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.
