Admittedly jumping in, midconversation. And we've tussled on COVID-related way early on in the past.
This is the first I've heard anyone assert HCA "simply doesn't work".
It was my understanding, those recommending HCQ said to give it prior to the viral amplification phase; in conjunction with Zinc. Further that the man study deb00nking it, waited until the COOF sufferers were hospitalized, and then did not give Zinc with the HCQ.
Would you happen to have a link handy, to either studies, or summary review papers, or similar, claiming that HCQ doesn't work?
Second, off the wall question. In light of the AstraZeneca/JNJ injections having (rare) side effects of clotting, what do you make of various medical articles suggesting Deep Vein Thrombosis is a side effect of coof infection? I've even seen some articles detailing patients where they had DVT -- and upon further eval, the characteristic ground-glass opacity on lung X-ray; but they had not reported any respiratory symptoms. Thoughts?
While we have tussled, I think you are spot on with some of your commentary and some of your statements.
As for HCQ simply not working, as I said, I think it is a weak prophylactic. Utilizing it in early infection did not reduce progression to severe disease, nor hospital time. While this was early in the pandemic, it seems to have held. Early in the pandemic, we were looking for anything that would help anticipating that we would either find the so called silver bullet or something would be therapeutically developed. I will work on literature searches to find the data, but most health care systems abandoned HCQ for therapy for hospitalized patients. You are correct that the mechanisms of action was for concentration of intracellular zinc by HCQ acting as an ionophore and in vitro higher levels of zinc prevent viral replications. This was not demonstrated in disease.
Not an off the wall second question. One of the early markers we measure of CoVID infection is D-dimer which is a product of thrombosis and clotting. In virtually all cases there is increased thrombotic activity (and elevated D-dimer) with CoVID infection. We actively anticoagulant many patients with elevated D-dimer to prevent thrombosis. So yes, thrombosis is a very large part of this disease.
Here are some of the interesting questions that are developing around the J&J and AstraZeneca vaccines. Since these vaccines are “more traditional” than the mRNA which is specific for the spike protein, what I think this tells us is that the dead viral particles in these injections still have a highly prothombotic nature, and it tells us a lot about Corona virus 19. From a straight non-political perspective, given that this is not seen with Pfizer and Moderna, I think this means that the thrombosis factors are not in the spike protein but in other regions of the viral genome.
Additionally here is the question that I am really curious about. The J&J was stopped because of 6 cerebral venous thromboses all of which occurred in women. I find it fascinating that there is not any males with this complication. I would be highly interested if these women were on oral contraceptive or other hormonal therapy that synergized with the injection to cause thrombosis. We know that progesterones and exogenous hormones promote thrombosis in young women so is there a correlation between progesterone and thrombosis in CoVID.
The next question I have is if we wish to continue J&J is there a population who would require some low level anticoagulation for a period of time? Then the question is would it be worth it?
Its a very curious outcome and one that bears close watching. I hope this genuinely answers the questions as best as I am able.
I hope you have a pleasant evening and thank you for your asking. I am trying to not be crusty any further — and appreciate your perspectives as well