has not been showed to be safe or effective for any use, Gilead’s chief medical officer Merdad Parsey said in a statement on Friday.
The firm is working with Chinese health authorities to conduct a clinical trial on patients with pneumonia symptoms to test its safety and efficacy, it said. Past clinical data on other coronaviruses give it “hope,” it added.


Edited by xEva, 06 February 2020 - 12:21 PM.

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#8 xEva

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Posted 06 February 2020 - 12:27 PM

Or this:


large doses of the flu drug oseltamivir combined with HIV drugs lopinavir and ritonavir, improved the conditions of several patients at the Rajavithi Hospital in Bangkok.


“From testing positive for 10 days under our care, after applying this combination of medicine the test result became negative within 48 hours.”



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#9 Kalliste

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Posted 06 February 2020 - 05:02 PM

The Vitamin C angle. A part of me want to believe that Of Course doctors would have tried this, but knowing how obsessed DR's are with their patented substances it's fully possible they have'nt even considered this.

If it was possible I would get IV-C of course.


I'm stocking up on ginger, quality curry powder, melatonin, garlic, MitoQ, colloidal silver, L-Lysine, AA, CoQ10, alcohol, manuca honey. Where I come from it's not possible to get any anti-viral meds without doctors recipe.




Mitochondria & The Coronavirus – The Vitamin C Connection (Part 3)

Why should you take vitamin C, ascorbic acid, to protect against infectious viruses like the recent outbreak of the novel human coronavirus in Wuhan, China [1]?  The answer lies in the way how coronaviruses affect mitochondrial functions, and how vitamin C, ascorbic acid (AA) protects and enhances a comprehensive defense network from immune support to mitochondrial bioenergetic integrity. 

The Role of Ascorbic Acid in Immunity

Ascorbic acid (AA) has been recognized for a long time as an antioxidant, with the ability to improve immunity [2]. More recent understanding demonstrated how AA protects against attacks by pathogens by strengthening epithelial defenses, while supporting both innate and adaptive immune systems, defending the body against invading microbes [4].  

Leucocytes including neutrophils have been shown to accumulate large amounts of AA. Increasing supplementation of ascorbic acid, led to improved neutrophil motility in patients with recurrent infections [5].   The accumulation of ascorbic acid in neutrophils results in improved chemotaxis, phagocytosis, and microbial killing, while decreasing necrosis/NETosis and potential tissue damages [4].


An increasing body of emerging evidence points to the possibility that AA can positively influence lymphocyte development and function by stimulating the differentiation and proliferation of B- and T-cells [6, 7,8].  It is not surprising that infections can significantly deplete ascorbic acid levels [9]. Two controlled trials found a significant dose-dependent response in the inhibition of common cold symptoms when ascorbic acid was supplemented up to 8 g/day [10]. 

The ability of ascorbic acid to influence the immune system is perhaps only a part of the story in how it can protect us from infectious viruses such as the coronavirus.  To fully understand how AA functions, we first need to realize that AA is not just an antioxidant, it is a REDOX molecule, used by our body to balance electron exchanges in vital biochemical processes.  This is actually the key to understanding how AA truly functions inside our body. 


Why is the balance of electrons important in pathogenesis initiated by coronaviruses? 

Coronaviruses, Cytokine Storms & Apoptosis – A Story About Mitochondrial Membranes

The 2019 novel coronavirus (2019-nCoV), identified in patients with viral pneumonia late December 2019 in Wuhan, China [17] is a betacoronavirus that bears 88% identity to two bat-derived severe acute respiratory syndrome (SARS)-like coronaviruses, bat-SL-CoVZC45 and bat-SL-CoVZXC21, both of which were collected in 2018 in Zhoushan, eastern China [11].  

Coronaviruses (CoVs) are enveloped, single-stranded RNA viruses divided into four subtypes of Alphacoronavirus (αCoV), Betacoronavirus (βCoV), Deltacoronavirus (δCoV), and Gammacoronavirus (γCoV) [12].  Alpha and beta CoVs originate from bats and rodents while delta and gamma CoVs originate from avian species. 

CoVs have become important pathogens as they can induce severe acute respiratory syndrome (SARS), such as the epidemic that infected 8000 patients causing 800 deaths in China during 2002-2003. The MERS-CoV that is responsible for a persistent epidemic in the Arabian Peninsula since 2012 [13] and the SARS-CoV both originated from bats and jumped to another mammalian host before crossing species barriers to infect humans.


This novel strain from Wuhan, China bears only 79% similarity to the SARS-CoV (2002-2003) and 50% similarity to the MERS-CoV (2012) [11].  However, both the to the SARS-CoV [14] and the 2019-nCoV are able to bind to the angiotensin converting enzyme 2 receptor (ACE2) in humans [15, 16]. 

Cell entry is an essential component of cross-species transmission, especially for the β-CoVs [40].  The role of ACE2 receptors is significant because it is the means by which betacoronaviruses (βCoV) like SARS-CoV and 2019-nCoV can gain entry into human cells [18].  Unfortunately, the ACE2 receptor is not the only route βCoVs gain entry into host cells.

Envelope Proteins and Membrane Permeability

The 2019-nCoV and other coronaviruses like SARS-CoV encode proteins known as envelope (E) protein that can modify host cell membrane permeability in order to gain entry into host cells, promoting replication, release and proliferation.  These proteins are able to form ion channels to induce membrane permeability changes [19, 23]. 

In the SARS-CoV, the E protein has been observed to translocate to the cell surface and is partially associated with lipid rafts [20].  This envelope (E) protein plays a diverse role in coronavirus morphogenesis, depending on the particular genus of the virus. However, the presence of the E protein has been shown to activate pathogenic inflammatory responses that may cause death in animal models and humans [21, 22].


The E protein is now accepted to be responsible for a significant proportion of the inflammation cascade caused by SARS-CoV [21]. Why would such a small protein like the E protein be able to dramatically enhance the replication of CoV’s and increase their pathogenicity and virulence?  

Cytokine Storms & Apoptosis – The Mitochondria Connection

One common clinical feature of critically ill patients infected with the 2019-nCov is the high concentrations of cytokines in their plasma. Analysis showed that 2019-nCoV caused clusters of fatal pneumonia with clinical presentation similar to SARS-coV.  Infected patients had a high probability of developing acute respiratory distress syndrome. 75% of patients showed bilateral pneumonia (affecting both lungs) [17]. 

During the outbreaks of SARS-CoV and MERS-CoV, increased amounts of proinflammatory cytokines in serum of infected patients were associated with pulmonary inflammation and extensive lung damage [24, 25, 38]   IL1B, IL6, IL12, IL15, IL17,TNFα. IFNγ, IP10 and MCP1 were among the elevated cytokines found in CoV patients. High amounts of IL1B, IFNγ, IP10, and MCP1 cytokines that might have led to increased activated T-helper-1 (Th1) cell responses have also been identified in 2019-nCoV patients [26].  

Similar to the SARS-CoV, absolute value of lymphocytes in most 2019-nCoV patients was markedly reduced, suggesting that 2019-nCoV main mechanism of action could be directed at lymphocytes, especially T lymphocytes.  

As virus particles spread and infect other cells, the body responds with a cascading event of immune response known as a cytokine storm that causes changes in peripheral white blood cells and immune cells including lymphocytes.  Cytokine storms maybe the reason why some patients progressed rapidly with acute respiratory distress syndrome and septic shock, followed by multiple organ failure and death eventually [17].

2019-nCoV and The Cytokine Storm

The term “Cytokine Storm”, first used in 1993 [26] describes a phenomenon where the inflammatory response in the immune system rages out of control [39].  The term is subsequently associated with virus infections including, Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis, group A streptococcus, influenza virus, and SARS-CoV. 

Cytokines are a group of proteins secreted by cells for signaling and communication in the regulation of angiogenesis, immune and inflammatory responses. These proteins can elicit a wide range of different responses depending on the cytokine and the target cell. 


Inflammation in cytokine storms usually begins at a local site and is subsequently spread throughout the body via systemic circulation.  Symptoms such as redness, swelling or edema, heat and pain are hallmarks of acute inflammation at a local site. These inflammatory responses often occur at the expense of local organ functions.  Compensatory repair processes are usually initiated after inflammation begins, and the repair process in most cases could completely restore tissue and organ function. However, when severe inflammation damages local tissue structures, healing could only proceed with fibrosis, which often results in persistent organ dysfunction [28].

SARS-CoV is a primary example of cytokine storm responses that result in severe lung infections, leading to the development of pulmonary fibrosis.  Clinical manifestations of 2019-nCoV seem to imply similar mechanisms, as infected patients exhibited high rates of bilateral pneumonia [17].

In most cytokine storms, acute-response cytokine proteins such as TNF, IL-1β,  IL-8 and MCP-1 appear within minutes to hours after infection, followed by more sustained increase in IL-6, while  cytokine IL-10 appears somewhat later, as the body attempts to control the acute systemic inflammatory response, as IL-10 is a counter-anti-inflammatory defence mechanism [28].  In severe infections such as those initiated by coronaviruses, the normal immune responses are manipulated by the virus that may result in an immune system gone awry. 

When the body initiates systemic production of IL-10 once a cytokine storm is initiated, a phase known as ‘immunoparalysis’ takes over where neutrophils and monocyte functions are downregulated in the attempt to control and reign in systemic inflammation responses to local infections [29, 30, 31].  However, it is possible that patients may not recover from immunoparalysis even though they survived the initial cytokine storm. These patients with severe immunosuppression would be challenged with onset of severe sepsis leading to eventual death [32]. 

Immune homeostasis is therefore critical during the progression of cytokine storms. The inability to clear apoptotic cells in a timely manner [33] may be one of the reasons for increased virulence of coronaviruses during cytokine storms. 

Mitochondria, Envelope Proteins and Apoptosis – A Tale of Depolarization

Apoptosis is an important biological function involving cell death for the purpose of regulating cell proliferation and differentiation in cell tissues, as well as the pathogenesis of various diseases [34]. The biochemical pathway required for apoptotic cell death is ubiquitous in practically ALL mammalian cells and can be activated by a variety of extra- and intracellular signals. 

At present, it is widely recognized that mitochondria play a critical role in the regulation of apoptosis [35].  In the early stages of apoptosis, different pro-apoptotic proteins including cytochrome c normally found in the intermembrane space are released into the cytosol. However, the key step that initiates the apoptotic process is the PERMEABILIZATION of the outer mitochondrial membrane [36].  Envelope proteins in coronaviruses induce membrane permeabilization [19, 23].


The 3b protein encoded by the SARS-CoV has been identified in mitochondria. The localization of the protein in mitochondria is believed to contribute to SARS pathogenesis in humans [37].  While another protein encoded by coronavirus SARS-CoV known as the 3a protein has been demonstrated to induce extensive cell death by induction of mitochondrial apoptotic pathways where cytochrome c was released into cytosol [41].  Why would coronaviruses cause membrane permeability so as to inject proteins into mitochondria, causing apoptosis and cell death?

Mitochondrial Dynamics is Essential in Antiviral Immunity

Viruses, including coronaviruses, have the ability to alter cellular functions to increase proliferation. The ability to evade immune responses is perhaps the most important aspect of viral persistence and proliferation.  Recent discoveries have shown that mitochondria is the central regulator of our immune system, controlling innate immune signaling and cell fate of immune cells [42]. 

Mitochondrial outer membranes have emerged as a major platform for important signaling molecules, and mitochondrial dynamics involving fusion and fission play critical roles in immune-cell activation [43].  Immunity and mitochondria are now accepted to be tightly interlinked, as mitochondria can regulate the activation, differentiation and survival of immune cells [44]. 


During viral infections, mitochondrial dynamics is altered as viruses manipulate mitochondrial dynamics to influence infection progression.  The disruption of mitochondrial dynamics caused by viruses, including coronaviruses, can severely increase viral pathogenesis [45]. This is the reason why coronavirus SARS-CoV encoded 3a, 3b proteins target mitochondria to inflict damage and injury, causing apoptosis in order to deregulate the host immune system [37, 41].  

During infection, damaged mitochondria would normally be cleared quickly via combined processes in mitochondrial dynamics and mitophagy.  Fission is a process that facilitates the segregation of damaged mitochondria, which is subsequently removed by mitophagy. The remaining healthy mitochondria would be fused with existing mitochondrial network through fusion processes. In this way, mitochondria can maintain energy production to sustain cellular homeostasis [46].  

However, if mitochondria become highly depolarized and therefore irreversibly damaged, these mitochondrial will be eliminated permanently with no possibility of being reincorporated via fusion events. The mitochondrial membrane potential  (∆Ψm) becomes the determining factor in sorting out which mitochondria can be repaired and restored, and which must be segregated and permanently eliminated [45]. 

Membrane Permeabilization and Depolarization

The onset of mitochondrial depolarization is always coupled with depolarization of the plasma membrane potential.  Studies have also shown that permeabilization of the outer mitochondrial membrane is necessary for the depolarization of membrane potential during apoptosis [47].  Mitochondrial membrane permeabilization and the loss of mitochondrial transmembrane potential, or ΔΨm depolarization are often used as biomarkers of apoptosis [53]

During mitochondrial depolarization, release of large quantities of cytochrome c slows down electron flow, interrupting the production of ATP that eventually leads to the formation of increased free radicals that will disturb cellular homeostasis [47]. 

The mitochondrial membrane potential (ΔΨm) is the main source of chemical energy that is responsible for driving proton re-entry from the intermembrane space through the ATP synthase back into the mitochondrial matrix [48].  The maintenance of appropriate ΔΨm is critical for mitochondrial energy production as the energy available for ATP synthesis is directly derived from mitochondrial membrane potential (ΔΨm). Depolarization translates into decreased energy available for ATP synthesis.

It is now understood that mitochondria contain individual interconnected powerhouses called cristae [49]. Individual crista is able to maintain different membrane potential along the inner mitochondrial membrane. During transient depolarization events, some cristae can maintain polarity despite the collapse of ΔΨm in adjacent cristae [50].  

This means that during depolarization, the cristae that can sustain membrane potential can be rescued and fused into existing healthy mitochondria. However, fusion must happen before the cristae loses polarity permanently because reduced membrane potential can decrease the level of fusion protein OPA1, generating non-fusing mitochondria as a result [51]. Simultaneous tracking of fission and Δψm revealed that depolarized mitochondria produced during fission events are SIX times less likely to be fused within the next 10 minutes [52]. 

What can facilitate the rescue of depolarized mitochondria?

Ascorbic Acid, Mitochondria & Depolarization – the Plasma Membrane Redox System Revisited

Recent discoveries showed that ascorbic acid has the ability to return mitochondrial fusion rates to normal in a model for Parkinson’s disease [54].  Many earlier studies already demonstrated that ascorbic acid, vitamin C, can prevent loss of mitochondrial membrane potential. When cells were treated with uncoupling agents that can inhibit oxidative phosphorylation like CCCP (carbonyl cyanide m-chlorophenyl hydrazone), membrane potential was lowered together with the induction of membrane permeabilization, while cytochrome c proteins were released to initiate apoptosis.  The addition of ascorbic acid to these cells prevented depolarization and ensuing apoptotic cascade events [55]. 

The ability of ascorbic acid to prevent depolarization in mitochondrial membrane confers anti-cytotoxic effects resulting in dose-dependent decrease in apoptosis in cells during in vitro experiments [56]  Ionizing radiation induce mitochondrial membrane depolarization in cells and causes apoptosis [57]. Pretreating cells with ascorbic acid protected cells against ionizing radiation induced apoptosis [58]. 

Coronavirus & Membrane Depolarization – The Ascorbic Acid Connection

The N-protein of SARS-CoV has been demonstrated to cause apoptosis via the mitochondrial apoptotic pathway under starvation of serum.  Zhang et al. in 2009 found that the N-protein could cause increased generation of reactive oxygen species, leading to loss of membrane potential, increased membrane permeability, cytochrome C release and ultimately cell death after bovine serum was withdrawn for 24 hours [59].  Why is bovine serum important? Bovine serum contains various micronutrients [60] but most of all, it contains ascorbic acid [61]. 

There is no doubt that coronaviruses like 2019-nCoV, SARS-CoV, and MERS-CoV target mitochondria to induce apoptosis in order to disrupt host immune system in order to facilitate proliferation.  Protecting mitochondrial dynamics in fusion and fission events allow depolarized mitochondria to regain functional control.  How does ascorbic acid maintain membrane potential to protect mitochondrial dynamics? 

CYB5R3 & VDAC1 – A Tale of Membrane Potential & Ascorbic Acid

There is an extensive, dynamic and influential network of plasma membrane enzymes that regulate redox balance in the cellular environment. These enzymes were not formally classified until the early 2000’s because they were primarily NADH or NADPH oxidases that had been known under various other names based upon their physiological electron acceptors. Most of these plasma membrane redox enzymes that have been identified so far use ascorbic acid almost EXCLUSIVELY as their electron acceptor and donor, due to the unique characteristics of ascorbic acid [62].

The CYB5R plasma membrane enzyme is encoded by four genes CYB5R1, CYB5R2, CYB5R3 and CYB5R4. The isoform CYB5R3 has ubiquitous cytoplasmic expression and its membrane-bound form is present in mitochondria, nucleus, endoplasmic reticulum and plasma membrane [64].

The CYB5R3 (membrane-bound NADH:cytochrome b5 oxidoreductase 3) enzyme catalyzes rapid exchange of electrons between ascorbate and its one electron oxidation metabolite, ascorbyl free radical (AFR), also known as semidehydroascorbate.  The CYB5R3 enzyme uses electrons from NADH to convert AFR back into ascorbate [64]. 

CYB5R3 is located on the outer mitochondrial membrane and is functionally connected to VDAC1 (voltage-dependent anion channel 1).  VDAC1 is the most abundant protein found on the outer mitochondrial membrane (OMM) [64]. The Cyb5R3/VDAC1 system is responsible for the conversion of AFR into ascorbate. VDAC1 has been shown to preserve mitochondrial membrane integrity, keeping cells intact when exposed to carcinogens that could induce depolarization and apoptosis [65, 66]. 

Mice bred without CYB5R3 show a loss of mitochondrial biogenesis, accompanied by 30% loss of total ATP, 50% loss of Complex IV activity, and 25% loss of Complex IV protein quality [67].  Why is CYB5R3 essential for maintaining normal functioning of mitochondria, including activity of mitochondrial ETC, oxygen consumption, ATP production and resistance to oxidative stress? CYB5R3/VDAC1 is actually an additional energy generating pathway that utilizes ascorbate/AFR as electron donors and acceptors [68]. 

When oxidative phosphorylation activity is not supported by the respiratory chain proteins due to collapsed membrane potential (depolarization), the activity of the CYB5R3/VDAC1 system is able to generate an electrochemical membrane potential catalyzed by electron transfers [69, 70, 71].  CYB5R3/VDAC1 transfer electrons from cytosolic NADH into mitochondria, utilizing Complex IV [69, 72]. Most surprisingly, when ascorbic acid, instead of NADH is supplied to intact mitochondria, the same non-enzymatic induction of this alternative energy production pathway was observed, where there was oxygen uptake, cytochrome c reduction and ascorbate oxidation [69,72].  

The rapid conversion of AFR back to ascorbate using NADH as electron donor restores the ascorbate pool and maintains a high NAD+/NADH ratio in cells [68].  However, if there is a lack of NADH, then it may be necessary to maintain a constant supply of fresh ascorbate so that CYB5R3/VDAC1 can utilize electrons from ascorbate to generate membrane potential to rescue depolarizing mitochondria.  

During severe infections, the ability of mitochondria to utilize plasma redox system CYB5R3/VDAC1 to generate transient supply of alternate energy would provide mitochondria the opportunity to maintain fusion and fission events to clear damaged mitochondria. Ascorbic acid provides electrons to CYB5R3/VDAC1 when NADH is inadequate as a result of disrupted oxidative phosphorylation. 

The importance of a continuous supply of adequate ascorbic acid during cytokine storms induced by coronavirus infections cannot be underestimated. 

Have you had your AA today? References

[1] Novel Coronavirus 2019 Situation Summary, Wuhan, China | CDC https://www.cdc.gov/coronavirus/2019-ncov/summary.html

[2] Ascorbic acid: its role in immune system and chronic inflammation diseases. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/24766384

[3] Mechanisms of attenuation of abdominal sepsis induced acute lung injury by ascorbic acid. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/22523283

[4] Vitamin C and Immune Function https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5707683/ 

[5] Effects of ascorbate on leucocytes: Part III. In vitro and in vivo stimulation of abnormal neutrophil motility by ascorbate. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/550365

[6] Lymphocytes 2018_Influence of Vitamin C on Lymphocytes: An Overview https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5874527/

[7] Technical advance: ascorbic acid induces development of double-positive T cells from human hematopoietic stem cells in the absence of stromal cells. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/25157026/

[8] Promotion of IL-4- and IL-5-dependent differentiation of anti-mu-primed B cells by ascorbic acid 2-glucoside. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/19201381/

[9] Vitamin C and Infection | Nutrition Reviews | Oxford Academic https://academic.oup.com/nutritionreviews/article-abstract/1/7/202/1874601?redirectedFrom=PDF

[10] Vitamin C and Infections. – PubMed – NCBI  https://www.ncbi.nlm.nih.gov/pubmed/28353648/ 

[11] Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding – The Lancet https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30251-8/fulltext

[12] Interspecies transmission and emergence of novel viruses: lessons from bats and birds. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/23770275

[13] Middle East respiratory syndrome coronavirus: another zoonotic betacoronavirus causing SARS-like disease. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/25810418

[14] ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/16282461

[15] Single-cell RNA expression profiling of ACE2, the putative receptor of Wuhan 2019-nCov | bioRxiv https://www.biorxiv.org/content/10.1101/2020.01.26.919985v1

[16] Functional assessment of cell entry and receptor usage for lineage B β-coronaviruses, including 2019-nCoV | bioRxiv https://www.biorxiv.org/content/10.1101/2020.01.22.915660v1.full

[17] Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study – The Lancet https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30211-7/fulltext

[18] Functional assessment of cell entry and receptor usage for lineage B β-coronaviruses, including 2019-nCoV | bioRxiv https://www.biorxiv.org/content/10.1101/2020.01.22.915660v1.full#ref-20 

[19] Expression of SARS-coronavirus envelope protein in Escherichia coli cells alters membrane permeability. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/15522242/

[20] Biochemical and functional characterization of the membrane association and membrane permeabilizing activity of the severe acute respiratory syndrome coronavirus envelope protein.- PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/16507314/

[21] CORONAVIRUS VIRULENCE GENES WITH MAIN FOCUS ON SARS-CoV ENVELOPE GENE https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4261026/

[22] Coronavirus envelope protein: current knowledge | Virology Journal | Full Text https://virologyj.biomedcentral.com/articles/10.1186/s12985-019-1182-0

[23] Genomic characterization of the 2019 novel human-pathogenic coronavirus isolated from a patient with atypical pneumonia after visiting Wuhan: Emerging Microbes & Infections: Vol 9, No 1 https://www.tandfonline.com/doi/full/10.1080/22221751.2020.1719902

[24] Plasma inflammatory cytokines and chemokines in severe acute respiratory syndrome https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808997/

[25] MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile. – PubMed – NCB Ihttps://www.ncbi.nlm.nih.gov/pubmed/29414327

[26] Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China – The Lancet https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30183-5/fulltext 

[27] Cytokine storm of graft-versus-host disease: a critical effector role for interleukin-1. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/8442093

[28] Into the Eye of the Cytokine Storm https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294426/ 

[29] Development of the adult respiratory distress syndrome: progressive alteration of neutrophil chemotactic and secretory processes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1900478/

[30] Monocyte deactivation in septic patients: restoration by IFN-gamma treatment. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/9176497

[31] Normal responses to injury prevent systemic inflammation and can be immunosuppressive. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/11179099

[32] Persisting low monocyte human leukocyte antigen-DR expression predicts mortality in septic shock. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/16741700

[33] Apoptotic Cells Induced Signaling for Immune Homeostasis in Macrophages and Dendritic Cells https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661053/

[34] Apoptosis: A Basic Biological Phenomenon with Wideranging Implications in Tissue Kinetics | British Journal of Cancer https://www.nature.com/articles/bjc197233

[35] Mitochondrial regulation of apoptotic cell death – ScienceDirect https://www.sciencedirect.com/science/article/abs/pii/S037842740300479X

[36] Multiple pathways of cytochrome c release from mitochondria in apoptosis – ScienceDirect https://www.sciencedirect.com/science/article/pii/S0005272806000715

[37] Mitochondrial location of severe acute respiratory syndrome coronavirus 3b protein. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/16682811

[38] Active Replication of Middle East Respiratory Syndrome Coronavirus and Aberrant Induction of Inflammatory Cytokines and Chemokines in Human Macrophages: Implications for Pathogenesis | The Journal of Infectious Diseases | Oxford Academic ttps://academic.oup.com/jid/article/209/9/1331/884110

[39] Mapping the innate signaling cascade essential for cytokine storm during influenza virus infection | PNAS https://www.pnas.org/content/111/10/3799

[40] Host cell proteases: critical determinants of coronavirus tropism and pathogenesis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465284/ 

[41] Severe acute respiratory syndrome coronavirus 3a  protein activates the mitochondrial death pathway through p38 MAP kinase activation https://www.ncbi.nlm.nih.gov/pubmed/18632968

[42] Mitochondria as central hub of the immune system – ScienceDirect https://www.sciencedirect.com/science/article/pii/S2213231719303076

[43] Mitochondria are the powerhouses of immunity | Nature Immunology https://www.nature.com/articles/ni.3704?draft=marketing

[44] Diverse Roles of Mitochondria in Immune Responses: Novel Insights Into Immuno-Metabolism | Immunology  https://www.frontiersin.org/articles/10.3389/fimmu.2018.01605/full

[45] Mitochondrial dynamics and viral infections: A close nexus – ScienceDirect https://www.sciencedirect.com/science/article/pii/S0167488915000099 

[46] The essential role of mitochondrial dynamics in antiviral immunity  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5988924/ 

[47] Outer mitochondrial membrane permeabilization during apoptosis triggers caspase-independent mitochondrial and caspase-dependent plasma membrane potential depolarization: a single-cell analysis | Journal of Cell Science https://jcs.biologists.org/content/116/3/525

[48] Coupling of Phosphorylation to Electron and Hydrogen Transfer by a Chemi-Osmotic type of Mechanism | Nature https://www.nature.com/articles/191144a0

[49] Cristae – The Powerhouses Within – EvolutaMente.it https://www.evolutamente.it/cristae-the-powerhouses-within/ 

[50]  Individual cristae within the same mitochondrion display different membrane potentials and are functionally independent | The EMBO Journal https://www.embopress.org/doi/full/10.15252/embj.2018101056

[51] Fission and selective fusion govern mitochondrial segregation and elimination by autophagy https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2234339/ 

[52] Fission and selective fusion govern mitochondrial segregation and elimination by autophagy. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/18200046/

[53] Role of mitochondrial membrane permeabilization and depolarization in platelet apoptosis – Leytin – 2018 – British Journal of Haematology – Wiley Online Library https://onlinelibrary.wiley.com/doi/full/10.1111/bjh.14903

[54] Exploring the Effect of Rotenone—A Known Inducer of Parkinson’s Disease—On Mitochondrial Dynamics in Dictyostelium discoideum https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6262481/

[55] Vitamin C enters mitochondria via facilitative glucose transporter 1 (Glut1) and confers mitochondrial protection against oxidative injury | The FASEB Journal https://www.fasebj.org/doi/full/10.1096/fj.05-4107com?ck=nck&legid=fasebj%3B19%2F12%2F1657&cited-by=yes

[56] Vitamin C Antagonizes the Cytotoxic Effects of Antineoplastic Drugs | Cancer Research https://cancerres.aacrjournals.org/content/68/19/8031 

[57] Ionizing radiation-induced, mitochondria-dependent generation of reactive oxygen/nitrogen. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/11358802

[58] Ascorbic acid inhibits apoptosis induced by X irradiation in HL60 myeloid leukemia cells. – PubMed – NCBI  https://www.ncbi.nlm.nih.gov/pubmed/10521923?dopt=Abstract

[59] SARS-CoV Nucleocapsid Protein Induced Apoptosis of COS-1 Mediated by the Mitochondrial Pathway: Artificial Cells, Blood Substitutes, and Biotechnology: Vol 35, No 2 https://www.tandfonline.com/doi/full/10.1080/10731190601188422#

[60] The Influence of Micronutrients in Cell Culture: A Reflection on Viability and Genomic Stability https://www.hindawi.com/journals/bmri/2013/597282/

[61] Chiral analysis of ascorbic acid in bovine serum using ultrathin molecular imprinted polyaniline/graphite electrode – ScienceDirect https://www.sciencedirect.com/science/article/pii/S1572665717302953

[62] Thioredoxin Reductase AFR NADH NADPH_Molecular biology of mammalian AFR reductases https://www.researchgate.net/publication/236015879_Molecular_biology_of_mammalian_AFR_reductases

[63] Characterization of the Trans-plasma Membrane Electron Transport System in the Myelin Membrane https://scholars.wlu.ca/cgi/viewcontent.cgi?referer=https://www.google.com/&httpsredir=1&article=2785&context=etd

[64] External mitochondrial NADH-dependent reductase of redox cyclers: VDAC1 or Cyb5R3? – ScienceDirect https://www.sciencedirect.com/science/article/abs/pii/S0891584914002573?via%3Dihub

[65] Paraquat toxicity induced by voltage-dependent anion channel 1 acts as an NADH-dependent oxidoreductase. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/19717555

[66] Paraquat induces oxidative stress and neuronal cell death; neuroprotection by water-soluble Coenzyme Q10. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/15519605

[67]Cytochrome B5 Reductase 3 Is Essential for Cardiomyocyte Function | Circulation https://www.ahajournals.org/doi/abs/10.1161/circ.136.suppl_1.20733

[68] Vitamin C versus Cancer: Ascorbic Acid Radical and Impairment of Mitochondrial Respiration? https://new.hindawi.com/journals/omcl/2020/1504048/

[69] Modulation of Cytochrome c-Mediated Extramitochondrial NADH Oxidation by Contact Site Density – ScienceDirect https://www.sciencedirect.com/science/article/abs/pii/S0006291X99907878

[70] Membrane potential generation coupled to oxidation of external NADH in liver mitochondria. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/9762923

[71] Cytochrome c-induced cytosolic nicotinamide adenine dinucleotide oxidation, mitochondrial permeability transition, and apoptosis. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/12573279 

[72] Porin and cytochrome oxidase containing contact sites involved in the oxidation of cytosolic NADH. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/15752713


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#10 adamh

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Posted 14 February 2020 - 04:22 PM

What masks will be effective against corona? I look on ebay and they are offering "n95" masks like that is the gold standard but they only filter out 95% of particles. What good is that? Others claim 99% or 99.9% and even if true that would not stop everything. Will we have to wear masks while indoors? Air conditioning filters only take out larger particles so the virus might come inside too.


Has anyone seen the videos of flocks of crows? Thousands of them flying in, not sure if they are all crows or a mixture 

of species. Each body on the street had a bunch of birds on it. Next will come a fly infestation, no wonder they are working frantically to incinerate the bodies


I heard it may cause sudden heart attacks, I have not seen the proof of that but they claim people are falling down suddenly and not even able to put hands out to break the fall, just a face plant. 


#11 resveratrol_guy

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Posted 16 February 2020 - 03:09 PM

My usual 2 cents:

1. We need to offer DRACO to consenting patients experiencing severe illness. It has cured various forms of coronavirus in rodent experiments, among other virus families. I'd bet the farm that this won't happen in the US, thanks to FDA intransigence and intellectual property considerations. I would also bet that this isn't even on the radar in the Chinese health system, so if you know folks over there, please point them to it. Their authoritarian government could actually do some good by making it available.


2. Blunt the cytokine storm, when it occurs, with rapamycin or analogs. Some patients are dying needlessly because their immune systems are too aggressive at responding to the infection.


3. I've used the following regimen many times over the years, and as recently as last week, when I just start feeling sick (sneezing, fever coming on, queasy, etc.). It has rarely failed me, and might be particularly useful in the elderly:


 * Carbon 60 olive/MCT oil providing about 4 mg of C60

 * 50 mg zinc gluconate (immune mythology that seems to work)

 * Shiittake-maitake extract (probably supplies beta glucan and some sort of natural killer cell booster)

 * Maybe also vitamin D (haven't taken consistently)


4. The similarities to HIV are striking, perhaps not coincidentally associated with the inclusion of various genes encoding pieces of the GP120 "harpoon". And then we have reports of reinfection, which might indicate rapid and ongoing mutation which moots antibody resistance or possibly even a durable and gradually mutating cellular reservoir, both of which occur in HIV. In other words, it may be that people who are "cured" of the virus are cured in the same sense as an HIV patient who has returned to health following their initial fever. I guess we'll know in a few months.

Edited by resveratrol_guy, 16 February 2020 - 03:24 PM.

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#12 Dorian Grey

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Posted 17 February 2020 - 06:31 AM

When I heard the COVID-19 coronavirus came from the same family of virus that causes the common cold, I thought of zinc as a potential therapy.  I've had excellent results from the old Zicam zinc nasal swabs (now banned due to anosmia issues), & more recently zinc acetate lozenges, both of which knocked out my head colds in record time.  In researching this, I see rinovirus & coronavirus are two different bugs???  




From the chart on the above linked page, it appears coronavirus are primarily associated with Winter colds, & rinovirus with Summer colds?  If this is true, I've had good results with zinc knocking out my Winter colds, which seem to be predominantly coronavirus.  The key seems to be getting high enough zinc concentrations where the bug actually lives in the nose, throat etc, & apparently zinc acetate lozenges are absorbed locally through the mucosa by keeping the lozenge in the mouth for extended periods, raising tissue levels of zinc high enough to kill the virus, or at least inhibit replication.  Systemic zinc supplements (absorbed in the gut) fail to raise zinc levels high enough locally in infected tissues to be effective, so the lozenge, and particularly the right type of lozenge (zinc aceatate) are vital.  Here's Chris Masterjohn describing how this works.  



The reports of COVID-19 spreading to the GI tract, with some patients reporting GI symptoms as their first sign of the disease are also intriguing.  If zinc is effective in high enough localized concentration, might extended bathing of the GI tract with multiple zinc lozenges over the first few days of infection possibly be helpful at inhibiting proliferation of COVID-19 in the GI tract?  


I always keep a bottle of the Life Extension "Enhanced Zinc Lozenges" (with the essential zinc acetate form Chris mentions) on hand to take at the first sign of a cold.  Don't know if this might work with COVID-19, particularly if it manifests initially in the lungs, but it probably couldn't hurt, & any effect at all on this bug in the throat or GI tract might tip the scales towards survival.  It is imperative to start treatment as early as possible, so you'd need to have this on hand day 1.  If the COVID-19 bug never shows up at your door, you can still use this to knock out your next head cold.  I've been very impressed with the results I've gotten with this therapy.  


What do you think about the potential for this angle?  

Edited by Dorian Grey, 17 February 2020 - 06:49 AM.

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#13 Ark

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Posted 18 February 2020 - 08:26 AM

Let's assume this is a Biowarfare weapon for fun, and you had to use everything you could think of. Whether FDA approved or Not.

What would your list look like?

#14 Dorian Grey

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Posted 18 February 2020 - 04:30 PM

The zinc acetate lozenges I posted on above would seem to cover the upper respiratory / oropharyngeal tissues, as well as upper and perhaps lower GI tract well.  


Other than this, restricting the virus access to iron with curcumin, quercetin and IP6 (Inositol Hexaphosphate) would seem logical.  




"Understanding how iron metabolism and viral infection interact might suggest new methods to control disease."


IP6 also activates natural killer cells: https://www.foundati...02/v7-3-244.pdf


In addition, IP6 has been shown to enhance NK-cell activity, thereby boosting NK-cell cytotoxicity


which are important in killing virus: https://en.wikipedia...ral_killer_cell


"NK cells provide rapid responses to virus-infected cells"  "NK cells are activated in response to interferons or macrophage-derived cytokines. They serve to contain viral infections while the adaptive immune response generates antigen-specific cytotoxic T cells that can clear the infection. NK cells work to control viral infections by secreting IFNγ and TNFα."


Secondary bacterial pneumonia is particularly dependent on free iron: 




"The proliferative capability of many invasive pathogens is limited by the bioavailability of iron."


Green Tea also sequesters free iron




"Green tea significantly decreased serum levels of iron, ferritin and MDA and increased TAC compared with control group"

Edited by Dorian Grey, 18 February 2020 - 04:49 PM.

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#15 izan82

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Posted 26 February 2020 - 10:45 PM

Dorian, great input as always, but are you sure IP6 would be effective against virus activity



Read this please. 




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#16 Dorian Grey

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Posted 27 February 2020 - 05:28 AM

Dorian, great input as always, but are you sure IP6 would be effective against virus activity



Read this please. 





Great find izan.  Thanks for this.  Will scratch IP6 off my list TFN.  


Meanwhile, I bought a "pulse oximeter" (aka oxygen saturation monitor) today. These things work by shining a light through your finger-tip and looking at how red your blood is from the light coming out on the other side.  How cool is that?  




$35 (available at most pharmacies, Walmart etc). These measure how much oxygen your blood is carrying.  Normal range between 94-99.  Pneumonia will drop this down into the 80's pretty quick.  




"This is the first large study to look at whether oxygen saturation might indicate pneumonia and the results do support using pulse oximetry in assessing patients in primary care"


If (WHEN?) I do get sick, I'd like to avoid the crunch down at the local hospital unless & until I actually need a major intervention.  It can be very difficult to tell exactly when you're sinking into deep doo-doo, but Oxygen Saturation will flag pneumonia remarkably well.  


These little gizmo's will probably sell out before too long now that we're due for more cases, and they are made in China, so there may not be any more in the post for quite a while.  Get 'em while they are available if like me, you're not looking forward to lining up at the make-shift triage tent down at the hospital parking lot until you absolutely have to. 

Edited by Dorian Grey, 27 February 2020 - 05:41 AM.

#17 Dorian Grey

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Posted 27 February 2020 - 06:14 AM

N-acetyl-cysteine: Pro's & (at least one) con.  


I was reading about the pathology found with COVID, & the "thick mucus" that was found to be associated & problematic with COVID




Covid-19 autopsy shows lungs full of mucus, different from SARS


"the lung of patients with Covid-19 is different from those infected with SARS. “The fibrosis in the lungs is not so severe as we expected. The final results have not come out yet. It seems that some alveoli are still there, but the inflammation is very severe and there is a lot of sticky mucus. This causes difficulty in breathing."




Autopsies reveal differences between SARS and coronavirus


"unlike those who perished due to SARS, autopsies of the first two deaths in the recent outbreak reveal that their lungs did not exhibit significant pulmonary fibrosis, or thickened and stiff lung tissue, reported Sina. Instead, their lungs were found to have severe inflammations and mucus buildup, which resulted in breathing difficulty"


I'd read N-acetyl-cysteine was used to thin mucus in cystic fibrosis patients...  




"Since the 1960s, N-acetyl cysteine (NAC) has been a commonly used mucolytic to clear the clogged airways in CF patients."


Thought this might be helpful with COVID, with little downside till I found this: 




N-acetyl-cysteine increases the replication of Chlamydia pneumoniae and prolongs the clearance of the pathogen from mice


Looks like Chlamydia pneumoniae is a bacterial infection commonly acquired in hospital patients.  Don't know if this would be likely during the early stages of COVID, but it would seem to me anything that prevented plugs of thick mucus deep in your lungs might be a good thing.  


Any other problems with this potential therapy?  


#18 Dorian Grey

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Posted 27 February 2020 - 06:23 AM

Cystic Fibrosis patients also benefit from postural drainage and percussive therapy to clear mucus plugs:




Basics of Postural Drainage and Percussion


"Chest physical therapy (CPT), or postural drainage and percussion (PD & P), uses gravity and percussion (clapping on the chest and/or back) to loosen the thick, sticky mucus in the lungs so it can be removed by coughing. Unclogging the airways is key to keeping lungs healthy."


Don't know how much this might help with the thick mucus found in COVID, but it shouldn't hurt to try.  The mucus in COVID is found primarily in the LOWER LUNGS, so this would be your area of focus.  

#19 Daniel Cooper

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Posted 27 February 2020 - 02:14 PM

Let's assume this is a Biowarfare weapon for fun, and you had to use everything you could think of. Whether FDA approved or Not.

What would your list look like?



DRACO without a doubt.  Why that research has been allowed to languish is beyond me.

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#20 ambivalent

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Posted 29 February 2020 - 10:54 PM

Regular fasting builds a strong immune system:





Edited by ambivalent, 29 February 2020 - 10:55 PM.

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#21 Oakman

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Posted 01 March 2020 - 04:55 PM

DRACO without a doubt.  Why that research has been allowed to languish is beyond me.


Reading about the sad tale of DRACO leaves me flabbergasted! It's as if the cure for cancer, or cure for aging had been discovered, but they couldn't get funding to finalize and approve it, so whatever, let it die in funding limbo. WTH? 

#22 HBRU

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Posted 01 March 2020 - 06:41 PM

IP6 may help both in senolitic protocols and virus infections ??


#23 ambivalent

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Posted 01 March 2020 - 09:54 PM

Another supplement is allicin, naturally poorly researched but with some suggestion of antiviral properties:




On vitamin C, this guy asserts that bowel tolerance of C sky rocket with ebola, influenza. Here he recounts putting a woman with HIV on high C dosage, claiming 25 years later, there was no trace of the virus. 




Also, I'm sure I've stumbled across claims and anecdotes of improved immune system function derived from cold baths and meditation. Any research supporting this or indeed breathing exercises chez Wim Hof?





Edited by ambivalent, 01 March 2020 - 10:10 PM.

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#24 ambivalent

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Posted 01 March 2020 - 10:52 PM

Also an alternative to strict fasting is the Fastic Mimic Diet developed by Prof Longo. It is expensive, though ($250). (There are DIY FMD's out there, though I have no experience of either.)




As far as I am aware he has conducted several studies using FMD and has found it to be as or more effective than water-fasting. 







Edited by ambivalent, 01 March 2020 - 10:53 PM.

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#25 Hip

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Posted 01 March 2020 - 11:22 PM

Another supplement is allicin, naturally poorly researched but with some suggestion of antiviral properties:





That paper does not actually test allicin in vivo for any antiviral effect. 


However, this paper does, and finds that in a placebo controlled test, the group given allicin had a lot fewer colds than the control group (24 colds for the allicin group versus 65 for the control group).


Remember, coronavirus is one of the viruses that causes the common cold, so if allicin can reduce the risk of catching a cold, it may reduce the risk of catching the COVID-19 coronavirus.


Thus an allicin capsule daily might buy some protection against catching COVID-19.

Edited by Hip, 01 March 2020 - 11:25 PM.

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#26 ambivalent

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Posted 02 March 2020 - 12:28 AM

Good find!


Here is an ebook written by the researcher in the linked paper:




Search 'viral' and you'll find the study mentioned as well as impressive testimonials from an MS and an AIDS patient.  

Edited by ambivalent, 02 March 2020 - 12:35 AM.

#27 albedo

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Posted 02 March 2020 - 07:24 AM

Always thought IP6 useful as immune booster and lower iron and NAC to help cleaning lungs. Should I reconsider?

#28 ambivalent

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Posted 02 March 2020 - 02:02 PM

Allicin is pretty unstable and ephemeral (iirc) and as such acts as something of a system shock wave. So I wonder if we can improve efficacy to coordinate with peak exposure. But when might this be? At T or T+2 hours after alighting tube or leaving the office, say? 

#29 Hip

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Posted 02 March 2020 - 02:12 PM

Allicin is pretty unstable and ephemeral (iirc) and as such acts as something of a system shock wave. So I wonder if we can improve efficacy to coordinate with peak exposure. But when might this be? At T or T+2 hours after alighting tube or leaving the office, say? 


Allicin rapidly breaks down into a number of different substances, but those substances themselves may have the antiviral effect:


Allicin breaks down in vitro to form:     

diallyl trisulfide (DATS) — also called allitridin
diallyl disulfide (DADS)
diallyl sulfide (DAS), 
In the presence of oil or organic solvents, allicin breaks down to:
In vivo, allicin can react with glutathione and L-cysteine to produce
S-allylmercaptoglutathione (SAMG)  
S-allylmercaptocysteine (SAMC)
Ref: here.
I believe ajoene and allitridin have been shown to have antiviral effects. 

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#30 Galaxyshock

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Posted 03 March 2020 - 10:59 AM

What about Echinacea Purpurea?


Anti-viral properties and mode of action of standardized Echinacea purpurea extract against highly pathogenic avian Influenza virus (H5N1, H7N7) and swine-origin H1N1 (S-OIV)



Echinacea—A Source of Potent Antivirals for Respiratory Virus Infections






Neutralizing activity of Echinacea purpurea on Coronaviruses including highly pathogenic Middle-East-Respiratory Syndrome Virus (MERS-CoV)



Edited by Galaxyshock, 03 March 2020 - 11:39 AM.

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