3083 replies to this topic

[lancebr]

I've explained several times that upregulation is desired.  You can go look at my previous posts in this thread.

 

What is your take on Chris Masterjonhn's recent post about this new study about smokers

and ACE2 and that "the higher ACE2 allows a greater rate of viral entry and thus a higher viral load,

and thus a worse disease course":

 

https://www.biorxiv.....03.28.013672v1

 

His conclusions from that study are:

 

"Altogether this shows that smoking increases mucus-producing cells as a means of protecting the airway

from the smoke. ACE2, which is a protective enzyme under ordinary circumstances, increases as a result.

Since it is the entryway of SARS-CoV-2 into cells, the higher ACE2 allows a greater rate of viral entry and

thus a higher viral load, and thus a worse disease course. This suggests that quitting smoking will be

protective, and it adds to the evidence that controlling ACE2 levels should be a primary strategy in

prevention and early treatment."

 

His post:

 

https://chrismasterj...ovid-19-updates

Edited by lancebr, 01 April 2020 - 06:44 PM.

[OP2040]

What is your take on Chris Masterjonhn's recent post about this new study about smokers

and ACE2 and that "the higher ACE2 allows a greater rate of viral entry and thus a higher viral load,

and thus a worse disease course":

 

https://www.biorxiv.....03.28.013672v1

 

 

Interesting, I would caution extrapolating this to ACE2 up-regulation with meds for hypertension.  There was a study just out that showed ACE inhibitors to be protective against the virus.  It seems ACE2 expression in the lungs may have an effect, but expressed elsewhere may not matter. 

 

To add to the mystery, we have a bias against smokers that assumes they probably have higher rates of everything.  But while they do have higher rates of atherosclerosis, they do not have higher rates of hypertension and some studies show lower rates.  Same goes for Alzheimer's/Parkinson's but probably for different reasons.  Nicotine is not the bad guy in most cases, but combustion and particulates.   Anyway, I'm skeptical of any ACE2 stuff and there should be other obvious reasons why smokers would do worse, perhaps just the lung tissue damage.  Occam's razor seems especially important during a pandemic.

Edited by OP2040, 01 April 2020 - 06:53 PM.

[Kalliste]

What is your take on Chris Masterjonhn's recent post about this new study about smokers

and ACE2 and that "the higher ACE2 allows a greater rate of viral entry and thus a higher viral load,

and thus a worse disease course":

 

https://www.biorxiv.....03.28.013672v1

 

His conclusions from that study are:

 

"Altogether this shows that smoking increases mucus-producing cells as a means of protecting the airway

from the smoke. ACE2, which is a protective enzyme under ordinary circumstances, increases as a result.

Since it is the entryway of SARS-CoV-2 into cells, the higher ACE2 allows a greater rate of viral entry and

thus a higher viral load, and thus a worse disease course. This suggests that quitting smoking will be

protective, and it adds to the evidence that controlling ACE2 levels should be a primary strategy in

prevention and early treatment."

 

His post:

 

https://chrismasterj...ovid-19-updates

 

 

 

The study presents an analysis of the current smoking prevalence among hospitalized patients with COVID-19 in China, compared to the population smoking prevalence in China (52.1% in males and 2.7% in females). We identified 6 studies examining the clinical characteristics of hospitalized COVID-19 patients that presented data on the smoking status. The expected number of smokers was calculated using the formula Expected smokers = (males x 0.521) + (females x 0.027). An unusually low prevalence of current smoking was observed among hospitalized COVID-19 patients (9.6%, 95%CI: 8.2-11.1%) compared to the expected prevalence based on smoking prevalence in China (31.2%, 95%CI: 29.0-33.4%; z-statistic: 19.16, P < 0.0001). This preliminary analysis does not support the argument that current smoking is a risk factor for hospitalization for COVID-19, and might suggest a protective role. The latter could be linked to the downregulation of ACE2 expression that has been previously known to be induced by smoking. No studies recording e-cigarette use status among hospitalized COVID-19 patients were identified. Thus, no recommendation can be made for e-cigarette users. Keywords. SARS-CoV-2, COVID-19, ACE2, expression, susceptibility, smoking, hospitalization, electronic cigarette.

https://www.qeios.com/read/article/550
 

[bladedmind]

Clinical hydroxychloroquine random-controlled-trial in China, preprint

https://www.medrxiv....3.22.20040758v2

 

31 patients control

31 patients treatment

5-day HCQ (400 mg/d) treatment

 

From abstract, but I revised into more idiomatic English:

Total time to recovery, body temperature recovery time, and cough remission time were significantly shortened in the HCQ treatment group. Additionally, pneumonia improved in a |arger proportion of patients in the HCQ treatment group (80.6%, 25 of 32) than in the control group (54.8%, 17 of 32). The 4 patients who progressed to severe illness were in the control group. However, there were 2 patients with mild adverse reactions in the HCQ treatment group.  .

[Mind]

FYI, I am attempting to produce a video series summarizing some of the thoughts in this thread. I am not a medical researcher, the videos are meant for a layman audience. I was hoping to get more people (general public) focused on real potential treatments, instead of the daily "crisis news". I have created a different thread for thoughts on improving the series. Check it out here.

[thompson92]

So then what is your take on Chris Masterjonhn's recent post about this new study about smokers

and ACE2 and that "the higher ACE2 allows a greater rate of viral entry and thus a higher viral load,

and thus a worse disease course":

 

https://www.biorxiv.....03.28.013672v1

 

His conclusions from that study are:

 

"Altogether this shows that smoking increases mucus-producing cells as a means of protecting the airway

from the smoke. ACE2, which is a protective enzyme under ordinary circumstances, increases as a result.

Since it is the entryway of SARS-CoV-2 into cells, the higher ACE2 allows a greater rate of viral entry and

thus a higher viral load, and thus a worse disease course. This suggests that quitting smoking will be

protective, and it adds to the evidence that controlling ACE2 levels should be a primary strategy in

prevention and early treatment."

 

I got limited time to sit and fight this 'battle' over ACE2.  Yesterday's Chris's comments on the pH of endosomes from chloroquine usage made crystal clear sense to me and I think he's smart and correct.  Today, I read this email from him this morning and I think the guy is just shortsighted and he's extrapolating things too far.

 

1.  I am not qualified to speak about why smokers have higher ACE2 in this subpopulation of cells.

 

2.  His comments on reducing ACE2 are at odds with broader/other epidemiological data and outside of the smoking population, doesn't dissuade me from the other material that points to ideally wanting higher ACE2 (see Chen, et al and other papers mentioned in the thread).

 

3.  Key proteases are also upregulated in smokers that facilitate the virus, which Chris fails to mention.  In the paper, the authors state as follows:

 

Coronavirus infections are facilitated by a set of host proteases that cleave and activate the viral spike (S) protein40. SARS-CoV-2 primarily relies on the serine protease TMPRSS2 but can also utilize an alternate pathway involving Cathepsin B/L in TMPRSS2-negative cells6. Interestingly, we observed that Cathepsin B expression, but not TMPRSS2 or Cathepsin L expression, was consistently increased in mice and humans exposed to cigarette smoke (Figure S3). Thus, smoking can upregulate both the coronavirus receptor as well as a protease that SARS-CoV-2 uses for viral activation.

 

 

It isn't just that smoking is increasing ACE2, it is also increasing cathepsin that is mediating the escape of the virus from endosome into the cell body.  The researchers say that only Cathepsin B (not Cathepsin L) is elevated in human smokers, but if you look at the mouse data in the same table Cathepsin L is significant upregulated.  Mice are not humans, but color me skeptical in saying that two key proteases are probably upregulated in smokers (See page 30, Figure S3).  So, why Chris doesn't mention that ... I have no idea.  Maybe because the authors emphasize ACE2 more than cathepsin.

 

4.  At the end of the day, we need sufficient ACE2 as a counter-regulatory factor against increased ANG-II and the RAS pathway.  Having less, makes you more vulnerable to a RAS imbalance.  It's fundamental.  If you don't have ACE2, you are in deep trouble.  So yea, the virus is co-opting this important receptor to sneak into our cells and do its dirty work, but it kind of is what it is. 

 

5.  Yes, higher ACE2 might make it easier for the virus to get into your cells.  But what matters most at the end of the day is the immune response to the virus and we don't know the trade-off with sacrificing Vitamin D as a supplement/vitamin (hormone really) for the benefit of less ACE2.  My guess is that it would be highly inadvisable and it is the quintessential case of not seeing the forest through the trees.  The people that get very severely sick during this virus are those that cannot effectively mount an immune response to the virus.  They are deficient in their immune (NKs/monocyte) response and this is complicated by the RAS pathway behavior.  Well, I'd rather have higher ACE2 levels and Vitamin D and mount an immune response.

 

How Chris goes from a chain of logic that says 1) "smokers are at risk for worse outcomes in SARS-Cov2" to 2) "smokers have higher ACE2" therefore conclusion 3) "we should all want lower ACE2 expression and should throw away our Vitamin D supplements" just does not wash for me.  Do smokers have as an effective immune response to a viral lung infection, all things being equal?  It's extrapolating things too far and at the end of the day, I don't even think ACE2 is the biggest problem w/ this virus.  It's really not a matter of more ACE2 or less ACE2.  If you were hypertensive w/ a losartan prescription, things get a little more complicated.  But what matters most is the immune response and containing the RAS cascade, therefore I come down on wanting Vitamin D and wanting higher ACE2 expression (because of the Vitamin D) ACE2 to counteract RAS.

 

I think one of the biggest things I disagree with Chris over is his very high focus on avoiding getting the virus at all costs.  This may sound silly to some, because I recognize that it is highly transmissible.  But I'm far more worried about having a strong immune system, than whether or not I get this virus.  I'm probably going to get it at some point, because I touch my face frequently.  And I'm ~40 yrs old and pretty healthy.  I care most about mounting an appropriate immune response, not going crazy about ACE2.  The people who do worse here, are the ones who come down with symptoms and never mount an effective immune response and they go down.

 

To analogize, I would care more about wearing a mask to avoid infection than my ACE2 levels as a result of taking Vitamin D.  That would be more effective than skipping Vitamin D and risking a weaker immune system, when I want my immune system as strong as possible.

Edited by thompson92, 01 April 2020 - 08:01 PM.

[thompson92]

stuff about ACE2

 

I went to the researchers webpages, twitter feed and pulled out this mouse study they cite on hACE2 (it kills all the mice w/ SARS).  If you notice, a lot of researchers are quibbling with their actual findings, similar to what I have and OP2040 say.

 

https://twitter.com/...015020339109888

 

And the key response in the entire thread is here:

 

https://twitter.com/...332972506697734

 

I think a critical question, which your research informs, is whether elevated ACE2 is helpful, harmful, or both (as in it may increase susceptibility to initial infection, but decrease mortality risk after infection, see e.g. https://ncbi.nlm.nih.gov/pubmed/16001071.)

 

 

IMO, she's right.  Yea, it might increase risk of infection, but it protects you from mortality at the end of the day.  Like I said in my prior posting, "it is what it is".

[thompson92]

Anyone who wants a deeper thought process on why Vitamin D is a good idea and why Chris Masterjohn/Andrew Weil are wrong, read this response to BMJ from Attila Garami, MD PhD.  He notes his views as 'hypothesized', but I think he is pretty much spot on.

 

https://www.bmj.com/.../bmj.m810/rr-24

 

 

[lancebr]

So they just mentioned on tv that the Bacillus Calmette–Guérin vaccine for TB has

shown to provide some protection against the Covid 19.

 

https://economictime...ow/74931591.cms

 

 

Edited by lancebr, 02 April 2020 - 06:34 AM.

[Iporuru]

COVID-19 and chronological aging: senolytics and other anti-aging drugs for the treatment or prevention of corona virus infection?

COVID-19, also known as SARS-CoV-2, is a new emerging zoonotic corona virus of the SARS (Severe Acute Respiratory Syndrome) and the MERS (Middle East Respiratory Syndrome) family. COVID-19 originated in China and spread world-wide, resulting in the pandemic of 2020. For some reason, COVID-19 shows a considerably higher mortality rate in patients with advanced chronological age. This begs the question as to whether there is a functional association between COVID-19 infection and the process of chronological aging. Two host receptors have been proposed for COVID-19. One is CD26 and the other is ACE-2 (angiotensin-converting enzyme 2). Interestingly, both CD26 and the angiotensin system show associations with senescence. Similarly, two proposed therapeutics for the treatment of COVID-19 infection are Azithromycin and Quercetin, both drugs with significant senolytic activity. Also, Chloroquine-related compounds inhibit the induction of the well-known senescence marker, Beta-galactosidase. Other anti-aging drugs should also be considered, such as Rapamycin and Doxycycline, as they behave as inhibitors of protein synthesis, blocking both SASP and viral replication. Therefore, we wish to speculate that the fight against COVID-19 disease should involve testing the hypothesis that senolytics and other anti-aging drugs may have a prominent role in preventing the transmission of the virus, as well as aid in its treatment. Thus, we propose that new clinical trials may be warranted, as several senolytic and anti-aging therapeutics are existing FDA-approved drugs, with excellent safety profiles, and would be readily available for drug repurposing efforts. As Azithromycin and Doxycycline are both commonly used antibiotics that inhibit viral replication and IL-6 production, we may want to consider this general class of antibiotics that functionally inhibits cellular protein synthesis as a side-effect, for the treatment and prevention of COVID-19 disease.

 

[thompson92]

 

Tang, F., Quan, Y., Xin, Z., Wrammert, J., Ma, M., & Lv, H. et al. (2011). Lack of Peripheral Memory B Cell Responses in Recovered Patients with Severe Acute Respiratory Syndrome: A Six-Year Follow-Up Study. The Journal Of Immunology, 186(12), 7264-7268. doi:10.4049/jimmunol.0903490

 

 

Recovered SARS patients were followed up to 6 y to estimate the longevity of specific Ab. The specific memory B cell and T cell responses to SARS-CoV Ags were measured by means of ELISPOT assay. Factors in relation to humoral and cellular immunity were investigated. Six years postinfection, specific IgG Ab to SARS-CoV became undetectable in 21 of the 23 former patients. No SARS-CoV Ag-specific memory B cell response was detected in either 23 former SARS patients or 22 close contacts of SARS patients. Memory T cell responses to a pool of SARS-CoV S peptides were identified in 14 of 23 (60.9%) recovered SARS patients, whereas there was no such specific response in either close contacts or healthy controls.

 

 

Antibodies appear to mostly gone after 6 years of SARS-CoV1 exposure from 2003 cohort.  SARS-CoV2 will probably be with us for a very long time....

[Daniel Cooper]

You know, convalescent patient blood plasma is being used in some hospitals to help covid 19 patients recover.  Old technology of course.  Popular for a few decades in the West before Salk showed the way for creating new and effective vaccines.  The convalescent patient has covid 19 antibodies circulating in their blood that tags covid 19 for destruction by the immune system.  The blood plasma simply conveys these antibodies to a patient who's own immune system hasn't yet had time to or is otherwise unable to produce these antibodies on it's own.

 

It seems obviously that isolating these antibodies (which has already been done) and using monoclonal or polyclonal techniques to make them on an industrial scale would be one way to go.  And you would think that as long as you successfully clone antibodies that recovered patients bodies have made that the FDA could fast track this as the risk should be low.  

 

I see a little discussion of this, but not much.  This seems like something you might have up and running in a year, maybe less if there's some real sense of urgency.  For most monoclonal therapies, for say arthritis or cancer, the real trick is coming up with designing an antibody that effectively targets what you're trying to block or destroy.  For this, we don't have that step since we have patients who's bodies have already done that for us.  All you've got to do is identify them and replicate then.  You would need some testing to verify that they aren't likely to generate some autoimmune condition, but even if they do you're no worse off than a person that has already had covid 19 and has recovered from it, as they will have the same antibodies in circulation.  If as they tell us 70 - 80% of the world's population is going to get this then it's hard to see how you'd be worse off in that respect.  

 

This one seems like a no-brainer.  I wonder why this isn't being discussed more vigorously.

 

 

 

[Mind]

You know, convalescent patient blood plasma is being used in some hospitals to help covid 19 patients recover.  Old technology of course.  Popular for a few decades in the West before Salk showed the way for creating new and effective vaccines.  The convalescent patient has covid 19 antibodies circulating in their blood that tags covid 19 for destruction by the immune system.  The blood plasma simply conveys these antibodies to a patient who's own immune system hasn't yet had time to or is otherwise unable to produce these antibodies on it's own.

 

It seems obviously that isolating these antibodies (which has already been done) and using monoclonal or polyclonal techniques to make them on an industrial scale would be one way to go.  And you would think that as long as you successfully clone antibodies that recovered patients bodies have made that the FDA could fast track this as the risk should be low.  

 

I see a little discussion of this, but not much.  This seems like something you might have up and running in a year, maybe less if there's some real sense of urgency.  For most monoclonal therapies, for say arthritis or cancer, the real trick is coming up with designing an antibody that effectively targets what you're trying to block or destroy.  For this, we don't have that step since we have patients who's bodies have already done that for us.  All you've got to do is identify them and replicate then.  You would need some testing to verify that they aren't likely to generate some autoimmune condition, but even if they do you're no worse off than a person that has already had covid 19 and has recovered from it, as they will have the same antibodies in circulation.  If as they tell us 70 - 80% of the world's population is going to get this then it's hard to see how you'd be worse off in that respect.  

 

This one seems like a no-brainer.  I wonder why this isn't being discussed more vigorously.

 

The near blackout of national media coverage of therapies to treat COVID-19 (current meds, nutrients, or donated plasma) is getting to be disturbing.

[OP2040]

All these things are being discussed.  The problem is that they are currently meaningless for people on this forum or anyone else for that matter.  None of us, I presume, have any control over whether we or our communities will benefit from them.  And we all know very well, they will probably never be used, at least not in time for anyone who actually needs them in the next year or so.

 

This is why I think we should focus our attention on supplements, tests and other things we may reasonably be able to procure now!  I don't know where others here live.  But where I am, we are one of the last to be hit and are just entering "peak" Coronavirus now.  By definition, this is the time we need to be prepared for, not two months from now and definitely not a year from now.  We will have an all summer lull to philosophize about the nature of Coronavirus and various mid to longer-term interventions.

 

If someone can get us all a BCG vaccine right now, you will then have a hard time shutting me up about it lol.

 

 

[OP2040]

The near blackout of national media coverage of therapies to treat COVID-19 (current meds, nutrients, or donated plasma) is getting to be disturbing.

 

The vitamin C and Zinc things are particularly annoying.  But even here on this forum some folks were trying to attack elderberry based on media lies and misinformation.  I believe it all started with a FB post of all things.  The idea seems to be that because these things do not outright prevent viral infections, specifically Coronavirus, then they are worthless.   It's a very black/white way of thinking when a couple days here, a smaller viral load there can make the difference between life or lung damage and death.  The studies show that these supplements probably can provide those couple days and smaller viral load.  Is the evidence unanimous?  No  Is the evidence for anything ever unanimous, particularly for biological interventions?  Hell no?  Some of the studies used to support blockbuster pharma drugs have much less scientific evidence than these three supplements.

[Dorian Grey]

Good point Mind.  Besides ignoring the potential of simple things like zinc supplementation, particularly in those known to develop deficiencies (BP meds, diabetics, PPI users) the news if full of "don't worry about your ibuprofen, Ace Inhibitors, etc". 

 

The war on hydroxychloroquine has been particularly impressive.  

 

Saw this on Yahoo news last night: Fact check: Getting flu shot doesn't make you more (or less) likely to get the coronavirus.  

 

Oh really?  "significantly blunted CD4 T-cell response" might not hamper immune response to COVID?

 

Evidence That Blunted CD4 T-Cell Responses Underlie Deficient Protective Antibody Responses to Influenza Vaccines in Repeatedly Vaccinated Human Subjects

 

“Despite the benefits of yearly influenza vaccination, accumulating evidence suggests that diminished vaccine efficacy may be related to repeated vaccination.” “We find a striking disparity in their responses, with previously vaccinated subjects exhibiting significantly blunted CD4 T-cell responses and diminished antibody responses.”

 

Just a couple weeks back yahoo ran a story that included an opinion from Ben Neuman PhD is head of the biology department at Texas A&M University-Texarkana. He has worked with coronaviruses for 24 years.: 

 

"In people who survive infections with coronaviruses and do well, if you check their blood afterward, as we found with SARS, you find out that they have a really good killer T cell response. And the ones who don’t do well did not really make a killer T cell response.”

 

Big Pharm & the Medical Industrial Complex certainly is going the extra mile to protect their interests.  Resistance is futile...  "Vaccines & ventilators for all!"

 

[mike_ag]

Frustrating. 

 

I guess the huge lack of anticipation of western countries now focus the public debate on the political side of things. 

Even the hydroxychloroquine idea is now hijacked into this sterile rep vs dem debate in the US.

 

I'm in Europe and situation is similar. Most media "scientists" and "doctors" try hard to discredit any experimental treatment possible, but they don't suggest anything other than wait 3 months for the first clinical trial results.

 

And yeah, I've yet to hear the word zinc on the medias here.

I thought we were "in war" ...

Edited by mike_ag, 02 April 2020 - 04:37 PM.

[mike_ag]

The debate around elderberry is getting interesting.

 

Initial study from 2001 where elderberry is said to increase IL-6

https://www.ncbi.nlm...pubmed/11399518

 

Manufacturers now respond : 

https://sambucolusa....t-are-the-facts

https://www.gaiaherb...ry-and-covid-19

 

Some paper from February 2020 

https://www.research...ucus_nigra_a_sy

 

Pro elderberry blog post 

https://eu.marconews...sts/2922891001/

" You see, there are good cytokines and bad ones. Elderberry raises the good ones, COVID-19 raises the bad ones. It doesn’t worsen any virus in my professional opinion."

 

Longecity experts what do you think ?

 

 

 

 

[OP2040]

Right, the IL-6 is what scared people, but IL-6 is not and should not be a deciding factor in whether an antiviral is effective or not.  IL-6 should go up upon viral infection, and if it doesn't you will be dead from the virus!

 

The last article you posted I read last night and it was very nice to see my very own thoughts on paper as I thought I was going crazy lol.  There are other studies out there, too lazy to do the search right now.

 

I don't give much weight to anything in vitro.  However, some of these things, lets say elderberry, garlic, vitamin C, D and Zinc, have all shown antiviral activity in vivo,  For me, the compelling nature of it is because they have shown generic antiviral activity across a number of different viruses in different families.  This is true particularly for Zinc which seems to show up in the very bowels of antiviral machinery.  Yes, Coronavirus is somewhat unique and of course it is new to our immune defenses.  But still well worth the gamble considering the safety and rapid accessibility of these things. 

 

 

 

 

Edited by OP2040, 02 April 2020 - 05:14 PM.

[BlueCloud]

 

... the news if full of "don't worry about your ibuprofen, Ace Inhibitors, etc". 

 

The war on hydroxychloroquine has been particularly impressive.  

 

...

 

 

In France, the government issued a national warning against ibuprofen a while back , as well as oral corticoids. The next day, people were lining up at the pharmacy to buy paracetamol. The scepticism against HCQ was strong as well in the beginning, but the health authorities finally authorized it, yet strongly advise to only use it on severe cases, which goes against what Dr Raoult recommends to use it very early on because it's useless once the symptoms have progressed severely. Go figure...

[lancebr]

 

The debate around elderberry is getting interesting.

 

Initial study from 2001 where elderberry is said to increase IL-6

https://www.ncbi.nlm...pubmed/11399518

 

Manufacturers now respond : 

https://sambucolusa....t-are-the-facts

https://www.gaiaherb...ry-and-covid-19

 

Some paper from February 2020 

https://www.research...ucus_nigra_a_sy

 

Pro elderberry blog post 

https://eu.marconews...sts/2922891001/

" You see, there are good cytokines and bad ones. Elderberry raises the good ones, COVID-19 raises the bad ones. It doesn’t worsen any virus in my professional opinion."

 

Longecity experts what do you think ?

 

 

I notice that the majority of people recommending the use of Elderberry always seem to use a disclaimer

when they are recommending it.  Like the following:

 

Dr. Andrew Weil:

 

"Elderberry extracts may help to prevent the early stage of corona virus infections, which includes COVID-19.

Elderberry contains compounds which decrease the ability of viruses to infect cells. Elderberry is considered

generally safe and in influenza B (cause of common cold), use of elderberry shortens the duration of symptoms.

However, as a part of its immune supportive actions, elderberry increases immune cell release of tiny chemicals

called cytokines. Specifically, elderberry increases the release of a cytokine called IL-1B which is a part of the

inflammatory reaction to COVID-19 that can result in acute respiratory distress. For this reason, to minimize the

possibility that elderberry could aggravate the inflammatory “cytokine storm” associated with the more severe

COVID-19 infections, it is recommended to stop elderberry at the first signs of infection (fever, cough, sore throat)

and/or if you test positive for the virus."

 

Since there can be a long incubation period of up to 14 days before you even know you have the virus and during that

time it is in your body replicating and potentially causing damage then how would you know to discontinue it at the exact

time you were infected with the virus if you are someone who is not showing symptoms until a week later or 2 weeks later.

 

There have been reports from doctors that for some patients once they became symptomatic the CT scans of their lungs had

shown that there was already damage to their lungs.  So, even if there is any protection from elderberry preventing Covid 19,

which there have been no studies to show that, then why take something that even the people recommending it say that it can

increase the very thing that is part of the inflammatory reaction that can result in respiratory distress.

 

So for example:  Lets say a person contracts the virus. Doctors say that some people are asymptomatic and never have

symptoms, and then there are people that show symptoms within 2 days and some that don't show symptoms for up

to 14 days.  So if this person is not going to show symptoms for lets say 8 days (the midpoint of 2 and 14 days) then for

those 8 days they have no idea they have the virus so they would not think to stop taking elderberry as these people's

disclaimers recommend.  So for those 8 days they are taking elderberry and unknowingly increasing inflammatory

cytokines along with what the virus is putting out.  So when day 8 comes and they are still taking elderberry but they

notice a fever or shortness of breath from lung inflammation and/or lung damage they then decide to stop the elderberry.

Well for those 8 days did that elderberry cause more damage because they didn't know they had the virus and stop

taking it when they first contracted the virus.....potentially yes.  So, why take the chance.

 

Edited by lancebr, 02 April 2020 - 07:35 PM.

[Mind]

Another more recent article about Dr. Zelenko.

 

It seems to throw extra wrenches into the story. Caution, it is a mainstream media report - not always the most accurate. They often get the numbers wrong.

 

Dr Zelenko claims to have now treated 900 patients (according to the article) but only 200 have received his regimen (seems to contradict his earlier videos). The article claims 6 needed hospitalization and 3 are on ventilators. Depending upon the age of the patients, those numbers would seem to indicate that the regimen is not much better than regular treatment. If they are all elderly or have underlying health conditions, then it would be a good treatment. If they are from a younger cohort, then the regimen doesn't seem all that great.

[Dorian Grey]

Looks like a full 2 out of 3 patients (in England) who go onto a vent wind up on ice.  

 

https://www.dailymai...lators-die.html

 

What's the TRUE risk of dying from coronavirus if you are in hospital? NHS data shows 66% of patients hooked up to ventilators will succumb to the killer infection

 

Upping my intake of Lactoferrin, Tonic Water, Zinc, Green Tea, Vitamin-C, EVERYTHING!  The healthcare option looking less appealing all the time (unless you can find a doc who's not scared of the chloroquine meds).  

[lancebr]

Band-Aid Vaccine:

 

https://triblive.com...animal-testing/

[zorba990]

Looks like a full 2 out of 3 patients (in England) who go onto a vent wind up on ice.

https://www.dailymai...lators-die.html

What's the TRUE risk of dying from coronavirus if you are in hospital? NHS data shows 66% of patients hooked up to ventilators will succumb to the killer infection

Upping my intake of Lactoferrin, Tonic Water, Zinc, Green Tea, Vitamin-C, EVERYTHING! The healthcare option looking less appealing all the time (unless you can find a doc who's not scared of the chloroquine meds).

\

Just spoke with a health professional today that said many docs have been setting the ventilators too high. Apparently this virus cause a lung spasm in this case that pushes up BP and also causes heart issues.
Ventilators need to be turned down as low as possible to reduce this side effect while maintaining acceptable O2 Sat. Just a data point.

[lancebr]

The study presents an analysis of the current smoking prevalence among hospitalized patients with COVID-19 in China, compared to the population smoking prevalence in China (52.1% in males and 2.7% in females). We identified 6 studies examining the clinical characteristics of hospitalized COVID-19 patients that presented data on the smoking status. The expected number of smokers was calculated using the formula Expected smokers = (males x 0.521) + (females x 0.027). An unusually low prevalence of current smoking was observed among hospitalized COVID-19 patients (9.6%, 95%CI: 8.2-11.1%) compared to the expected prevalence based on smoking prevalence in China (31.2%, 95%CI: 29.0-33.4%; z-statistic: 19.16, P < 0.0001). This preliminary analysis does not support the argument that current smoking is a risk factor for hospitalization for COVID-19, and might suggest a protective role. The latter could be linked to the downregulation of ACE2 expression that has been previously known to be induced by smoking. No studies recording e-cigarette use status among hospitalized COVID-19 patients were identified. Thus, no recommendation can be made for e-cigarette users. Keywords. SARS-CoV-2, COVID-19, ACE2, expression, susceptibility, smoking, hospitalization, electronic cigarette.

 

https://www.qeios.com/read/article/550
 

 

He commented on this study you posted, since it was contrary to his theory and someone

mentioned it, and he said that it is an inferior study to assess the outcome of smokers

who contract COVID-19.

 

I did notice on his latest update that he now recommends spraying copper in the mouth/nose.

He even provides product recommendations in his update with what appears to be affiliate links to

the products. 

 

What exactly is that saying....never let a bad situation go to waste, especially when you can make money

from it.

Edited by lancebr, 03 April 2020 - 03:41 AM.

[resveratrol_guy]

I have a few tidbits to add to various posts above:

* Iporuru, rapamycin is great for quelling cytokine storms and it does indeed inhibit protein synthesis, which would be expected to slow viral replication. There is modest evidence that it also improves vaccine response by reducing immune noise even though it suppresses immune aggression generally. However, I would not give it to patients attempting to fight off the virus, but rather only to those continuing to react excessively to a dying or dead viral infection. Those who need a stronger immune response are better off using GCSF, Stem Kine, or hematopoeitic stem cell therapy (hint: BioViva or Celltex). I'm speaking as someone with firsthand experience, having taken it in various forms and doses on and off since 2018.

* Daniel Cooper, the monoclonal antibody thing is spot on. Distributed Bio in California took SARS antibodies and reoptimized them for COVID19 last week, with high binding affinity. I posted about this elsewhere and you can find several copies of the interview on YouTube. Very promising, but money and time needed for mass production. Might hack off the tail end of the curve later this year. Meanwhile, convalescent plasma is probably a good idea, and the "good" news is that the supply of eligible donors is expanding exponentially.

* sciack, as I explained previously, I don't think the kidney issues posed by IV megadose vitamin C justify it not being offered to consenting patients. Such complications are in general transient and easily rectified. AFAIK there is no theoretical basis for stone formation, but even if I'm wrong, it's not going to occur in the span of a week.

* OP2040, the problem is that medicine is mostly polarized. The professionals are threatened by losing their jobs. So, even if they don't really operate on a black-and-white basis deep down, they have to fake it when addressing the public: nothing is "proven" until it's true to within 95% confidence, for the most part in medicine. If it's 94% certain to be true, then it's pseudoscience based on a quack research. On the other hand, we have millions of morons who read some rumor on Facebook and swallow it whole, assuming that all the real solutions are being suppressed by conspiracies. We need to take a lesson from so many neural networks which have defeated our best players at so many games: do the best with the information you have, and adjust your behavior over time as information quality improves. Optimize for minimum deaths, not maximum certainty, and certainly not for some personal reputational consideration. Don't stand there complaining that nothing has been absolutely proven, so we need to wait for all the patients to die before we have any idea how to save them. This may, in fact, be a longterm benefit from the pandemic, in the sense that we might finally admit that patients informed about risks and uncertainties deserve the right to try experimental therapies, and most definitely when they pay out of pocket.

* BlueCloud, waiting for patients to become severe before administering HCQ (and azythromycin, zinc, etc.) is indeed a huge mistake. This same foolishness has happened on a regular basis in drug trials involving other diseases. It happens become some idiot in charge of study design doesn't do his homework, then not only wastes years and millions of dollars, but ends up "proving" that the therapy doesn't work. We don't have time for this clowning anymore. People need to be fired.

* Mind, Dr. Zelenko said in his Guiliani interview that he only treats patients who are: (1) above 60, (2) experiencing shortness of breath, or (3) immunocompromised. He explained that even having the symptoms isn't sufficient for him to justify treatment with his protocol.

* Dorian Grey, check out the John Hopkins exit survival ratios (recovered over (recovered plus deaths)). UK and Netherlands lead the world at killing their patients. The NHS is the indisputed world leader at treating symptoms for the lowest possible cost!
 

* All, mask up when heading outside, and if using a surgical mask, pinch it at the nose bridge so as to minimize the air bypass cross section. Don't touch your face until you wash your hands (and before you touch a used hand towel). Sorry if I sound like a kindergarten teacher; if I save one of you, it's worthwhile. And listen to the advice from WHO which confirms that healthy people don't need to wear masks, then have a good laugh, and unsubscribe from their channel.

Edited by resveratrol_guy, 03 April 2020 - 03:54 AM.

[Florin]

Just spoke with a health professional today that said many docs have been setting the ventilators too high. Apparently this virus cause a lung spasm in this case that pushes up BP and also causes heart issues.
Ventilators need to be turned down as low as possible to reduce this side effect while maintaining acceptable O2 Sat. Just a data point.

Besides lower ventilator pressure, putting the patient in the prone position also seems to help.
 

"It is only a small number of patients, but our study shows that many patients did not re-open their lungs under high positive pressure and may be exposed to more harm than benefit in trying to increase the pressure," said Chun Pan, MD, also a professor with Zhongda Hospital, School of Medicine, Southeast University. "By contrast, the lung improves when the patient is in the prone position."

Wuhan study shows lying face down improves breathing in severe COVID-19
https://www.eurekale...s-wss032420.php

Edited by Florin, 03 April 2020 - 04:05 AM.

[lancebr]

This information was forwarded to me so for anyone who knows more about the immune system does this

sound like something worth using?

 

"Carvacrol (CVC) - Oregano

 

     Rosmarinic Acid (RA), which is found in Oregano, has been shown to increase the ACE2/ACE ratio [9].

 

     CVC inhibits ROS and MAPK-mediated signaling of NF-κB [2]

 

     CVC moderately inhibited TLR-4-mediated activation of NF-κB. Inhibitory effect on the IL-6/STAT3 pathway has been shown in a study [3].

 

     CVC reduces TGF-β levels significantly and increases IFN-γ levels moderately, and normalizes IL-4 [5] [10] [11].

 

     CVC inhibit LPS-induced NLRP3 activation [6].

 

     CVC reduces cytokine stress of IL-1beta, IL-6, and TNF-α (IL-8 is not affected) [1].

 

     CVC stimulates CD4+ and CD8+ T cell growth [7]. CD4+ CD8+ double-positive T cell ratio was increased.

 

     CVC alleviates ovalbumin-induced Th2 disorder [10]. Increased the Th1/Th2 ratio and the number of regulatory T cells.

 

CVC appears to be an effective treatment (1) to inhibit the pathways that SARS-CoV-2 uses, (2) to significantly decrease TGF-β

levels, (3) to enhance CD4+ and CD8+ T cell proliferation without augmenting them into the Th2 sub-type."

[tolerant]

...

Upped my UVB exposure to Daily.

...

 

How does UVB help with immunity? By synthesising Vitamin D3? If so, is this somehow better than supplementing D3? And how do you increase your exposure? With a UVB lamp? If so, can you recommend one? Thanks.