Why would pulmonary hypertension, which increases RV afterload and can contribute to shock, be beneficial?
What evidence do you have that zinc deficiency, rather than an infection causing a global pandemic, is causing hypoxemic respiratory failure right now?
To me, these seem totally irrelevant to COVID, but can you elaborate a direct connection?
I was just using the PAH as an example, but the issue in the lungs results from vasodilation (please correct me anyone if I am wrong). So vasocontriction might slow the leaking of fluid into the intercistal space.
Regarding the zinc deficiency; we see a large variation in outcomes after infection. Part could be viral load, but since we know people with "comorbidities" are more vulnerable to bad outcomes this delta should be an area of interest. Some people are totally asymptomatic!
The comorbidities (let's say heart disease) are caused by environmental or genetic variables. It seems zinc deficiency, to me, might be a common thread to both comorbidity and infection outcomes.
Since ACE2, a zinc metalloprotein which uses zinc as a cofactor, is in the alveoli and is the receptor for the virus, it would make sense to look at this as a serious possibility. ACE2 is a "Therapeutic Target for Heart Failure"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3944399/
And zinc plays a role in the lung disease as well:
Interleukin-1α (IL-1α) production by alveolar macrophages in patients with acute lung diseases: the influence of zinc supplementation
"These results suggest that zinc can regulate the production of IL-1α from AM in patients with pulmonary tuberculosis or bacterial pneumonia."
Both anecdotally and experimentally there is evidence that zinc inhibits the replication of several virii. So zinc deficiency might make infection more likely and weaken the immune system to make outcome worse.
It's fine to speculate, but there is no real connection between these ideas and COVID beyond pure speculation. Vasodilation is not the issue with the lungs (unless you mean V/Q mismatch for specific vascular beds, in which case this is the accepted dogma and is unrelated to pulmonary hypertension). The other hypotheses are at the level of preclinical evidence. Some (e.g., zinc deficiency being a common cause of causing heart disease) would upend all known clinical data.
Yes, speculation is the fertilizer of hypothesis. All anyone has at this point with COVID is speculation.
How can you say vasodialtion is not a vector in COVID19 outcomes? It is vasodialtion that increases capillary permeability leading to fluid in the intercistal space, am I correct? I may be wrong because I am reading that they are showing signs it appears as HAPE initially.
ACE2 uses Zinc as a cofactor. So a zinc deficiency could mean less ACE2 and a greater risk of HAPE.
Regarding zinc and heart disease, I am not saying it is THE cause, just a part of the cause. It is demonstrated very well that zinc deficiency is common in people with diabetes and heart disease. The clinical data is there, I just showed you part of it.
You were talking in favor of pulmonary hypertension and now you’ve shifted. And you’re pushing vitamin deficiencies as some cause-all. I’m not continuing this discussion with you.
I do not think I will be here long. It is even worse than it has been in academia.
I will share this with you, I do not think hydroxychloroquine is needed, only high dose zinc. It is looking more like lower ACE2 activity is causing the majority of issues. Since ACE2 needs zinc as a cofactor, well...
"Covid-19 enters the lungs via the ACE2 receptor. The virus binds to the receptor, which then pulls it into the lung cell where the virus can multiply. In case of a massive infection, this process makes the ACE2 receptors disappear from the outside of the cell. With that, their function also disappears."
Can you share what's a high dose in this case, how many milligrams of zinc per day ?
Also, with zinc it's important to increase the dose slowly or there might be some adverse effects, like hair loss.
I think it may matter more if you are zinc deficient when you are infected.
But Zinc does not need to be in the cell to help. It will also increase ACE2 activity, which is more important they are finding. When the ACE2 is destroyed, there is a build up of ANGII, which seems to be causing a majority of the issues. They are in a trial giving ACE2 directly to patients.
I've looked at the findings from France (although I'm not a doctor, I can still look at the numbers and try to make sense of them). It does seem that people on ACE inhibitor blood pressure medication have worse outcomes than almost any other group. Which is relevant to me, since I've been taking lisinopril (an ACE inhibitor) for the past 5 years. The "official" medical recommendation is to continue taking it, but I'm pretty certain at this point that the official recommendations are more or less full of shit when it comes to C19. It's not their lungs that are on the line. If I get any symptoms, I'll stop taking it as a precaution, my blood pressure issues weren't that bad to begin with.
Thanks for this comment, this stuff is super confusing. The effect must have been dominated by age distribution then. A lot of the older folks take ACE inhibitors, so it could be that they fared worse just because they're older.
What evidence do you have that zinc deficiency, rather than an infection causing a global pandemic, is causing hypoxemic respiratory failure right now?
To me, these seem totally irrelevant to COVID, but can you elaborate a direct connection?