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Comment by carbocation | Hacker News Reader

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?

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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:

https://link.springer.com/article/10.1007/BF00944606

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.

https://www.ncbi.nlm.nih.gov/pubmed/32226695

But these patients, from what I have read, also see a dramatic drop in blood pressure at some point as well.

so the connection with zinc is that they also treat HAPE patients with ACE2

https://www.ncbi.nlm.nih.gov/pubmed/22441085

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.

Here is a great study, 2017, establishing a clear link beween zinc deficiency and diabetes: https://www.ncbi.nlm.nih.gov/pubmed/28138861

It still shocks me that in 2020 we still have people that think vitamin cofactors play no role in health and should be ignored.

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.

You think I shifted, but I did not. If you would have given me an opportunity I would have explained.

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