3083 replies to this topic

[Mind]

Mass media news article:
 
Covid-19 Research Updates: Chinese Study Reveals That Hypokalemia Present In Almost All Covid-19 Patients
 
Paper on which that article is based:
 
Hypokalemia and Clinical Implications in Patients with Coronavirus Disease 2019 (COVID-19)

 

Can someone clarify.

 

Is the gist of this study that Covid-19 causes hypokalemia and that restoring K+ helps with recovery?

 

Or that people with hypokalemia more susceptible to severe Covid-19 symptooms?

 

Also, they used 3 grams of K+ per day. That seems like quite the megadose.

Edited by Mind, 25 March 2020 - 05:04 PM.

[OP2040]

I don't see the data in there to support either position, as you would need to know hypokalemia as a previously existing condition before the infection.  It's just as likely they started off with hypokalemia as developed it with the infection.  I could be wrong as I just skimmed through it.  Here's the full link if anyone wants to do the work.

 

https://www.medrxiv....8530v1.full.pdf

[Daniel Cooper]

Can someone clarify.

 

Is the gist of this study that Covid-19 causes hypokalemia and that restoring K+ helps with recovery?

 

Or that people with hypokalemia more susceptible to severe Covid-19 symptooms?

 

Also, they used 3 grams of K+ per day. That seems like quite the megadose.

 

 

Looks to me that covid-19 causes hypokalemia.

 

I think the normal intake of K is supposed to be around 4 grams/day from diet, though most people don't get that much.  So for someone that is dangerously low on potassium and may be flushing it out their kidneys due to this virus, I suppose 3g per day isn't overly dramatic.

 

Article also said that those with pre-existing low potassium that the situation is made radically worse with the infection.  Since many high BP patients are on diuretic type BP lowering drugs that tend to wash out potassium, that could be one of the links between high BP and worsened outcomes.

Edited by Daniel Cooper, 25 March 2020 - 05:44 PM.

[lancebr]

Maybe there is another way to block this virus from infecting the host cells.

 

Studies are finding that the way this virus infects the body is through the following process:

 

Cell entry of 2019-nCov depends on binding of the viral spike proteins to cellular receptors ACE2 and on S protein priming by

host cell protease TMPRSS2 . A TMPRSS2 inhibitor approved for clinical use blocked entry of 2019-nCov.

 

https://www.ncbi.nlm...pubmed/32142651

 

So my understanding of this process is that the 2019-nCov uses its viral spike to attach to the ACE2 receptors and then the

virus uses the cell protease TMPRSS2 to prime itself so it can enter the host cell and start to replicate.  A TMPRSS2 inhibitor

stops this process from happening causing the virus to be unable to enter the cell and replicate.

 

But an issue with ACE2 is that....."ACE2 did not show a high or specific expression in the lung, which is the major infected tissue in
the human body by this virus. It remains unclear why the lung is mainly infected, but not other tissues among which ACE2 is highly

expressed. We hypothesized that there could be some other gene playing key roles in the entry of 2019-nCoV into human cells."

 

So they are saying that the lung is the primary organ infected by this virus, but the lungs do not show a high or specific expression of ACE2,

And that tissues that do have a high expression of ACE2 are not being infected by the virus like the lungs are. So there must be something

special to the lungs that this virus is using.

 

Well, researchers found that "AGTR2 (angiotensin II receptor type 2), a G-protein coupled receptor, has interaction with ACE2 and is highly

expressed in the lung with a high tissue specificity. More importantly, simulation of 3D structure based protein-protein interaction reveals that

AGTR2 shows a higher binding affinity with the spike protein of 2019-nCov than ACE2 (energy score: -15.7 vs. -6.9 [kcal/mol])"

 

So then based upon the research we need to find something that can inhibit AGTR2 and also inhibit TMPRSS2 to cover all angles. And there

is actually a substance that can inhibit both of those.

 

The herb Andrographis

 

In reference to AGTR2:

 

"Through screening CMap and JMap, we identified the potential agents to decrease the expression level of AGTR2. A number of agents that

decreased the expression of AGTR2 included Urtica, Andrographis, lipopolysaccharide."

 

In reference to TMPRSS2:

 

"Studies have shown that inhibiting the enzyme activity of TMPRSS2 can prevent coronaviruses from entering host cells. As a possible target

for anti-viral drug discovery, the virtual screen results predicted many anti-bacterial drugs (pivampicillin, hetacillin, cefoperazone and clindamycin)

and anti-virus natural compounds (phyllaemblicin G7, neoandrographolide, kouitchenside I), etc. to be potential TMPRSS2 inhibitors."

 

Neonandrographolide is a compound of the andrographis herb.

 

Also there is some belief that Chloroquine works by raising the pH of the endosomes since a virus can not seem to replicates in that type of enviroment. Andrographis has been found to also raise pH to prevent virus from replicating:

 

https://www.ncbi.nlm...les/PMC6186950/

 

In addition to those benefits, Andrographis also appears to inhibit the cytokine IL-6 which was found to cause significant damage to the lungs in the  

2019-nCov virus.

 

https://www.ncbi.nlm...pubmed/21442031

Edited by lancebr, 25 March 2020 - 08:23 PM.

[lancebr]

There was a doctor who gave some assessments of what he has seen in the treatment of patients with Covid 19.

 

He said that he has been surprised at the levels of Interleukin-6 in some of the patients he has treated. Their levels

have been higher than what is usually seen in AIDS patients that have Kaposi Sarcoma Inflammatory Cytokine Syndrome.

 

He also said that at the hospital he is working at they are utilizing Plaquenil, but that it doesn't appear to be the

wonder treatment that everyone is expecting it to be.  His colleagues believe that it would be more useful as a

prophylactic.....since the utilization of it as a treatment after contracting the virus is not showing the results they

were hoping for.

 

There are so many different takes on how good or bad this treatment is that it is hard to know what to believe.

 

Here is information of what dosages some doctors are using to use it as a prophylactic:

 

 Prophylaxis-for-Exposed.jpg   133.81KB   3 downloads

Edited by lancebr, 26 March 2020 - 07:07 AM.

[thompson92]

 

Here is information of what dosages some doctors are using to use it as a prophylactic:

 

 

Needs zinc co-administered with it.  And now we know a couple grams of potassium is ideal also.

[thompson92]

https://www.bmj.com/...68/bmj.m1206/rr

 

Comment to BMJ pointing out the value of HSPG role in coronaviruses attachment to cells prior to entry via ACE2.  I'm still mystified as to how lactoferrin and heparin isn't getting much excitement.  I know it's been mentioned in prior comments in this thread and we don't have definitive data showing its interference with this strain of virus.  But I'm taking it daily and it's at the top of my list.

[lancebr]

https://www.bmj.com/...68/bmj.m1206/rr

 

Comment to BMJ pointing out the value of HSPG role in coronaviruses attachment to cells prior to entry via ACE2.  I'm still mystified as to how lactoferrin and heparin isn't getting much excitement.  I know it's been mentioned in prior comments in this thread and we don't have definitive data showing its interference with this strain of virus.  But I'm taking it daily and it's at the top of my list.

 

They have actually found that SARS-CoV-2 is using TMPRSS2 to gain entry into the the cell and then to

replicate.  A TMPRSS2 inhibitor was found to block entry of the virus.

 

https://www.ncbi.nlm...pubmed/32142651

Edited by lancebr, 26 March 2020 - 04:15 PM.

[xEva]

I'm doubtful that ACE2 plays role here. See comments above citing studies that show that ACE2 is poorly expressed in lungs, where covid19 causes critical damage, and is plentiful in other, unaffected tissues.

[DanCG]

Maybe there is another way to block this virus from infecting the host cells.

 

 

In reference to AGTR2:

 

"Through screening CMap and JMap, we identified the potential agents to decrease the expression level of AGTR2. A number of agents that

decreased the expression of AGTR2 included Urtica, Andrographis, lipopolysaccharide."

 

 

This part caught my eye because I regularly take Urtica. It turns out that an agglutinin from Urtica was previously shown to inhibit SARS-CoV replication. I'm new, so I can't post links, but the reference is Antiviral Res. 2011 Apr;90(1):22-32.

 

Yet another potentially useful natural product that too few people know about.

[p75213]

Maybe there is another way to block this virus from infecting the host cells.

Studies are finding that the way this virus infects the body is through the following process:

Cell entry of 2019-nCov depends on binding of the viral spike proteins to cellular receptors ACE2 and on S protein priming by
host cell protease TMPRSS2 . A TMPRSS2 inhibitor approved for clinical use blocked entry of 2019-nCov.

https://www.ncbi.nlm...pubmed/32142651

So my understanding of this process is that the 2019-nCov uses its viral spike to attach to the ACE2 receptors and then the
virus uses the cell protease TMPRSS2 to prime itself so it can enter the host cell and start to replicate. A TMPRSS2 inhibitor
stops this process from happening causing the virus to be unable to enter the cell and replicate.

But an issue with ACE2 is that....."ACE2 did not show a high or specific expression in the lung, which is the major infected tissue in
the human body by this virus. It remains unclear why the lung is mainly infected, but not other tissues among which ACE2 is highly
expressed. We hypothesized that there could be some other gene playing key roles in the entry of 2019-nCoV into human cells."

So they are saying that the lung is the primary organ infected by this virus, but the lungs do not show a high or specific expression of ACE2,
And that tissues that do have a high expression of ACE2 are not being infected by the virus like the lungs are. So there must be something
special to the lungs that this virus is using.

Well, researchers found that "AGTR2 (angiotensin II receptor type 2), a G-protein coupled receptor, has interaction with ACE2 and is highly
expressed in the lung with a high tissue specificity. More importantly, simulation of 3D structure based protein-protein interaction reveals that
AGTR2 shows a higher binding affinity with the spike protein of 2019-nCov than ACE2 (energy score: -15.7 vs. -6.9 [kcal/mol])"

So then based upon the research we need to find something that can inhibit AGTR2 and also inhibit TMPRSS2 to cover all angles. And there
is actually a substance that can inhibit both of those.

The herb Andrographis

In reference to AGTR2:

"Through screening CMap and JMap, we identified the potential agents to decrease the expression level of AGTR2. A number of agents that
decreased the expression of AGTR2 included Urtica, Andrographis, lipopolysaccharide."

In reference to TMPRSS2:

"Studies have shown that inhibiting the enzyme activity of TMPRSS2 can prevent coronaviruses from entering host cells. As a possible target
for anti-viral drug discovery, the virtual screen results predicted many anti-bacterial drugs (pivampicillin, hetacillin, cefoperazone and clindamycin)
and anti-virus natural compounds (phyllaemblicin G7, neoandrographolide, kouitchenside I), etc. to be potential TMPRSS2 inhibitors."

Neonandrographolide is a compound of the andrographis herb.

Also there is some belief that Chloroquine works by raising the pH of the endosomes since a virus can not seem to replicates in that type of enviroment. Andrographis has been found to also raise pH to prevent virus from replicating:

https://www.ncbi.nlm...les/PMC6186950/

In addition to those benefits, Andrographis also appears to inhibit the cytokine IL-6 which was found to cause significant damage to the lungs in the
2019-nCov virus.

https://www.ncbi.nlm...pubmed/21442031

For what it's worth:
https://www.bangkokp...rbal-medication

https://www.reuters....s-idUSKBN21D0EF

I haven't done any analysis but for a population of 70 million that looks pretty good.

Edited by p75213, 26 March 2020 - 07:18 PM.

[lancebr]

For what it's worth:
https://www.bangkokp...rbal-medication

https://www.reuters....s-idUSKBN21D0EF

I haven't done any analysis but for a population of 70 million that looks pretty good.

 

I like the way that one doctor says that there is no research to confirm that the plant has

any protection toward the Wuhan Virus.  Well of course there is no research the virus

has just been spreading for a few months now. I assume he is one of those doctors that

will tell you that Vitamin C or Zinc is not good against it because there is no studies for that

either against the Wuhan virus.

 

Actually andrographis has several good studies showing its value. 

 

https://www.ncbi.nlm...pubmed/27896563

https://www.ncbi.nlm...pubmed/28783743

hhttps://www.ncbi.nlm...pubmed/20092985

https://www.ncbi.nlm.../pubmed/1797953

https://www.ncbi.nlm...ubmed/20307638/

https://www.ncbi.nlm...ubmed/21034865/

https://www.ncbi.nlm...ubmed/20728594/

https://www.ncbi.nlm...pubmed/16372376

 

And this is just a few of them.

Edited by lancebr, 26 March 2020 - 08:33 PM.

[Mind]

So now we have 4 small trials of hydroxychloroquine (one very uncontrolled), alone or in combination with azythromycin and zinc. (Bahrain, France, Belgium, and New York) showing some promise, plus one Chinese study showing some positive results from administering potassium.

 

Also one Chinese study (27 subjects) showing no difference between hydroxychloroquine (alone) and standard coronavirus treatment.

 

I know some trials are ongoing, but does anyone know any entrepreneurial doctors willing to try the combination of hydroxychloroquine, azythromycin, zinc, and potassium. Maybe there is some synergy in the combination. I might also through in a braodspectrum probiotic (to maintain gut health during the treatment). These are the only substances so far the have shown some potential thus far.

 

I don't like sitting around wondering about the other trials, listening to politicians drone on about everyone staying locked up in your house and flattening the curve for months or years, and national media outlets constantly updating the body count day after day.

[lancebr]

I'm doubtful that ACE2 plays role here. See comments above citing studies that show that ACE2 is poorly expressed in lungs, where covid19 causes critical damage, and is plentiful in other, unaffected tissues.

 

Maybe this might answer the question to the debate about whether should up-regulate or down-regulate ACE2.

 

If the lungs have ACE2 that is poorly expressed and other tissues in the body have higher expression of ACE2

and they are not being infected like the lungs....then maybe the higher expression of ACE2 has some protective

effect to it.  So maybe the up-regulation is the way to go.

 

 

[xEva]

Maybe this might answer the question to the debate about whether should up-regulate or down-regulate ACE2.

 

If the lungs have ACE2 that is poorly expressed and other tissues in the body have higher expression of ACE2

and they are not being infected like the lungs....then maybe the higher expression of ACE2 has some protective

effect to it.  So maybe the up-regulation is the way to go.

 

this logic makes sense, HOWEVER ace2 appeared in the discussion based on the idea that covid19 uses ACE2 receptor to gain entry in the cell.

 

You seem to have dug this issue thoroughly. Was it an in vitro study that showed that covid19 gains entry into cell via ACE2 receptor? What cell line they used?

 

what I'm saying is that this whole ACE2 receptor idea may be a distraction

Edited by xEva, 26 March 2020 - 10:20 PM.

[Florin]

Wuhan study shows lying face down improves breathing in severe COVID-19

https://www.eurekale...s-wss032420.php

[xEva]

Wuhan study shows lying face down improves breathing in severe COVID-19

https://www.eurekale...s-wss032420.php

 

that's on  a ventilator. The headline omits this 'detail'.

[Izan]

Interesting:

 

Iceland

 

population: 360000

 

People tested for COVID-19: 10300 (even people with NO known symptoms/who didn't know they had COVID-19)

 

One of the results: Half of those who were tested positive have no coronavirus symptoms whatsoever.

 

https://www.bloomber...om-scmp-reports

 

 

Now, check out Iceland's blood type distribution:

 

http://www.blodbanki...flokkamotefnum/

 

O:56 A:32 B:10 AB: 3

 

 

 

[bladedmind]

 

 

He also said that at the hospital he is working at they are utilizing Plaquenil, but that it doesn't appear to be the

wonder treatment that everyone is expecting it to be.  His colleagues believe that it would be more useful as a prophylactic.....since the utilization of it as a treatment after contracting the virus is not showing the results they were hoping for.

 

There are so many different takes on how good or bad this treatment is that it is hard to know what to believe.

 

Here is information of what dosages some doctors are using to use it as a prophylactic:

 

The dosage recommendations resemble those for malaria prophylaxis. 

 

Before going further, I affirm that people who do not thoroughly examine options, benefits, and risks; who do not double-check and consult with others; should stick to mainstream medical advice.

 

I am dismayed that public-health authorities in the US have encouraged people to believe that masks are useless, when almost any kind of mask and eye protection reduces exposure.   I read one story where a doctor said to skip gloves because they are hard to put on and can break.  My heart breaks when I see the majority of retail clerks in my area not wearing gloves.

 

Maybe there are good public-health reasons to preserve stocks of chloroquines, and people should be cautioned to avoid misuse, but the recent publicity about Arizona and Nigeria is hysterical and misleading.   Headlines are not that Arizona man dies from eating aquarium cleaner, or that three people in Nigeria (population 190 million) foolishly overdose on chloroquine, but rather screech that chloroquine kills (and Trump is a fool).  

 

The current CDC document “Therapeutic Options for COVID-19 Patients” lists ONLY Remdesivir; Hydroxychloroquine and Chloroquine; and “Other Drugs,” with merely a link to https://clinicaltrials.gov/  The document is quite balanced about the chloroquines' positive potential and the need for better data.   

https://www.cdc.gov/...ic-options.html

 

However, if  you search online for “self-medication chloroquine” there is overwhelming official and popular negativity (e.g. “fake coronavirus cure”), especially on social media.  You would be a fool to touch this dangerous drug with dozens of horrifying side effects!

 

There are, as usual, warnings, precautions, interaction effects associated with the use of chloroquines; and they should be well considered if someone were to contemplate self-administration of prophylaxis.   However, not dismissing those cautions, in the past more widely and presently in areas where malaria is not chloroquine-resistant, chloroquine prophylaxis is routine.

      

 

Remember that your doctor has prescribed this medication because he or she has judged that the benefit to you is greater than the risk of side effects. Many people using this medication do not have serious side effects. Tell your doctor right away if you have any serious side effects, including…

https://www.webmd.co...en-oral/details

 

 

I think it's worth repeating what I wrote here once before.  Hydroxychloroquine, chloroquine base, and chloroquine base each are differently dosed.  Know exactly which kind will be administered.

 

 

[Florin]

The following papers and pages contain lists of potentially repurposable drugs and substances for SARS-CoV-2. Some of the listed substances are relatively safe and readily available stuff like aspartame, riboflavin, melatonin, and andrographis.

 

Analysis of therapeutic targets for SARS-CoV-2 and discovery of potential drugs by computational methods
https://www.scienced...211383520302999

 

Network-based drug repurposing for novel coronavirus 2019-nCoV/SARS-CoV-2
https://www.nature.c...1421-020-0153-3

 

Assessment of Evidence for COVID-19-Related Treatments
https://www.ashp.org...ence-Table.ashx

 

Covid2019 / SARSCoV2 coronavirus antivirals
https://www.datapunk...9/antivirals.pl

 

Coronavirus disease 2019
https://en.wikipedia...e_2019#Research

Edited by Florin, 27 March 2020 - 12:08 AM.

[thompson92]

 

Analysis of therapeutic targets for SARS-CoV-2 and discovery of potential drugs by computational methods
https://www.scienced...211383520302999

 

I didn't follow that paper entirely, but it practically screamed Hesperidin at me.  I'm not sure how much stock we should put in these analytical docking papers.  We already know that hydroxychloroquine is rather effective and there is limited docking going on here between any chloroquine and the virus, and it doesn't matter because the mechanism of action is zinc transport.  I guess in a combination therapy it makes sense though.

[Dorian Grey]

Don't know if you might have heard about the latest early warning of asymptomatic, early stage or mild COVID, but several ENT docs are reporting patients coming in with loss of taste and/or smell who turn out to have COVID.  Patient recovery stories are reporting loss of taste/smell and even hearing associated with their COVID experience. 

 

I'd heard zinc was important for taste & smell and was watching a youtube on signs of zinc deficiency.  The presenter said the body can't effectively store zinc, but when it is in short supply it prioritizes zinc towards the immune system and withholds it from other rapidly turning over cells.  He described hair loss & gut issues as common with chronic deficiency but went on to say loss of taste & smell was often a sign of acute deficiency.  

 

I know when I've had the flu in the past, I always had a terrible time eating (starve a fever), but I didn't realize the body can't store zinc and will quickly become depleted without adequate dietary intake (and absorption!).  Also realize head cold & upper respiratory infection might inhibit sense of smell simply due to mucus or inflammation.  An unusual loss of taste/smell where patients are seeking help from ENT doctors and reporting it in their COVID recovery stories struck me as impressive.  

 

We've seen evidence the body may burn through potassium, causing deficiency during the course of COVID.  Does fighting COVID also burn through zinc, rapidly creating a deficiency acute enough to be noticed through taste/smell?  Perhaps yet another clue for us all on the important role of zinc plays with this disease, and the very real danger of deficiency in the possible potentiation of advanced COVID.  

Edited by Dorian Grey, 27 March 2020 - 02:14 AM.

[ta5]

Covid2019 / SARSCoV2 coronavirus antivirals

https://www.datapunk...9/antivirals.pl

 

One of the references on that page is to Possible inhibitors of ACE2, the receptor of 2019-nCoV, which includes some evidence that Andrographis, Urtica, and Sambucus all decrease ACE2 expression:

The 4 TCM showed significant ability to decrease ACE2 expression, especially Andrographis (FC=21.57), Urtica (FC=11.59), and Sambucus (5.99). Indeed, some studies reported potential effects of anti-pneumonia for active ingredients from Andrographis[18,19], Urtica[20], Sambucus[21], and Astragalus[22].

 

This disappoints me. I want to take those, but I preferred the theory that ACE2 was good. 

Edited by ta5, 27 March 2020 - 02:17 AM.

[lancebr]

They have a Dr. Haseltine on CNN right now saying that a new study just released from China

shows that hydroxychloroquine was not effective in treatment and he said that patients that

were on the treatment actually did worse then patient not on the treatment.

 

Here is his article about it:

 

https://www.forbes.c...w/#a558a46409be

 

What is the deal with these doctors....some say it works great others say it doesn't work at all.

[lancebr]

Here is a good explanation of how the virus enters the cells.  It even has pictures to makes it easier to understand.
 
 MWSnap343 2020-03-26, 22_05_55.jpg   68.67KB   1 downloads
 
(A) Spike protein receptor binding domains (RBD) on the surface of the SARS-CoV-2 bind to angiotensin-converting enzyme-2 (ACE-2)
receptors on the surface of the target cell; (B) The TMPRSS2 binds to and cleaves the ACE-2 receptor. In the process, the spike protein
is activated; (C) Cleaved ACE-2 and activated spike protein facilitate viral entry into the cell. TMPRSS2 expression increases cellular
uptake of the SARS-CoV-2.
 
The concern with the binding to the ACE2 receptor is that if a compound binds to the ACE2 receptor that does not guarantee that where
it binds on that receptor will prevent another compound, such as the virus, from binding to that receptor.  Especially if the virus has a
stronger affinity to bind to the receptor compared to the other compound that binds to the receptor.
 
The following statements from that paper raise that concern about hesperdin and the other compounds:
 
"Based on the virtual screening results of ACE2 protein, anti-diabetes drug troglitazone, anti-hypertensive drug losartan, analgesia drug
ergotamine, anti-bacterial drug cefmenoxime, and hepatoprotective drug silybin, etc., were predicted to bind with ACE2 with low energy.
The natural products, such as phyllaemblicin G7 from Phyllanthus emblica, xanthones from the plants of Swertiagenus, neohesperidin
and hesperidin from Citrus aurantium, exhibited potentially high binding affinity to ACE2 protein. However, none of above ACE2
binding compounds was predicted to target the ACE2–RBD interface."
 
So based upon that comment they do not predict that those binding compounds will target the ACE2-RBD interface.  So if that is true then
those compounds will bind to the ACE2 receptor, but just not where it is needed to target the ACE2-RBD interface.
 
It appears that the most important place to target the virus would be inhibiting the TMPRSS2 so that it would not activate the virus and allow
entry to the cell to replicate.
 
This shows that a TMPRSS2 inhibitor could block entry into the cell.
 
https://www.ncbi.nlm...pubmed/32142651
 
Here are some potential TMPRSS2 inhibitors:
 
Drugs: pivampicillin, hetacillin, cefoperazone and clindamycin
 
Natural substances: phyllaemblicin G7, neoandrographolide, kouitchenside I.

 

 

.

[Dorian Grey]

DOH!  Just got my hesperidin in the post today.  This looked so good.  

 

https://www.scienced...211383520302999

 

"However, most of above compounds were not predicted to bind with the binding interface of the Spike–ACE2 complex. The only compound that could target the binding interface between Spike and ACE2 was hesperidin"

 

That diagram of the virus entering the cell is going to give me nightmares.  

 

Oh well, back to my zinc fetish.  Been buying more tonic water.  Got to make that zinc more effective!  Got Quinine?  

Edited by Dorian Grey, 27 March 2020 - 03:32 AM.

[Dorian Grey]

They have a Dr. Haseltine on CNN right now saying that a new study just released from China

shows that hydroxychloroquine was not effective in treatment and he said that patients that

were on the treatment actually did worse then patient not on the treatment.

 

Here is his article about it:

 

https://www.forbes.c...w/#a558a46409be

 

What is the deal with these doctors....some say it works great others say it doesn't work at all.

 

The variables as I see it are: At what point in the disease process did they initiate hydroxychloroquine therapy?  Were these patients already near death?  Or was therapy initiated immediately upon diagnosis?  

 

Were the patients in your study ALL taking zinc depleting BP or PPI meds?  If the beneficial effect of hydroxychloroquine is in acting as an ionophore to transport zinc into the cell to inhibit viral replication, how well would this be expected to work in an acutely zinc deficient patient?  

[Dorian Grey]

Well, here's at least one Happy Hydroxychloroquine patient: 

 

https://www.yahoo.co...-134453632.html

 

"According to the account Giardinieri provided to Yahoo News, doctors never told him his diagnosis of the coronavirus compounded with pneumonia would be fatal, but by Friday he’d become convinced that he was unlikely to survive."  “It was my feeling based on how it was progressing, how my heart was doing, how my breathing was doing. It was getting shallower and shallower by the day,” Giardinieri said. So he began reaching out to family and friends to say goodbye".

 

"Giardinieri said he asked a nurse about the medication, who then relayed his request to the doctor. Though the physician informed Giardinieri that he could not provide him with the drug, he put him in touch with an infectious disease doctor who, after speaking to Giardinieri on the phone, agreed to authorize the use of hydroxychloroquine. Thirty minutes later, Giardinieri said, a nurse was giving him his first dose in pill form. The next morning, he says, he woke up completely symptom-free."

Edited by Dorian Grey, 27 March 2020 - 04:05 AM.

[lancebr]

DOH!  Just got my hesperidin in the post today.  This looked so good.  

 

https://www.scienced...211383520302999

 

"However, most of above compounds were not predicted to bind with the binding interface of the Spike–ACE2 complex. The only compound that could target the binding interface between Spike and ACE2 was hesperidin"

 

That diagram of the virus entering the cell is going to give me nightmares.  

 

Oh well, back to my zinc fetish.  Been buying more tonic water.  Got to make that zinc more effective!  Got Quinine?  

 

Well there actually might be something better for binding to the Spike RBD to ACE2 complex.

 

https://www.research...cle/rs-17806/v1

 

The paper states the following:

 

"We have developed a strategy that may be utilized to block or weaken the viral infections like COVID-19, via disruption of

the electrostatic interaction of the interacting viral protein with the ACE2 receptor. In this regard, phytochemicals present

in Indian medicinal herb Withania somnifera (Ashwagandha) were screened by molecular docking, and simulated with

the selected phytocompound, Withanone.

 

Protein-protein interactions were studied by calculating the electrostatic component of binding free energy between the

viral RBD and its ACE2 receptor in the presence or absence of Withanone. Salt bridges’ occupancies also decreased

in the trajectories simulated with the Withanone, along with the concurrent decrease in the electrostatic components

of binding free energy. We also observed the stabilizing salt bridges turning into destabilizing, at the end of simulation.

 

This study highlights the importance of natural origin phytochemicals in controlling COVID-19 entry into host cells, and

provides an attractive and alternative means for the management of COVID-19 infection. W. somnifera could well be the

first choice of medicinal herbs in these directions, to control the COVID-19 infectivity."

 

So would Ashwagandha be a good preventative herb to take?  I don't know a lot about this herb....is it a safe

herb to take on a daily basis?

Edited by lancebr, 27 March 2020 - 04:32 AM.

[Dorian Grey]

Oh my God...  Just looked into the "China Study" that's all over the news saying Hydroxychloroquine is no more effective than bed rest & fluids.  

 

"The study involved just 30 patients & half the patients didn't get the drug. Of the 15 patients given the malaria drug, 13 tested negative for the coronavirus after a week of treatment. Of the 15 patients who didn’t get hydroxychloroquine, 14 tested negative for the virus. The results of the study weren’t statistically significant."

 

No other details...  Looks like small potatoes to me.  How 'bout we do a New York City sized trial?  Half get Hydroxychloroquine, the other half don't. 

 

Now that's what I'd call a real/proper trial!