2 votes
Posted 13 March 2020 - 10:43 AM
Maybe worth to share this on potential benefit of AT1R antagonists (as Losartan) for hypertension (look at the video, its a bit technical but clear). Also it might explain WHO reported in China higher mortality for people w/ hypertension? The host immune response to common cold (HCov-229E) and SARS-CoV-2 seems quite different.
"Treatments of Covid-19 should aim at:
1) preventing the virus from entering the cell
2) while preventing ACE2 deficiency at the same time
Current treatments don’t match both criteria. AT1R antagonists do.
As a group of doctors and researchers, we believe that AT1R antagonists, such as Candesartan, Losartan or Valtarsan, might provide substantial clinical benefit to acutely ill SARS-CoV-2-infected patients. These drugs have a good safety profile, are widely available and inexpensive.
They should be tested without delay."
https://www.closingt...ortocorona.org/
Also: https://www.ncbi.nlm...pubmed/32129518
(editing: add links)
Edited by albedo, 13 March 2020 - 11:21 AM.
Posted 13 March 2020 - 01:58 PM
Maybe worth to share this on potential benefit of AT1R antagonists (as Losartan) for hypertension (look at the video, its a bit technical but clear). Also it might explain WHO reported in China higher mortality for people w/ hypertension? The host immune response to common cold (HCov-229E) and SARS-CoV-2 seems quite different.
"Treatments of Covid-19 should aim at:
1) preventing the virus from entering the cell
2) while preventing ACE2 deficiency at the same timeCurrent treatments don’t match both criteria. AT1R antagonists do.
As a group of doctors and researchers, we believe that AT1R antagonists, such as Candesartan, Losartan or Valtarsan, might provide substantial clinical benefit to acutely ill SARS-CoV-2-infected patients. These drugs have a good safety profile, are widely available and inexpensive.
They should be tested without delay."
https://www.closingt...ortocorona.org/
Also: https://www.ncbi.nlm...pubmed/32129518
(editing: add links)
What dosage?
Thanks
Posted 13 March 2020 - 02:30 PM
Could regular zinc supplementation be as effective as zinc lozenges? I couldn't find any comparative research of delivery forms, only stuff like efficacy of acetate vs gluconate lozenges.
There doesn't seem to be that much research about the different forms and comparisons of which one is better.
For my daily zinc supplementation I am taking Zinc Monomethionine (Optizinc) every other day and then Zinc Picolinate
the other days. Supposedly, these two forms are suppose to be more absorbed by the body.
I also have the zinc acetate and zinc gluconate lozenges to take whenever I feel a cold coming on.
It would be nice to know which forms are better overall.
Posted 13 March 2020 - 02:46 PM
This is HUGE!
https://www.thelance...(20)30116-8.pdf
ACE inhibitor & ARB/sartan blood pressure meds and even ibuprofen INCREASE the risk of severe disease with COVID? YIKES!
Don't understand. If the ACE2 cells of the lung are where the virus enters, I would think ACE inhibitor would be protective.
We need to work this out!
Posted 13 March 2020 - 02:53 PM
This is HUGE!
https://www.thelance...(20)30116-8.pdf
ACE inhibitor & ARB/sartan blood pressure meds and even ibuprofen INCREASE the risk of severe disease with COVID? YIKES!
Don't understand. If the ACE2 cells of the lung are where the virus enters, I would think ACE inhibitor would be protective.
We need to work this out!
Guess related to inflammation response homeostasis, see my link just above but need to think more on this...
"...AT1R inhibition would prevent the entry of SARS-CoV-2 inside the cell, without inactivating ACE2 activity which is anti-inflammatory, nor disrupting ACE2 regulation of vital processes. ARB’s (angiotensin receptor blockers) as are cheap, widely available and safe. As a growing group of doctors and researchers, we believe ARB’s should be tested in acutely ill SARS-CoV-2-infected patients without delay. Doctors may consider AT1R antagonists as a Covid-19 treatment and share their experiences..." (bold mine)
(editing: add link)
Edited by albedo, 13 March 2020 - 03:02 PM.
Posted 13 March 2020 - 03:12 PM
This is HUGE!
https://www.thelance...(20)30116-8.pdf
ACE inhibitor & ARB/sartan blood pressure meds and even ibuprofen INCREASE the risk of severe disease with COVID? YIKES!
Don't understand. If the ACE2 cells of the lung are where the virus enters, I would think ACE inhibitor would be protective.
We need to work this out!
So is it correct to assume that we should not be taking any ibuprofen with this virus?
Also, I wonder what effect aspirin, Tylenol or Naproxene has on this virus...good or bad.
Because once poeple catch this and self-medicate at home a lot will use different pain killers
so wold be nice to know which are safe and which are not for this virus.
Edited by lancebr, 13 March 2020 - 03:13 PM.
Posted 13 March 2020 - 09:00 PM
Don't understand the nuts & bolts of why some doc's might think an ARB might be helpful while other see danger, but when in doubt, I'll punt on this as a potential therapy.
Regarding the aspirin/tylenol/naproxen possibly having the same risk as ibuprofen... Don't know, but I would think they would have considered and mentioned this if they were similarly antagonistic to recovery.
If the Lancet paper is correct, this would explain a lot regarding the aggressive disease seen with oldsters.
Posted 13 March 2020 - 09:08 PM
Don't understand the nuts & bolts of why some doc's might think an ARB might be helpful while other see danger, but when in doubt, I'll punt on this as a potential therapy.
Regarding the aspirin/tylenol/naproxen possibly having the same risk as ibuprofen... Don't know, but I would think they would have considered and mentioned this if they were similarly antagonistic to recovery.
If the Lancet paper is correct, this would explain a lot regarding the aggressive disease seen with oldsters.
So in your opinion do you think that it is prudent to down-regulate ACE2 like the Lancent paper says,
or up-regulate ACE2?
Posted 13 March 2020 - 10:26 PM
From what I understand, down-regulating ACE2 paradoxically up-regulates ACE2 receptor sites? which is what COVID uses to enter lung cells?
Haven't dug deep into the weeds yet, but this is something that may be explained by the boffins in the days to come.
Posted 14 March 2020 - 01:46 AM
From what I understand, down-regulating ACE2 paradoxically up-regulates ACE2 receptor sites? which is what COVID uses to enter lung cells?
Haven't dug deep into the weeds yet, but this is something that may be explained by the boffins in the days to come.
So if my understanding of the paper is correct then there are two ACE's.
ACE: angiotensin-converting enzyme
and
ACE2: angiotensin-converting enzyme 2
When you try to inhibit the ACE then the ACE2 increases...is that correct?
The virus is using the ACE2 receptors to infect the lungs and cause damage and pneumonia.
So then it would seem that there needs to be some type of treatment that can block the virus
from attaching to the ACE2 receptors.
Posted 14 March 2020 - 02:13 AM
Statement from ESC Council on Hypertension regarding ACE inhibitors:
"The Council on Hypertension strongly recommend that physicians and patients should continue treatment with their usual anti-hypertensive therapy because there is no clinical or scientific evidence to suggest that treatment with ACEi or ARBs should be discontinued because of the COVID-19 infection."
Posted 14 March 2020 - 03:09 AM
Coconut Oil, MCTs, Monolaurin, and Lauric Acid
Posted 14 March 2020 - 03:39 AM
So if my understanding of the paper is correct then there are two ACE's.
ACE: angiotensin-converting enzyme
and
ACE2: angiotensin-converting enzyme 2
When you try to inhibit the ACE then the ACE2 increases...is that correct?
The virus is using the ACE2 receptors to infect the lungs and cause damage and pneumonia.
So then it would seem that there needs to be some type of treatment that can block the virus
from attaching to the ACE2 receptors.
Yes, this is what I've made of this.
Posted 14 March 2020 - 03:42 AM
Elderberry
Posted 14 March 2020 - 03:59 AM
Examine.com has a Coronavirus page
They list:
Posted 14 March 2020 - 04:14 AM
Statement from ESC Council on Hypertension regarding ACE inhibitors:
"The Council on Hypertension strongly recommend that physicians and patients should continue treatment with their usual anti-hypertensive therapy because there is no clinical or scientific evidence to suggest that treatment with ACEi or ARBs should be discontinued because of the COVID-19 infection."
From your link, they claim speculation on "social media" is creating a dangerous situation. Surprised they consider the Lancet social media!
https://www.thelance...0116-8/fulltext
As to the lack of "clinical or scientific evidence" ACE inhibitors and/or ARB's (or thiazolidinedines and ibuprofen) should be discontinued; this is not surprising, as the COVID disease in humans has only been in existence for a couple of months. Hardly enough time for anything other than hypothesis. Their statement gives the impression this issue has been carefully considered and "debunked", and I don't see how they've scientifically arrived at their dismissal.
I can see how they don't want patients flooding doctors with phone calls & frantic appointments or folks discontinuing their meds on their own, but as I mentioned above, this looks HUGE to me. This may well turn out to be a key factor in the high aggressive disease/fatality rate in the geriatric population. If I were in my 70's/80's and on these meds I would be very concerned and (perhaps) rightly so. If there were no alternative meds, this might be an "oh well" situation; but from what they state in the hypothesis, calcium channel blockers might be a bridge to control high BP until this epidemic passes, or further research can be done. As we're all sailing uncharted waters, I would hope all new data & hypothesis would warrant careful consideration.
Posted 14 March 2020 - 06:55 AM
Here is an interesting article that talks about 5 herbs that can bind to ACE2 and potentially keep the virus from binding.
It is interesting that some of the herbs are the same one that the Chinese used in their soup.
Baicalin (flavone of skullcap herb)
Scutellarin (skullcap herb)
Hesperetin
Nicotianamine
Glycyrrhizin (licorice root herb)
https://www.google.c...UdpWTXzI-Kuvnka
So I wonder if these would work to prevent infection?
.
Posted 14 March 2020 - 10:27 AM
Posted 14 March 2020 - 01:40 PM
Another reason why early wider testing would have been beneficial - increased resource:
https://www.nbcnews....tients-n1158476
Posted 14 March 2020 - 02:52 PM
This is HUGE!
https://www.thelance...(20)30116-8.pdf
ACE inhibitor & ARB/sartan blood pressure meds and even ibuprofen INCREASE the risk of severe disease with COVID? YIKES!
Don't understand. If the ACE2 cells of the lung are where the virus enters, I would think ACE inhibitor would be protective.
We need to work this out!
Health authorities in several European countries are now warning the population against the use of ibuprofen.
Posted 14 March 2020 - 03:02 PM
Don't belive in too strong immunisation... on the contrary seems il-6 to be reduced during infection. Probably what is usefull in the silent phase i less (or not) during the avare phase.
Don't know for sure if I have really passed but I've used quite a bit of omega 3 and aspirin to prevent the inflammation of lungs... Also TUDCA seems helped in that.
It does seem that Omega 3 plays a very important role in the control of IL-6.
"Increased intake of specific dietary components, such as omega 3 fatty acids (Molfino et al. 2014) also has anti-inflammatory
effects. Interestingly, the adoption of the mediterranean diet by older adults has also been associated improvement in immune
responses, particularly dendritic cell function (Clements et al. 2017)."
What source are you using to get your Omega 3? Fish oil supplements or non-fish oil supplements (i.e. flaxseed oil etc)
Thanks
Posted 14 March 2020 - 05:43 PM
AHCC
Minerva Gastroenterol Dietol. 2020 Mar 12.
Lactoferrin (1,2) has been shown to inhibit SARS Pseudovirus entry (3). Might Lactoferrin supplements help to fight off this virus?1) Lactoferrin from Milk: Nutraceutical and Pharmacological Properties2) Antimicrobial properties of lactoferrin3) Inhibition of SARS Pseudovirus Cell Entry by Lactoferrin Binding to Heparan Sulfate ProteoglycansJianshe Lang, Ning Yang, [...], and Chengyu Jiang
All the responses are interesting. A couple mention Vitamin D. This one talks about ACE2:
The SARS-CoV-2 virus enters into human cells via the same receptor, angiotensin-converting enzyme 2 (ACE2), as its relative the SARS-CoV (1). During the course of infection virus particles bind to ACE2 and get internalized into human cells. This way the virus particles bind to numerous ACE2 molecules and sequester them from the cell surface. Moreover SARS-CoV was shown to downregulate ACE2 protein expression in a replication dependent manner (2). This would imply that loss of ACE2 function may develop during SARS-CoV-2 infection. Since ACE2 is a key-player in the renin-angiotensin system (RAS), its loss of function can lead to serious consequences.ACE2 acts together in balance with angiotensin-converting enzyme (ACE), another major player in RAS, and a well-known target of antihypertensive drugs, during finely tuned processes, such as blood pressure regulation and inflammation, among others. In disease models, a RAS imbalance with higher ACE and/or lower ACE2 results in atherosclerosis, hypertension, heart failure, chronic kidney disease, serious lung injury. Conditions wherein ACE2 increases seem to be protective (3).RAS activity is intrinsically higher in the lung, where ACE2 is highly expressed as well, to balance ACE Angiotensin II production, which means, the stakes are raised here in the lung. This situation may be further enhanced in patients on ACE inhibitor hypertensives. In the known escape phenomenon of ACE inhibitors, there is a significant increase in renin that is accompanied by higher ACE2 levels, likely as a balancing factor (4). If RAS activity is balanced so much higher above normal, one has to count with more severe events upon RAS imbalances. This can be the case when SARS-CoV-2 starts downregulating ACE2. There the loss of ACE2 function can be a prime event that leads to increased neutrophil infiltration in the lung and results in exaggerated inflammation and injury, as it was observed in disease models (5). As soon as the ongoing lung infection results in hypoxia, the stakes are further raised by induction of renin release and increase in renin gene expression that can lead to a vicious circle (6). Hypertension is indeed a key risk factor in COVID-19 disease according to Chinese medics who fight the virus at the front-line. They also suggest to start ventilation as soon as the blood oxygenation cannot be maintained by other means (7). I believe early ventilation exactly would try to balance the vicious circle triggered by unbalanced, activated RAS; but unfortunately, it is often too late...Patients with chronic diseases exhibit lower ACE2 levels. Moreover, as others suggested, it decreases by age, which would explain the vulnerability of this part of the population. In addition, significantly lower ACE2 levels were seen in aged males (8). This could be explained by the fact that ACE2 gene is X chromosome located and so males have less of a reserve capacity of ACE2 production under the extreme challenge of a SARS-CoV-2 infection. Since ACE2 protein is also expressed in the heart, kidney, small intestine enterocytes, and testes, one can indeed expect COVID-19 patients developing pathological changes at these locations, if vireamia is present.
The Wikipedia ACE2 page has a new Coronavirus section:
ACE2 receptors have been shown to be the entry point into human cells for some coronaviruses, including the SARS virus.[10] A number of studies have identified that the entry point is the same for SARS-CoV-2,[11] the virus that causes COVID-19.[12][13][14][15]
This might lead some to suggest that decreasing the levels of ACE2, in cells, might help in fighting the infection. However, ACE2 has been shown to have a protective effect against virus-induced lung injury by increasing the production of the vasodilator angiotensin 1-7.[16] In fact, the interaction of the spike protein of the virus with the ACE2 induces a drop in the levels of ACE2 in cells,[10] possibly inducing lung damage. In other words, the relation between ACE2 and severity of infections due to coronavirus is paradoxical and difficult to predict. Furthermore, the available (AT1R) blockers or Angiotensin II receptor blocker, such as losartan, have been shown to increase the amount of ACE2, plausibly facilitating the infection. As such, claims that available AT1R blockers can help in curing COVID-19 need to be tested by datamining of clinical patient records.[17] Suggestions that high dosage of Vitamin D, which has been shown to increase expression of ACE2 in cells,[18] could be effective in fighting the infection suffer from a similar paradox. A possible way of combating the infection could be the injection of soluble ACE2 into the blood stream which will have the twofold effect of competing with cellular ACE2,thus, preventing the attachment of the virus to non-infected cells and replenishing ACE2 in infected cells.[19]
Edited by ta5, 14 March 2020 - 06:01 PM.
Posted 14 March 2020 - 08:36 PM
Maybe worth to share this on potential benefit of AT1R antagonists (as Losartan) for hypertension (look at the video, its a bit technical but clear). Also it might explain WHO reported in China higher mortality for people w/ hypertension? The host immune response to common cold (HCov-229E) and SARS-CoV-2 seems quite different.
"Treatments of Covid-19 should aim at:
1) preventing the virus from entering the cell
2) while preventing ACE2 deficiency at the same timeCurrent treatments don’t match both criteria. AT1R antagonists do.
As a group of doctors and researchers, we believe that AT1R antagonists, such as Candesartan, Losartan or Valtarsan, might provide substantial clinical benefit to acutely ill SARS-CoV-2-infected patients. These drugs have a good safety profile, are widely available and inexpensive.
They should be tested without delay."
https://www.closingt...ortocorona.org/
Also: https://www.ncbi.nlm...pubmed/32129518
(editing: add links)
In this video, from min 1:10 on, there is an animation explaining the idea called to be tested:
Posted 14 March 2020 - 10:25 PM
Translated with google and attached as .rtf
Expert consensus on comprehensive treatme.rtf
Thank you pamojja, that's great info.
Among other things, they recommend:
"Vitamin C is administered at a dose of 50 to 100 mg / kg per day,"
and
"broad-spectrum protease inhibitor, ulinastatin, at 600 to 1 million units / day until the pulmonary imaging examination improves."
That ulinastatin is sold only in China, Japan and India. It's an injectable. I found some in Indian online pharmacies. All prices are in rupees, so I doubt they'll ship to the US. But this is the wonder drug that should be given at the onset of deterioration of condition (one sign of it is more than 30 breaths per minute). Since this ulinastatin it is a natural compound (found in healthy human urine, according to wiki) no western pharma will touch it. But there gotta be some other drug, no?
So, anyone knows a "broad-spectrum protease inhibitor"?
The other sign of deteriorating condition is metabolic alkalosis (but I wonder if it's due to those >30 breaths per minute?).
Can somebody comment please?
Edited by xEva, 14 March 2020 - 10:29 PM.
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