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ACE Inhibitors & COVID-19

Have you guys seen the youtube video
The coronavirus pandemic update 37?
I found I couldn't link it.
D.
My post#14 in this thread has a working link - just checked it and my laptop displays it ok
 
Thanks oldvatr.
A lot of work needs doing, it would be interesting to know how low renin patients are affected by Covid19?

There are too many pathways, it is extremely complex but Covid19 latches on the Ang2 receptor. It would paradoxical if the blockers increased the receptors!

Very low salt diets cause the feedback system of renin to work in healthy people. Thus increasing bp by ang2 and increasing aldosterone which has been mentioned by one low carb guru.
Some authorities argue that high insulin in diabetics hacks the RAAS and increases Ang2.
Perhaps all we T2D's should keep our carbs down and our hyperinsulin in check.
regards
D.
 
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Have you guys seen the youtube video
The Coronavirus Pandemic update 37?
I found I couldn't link, it but it was excellent on the subject Ace inhibitors and Arbs and comes up early in a search.
D.
I accessed this video quite easily - it is not my forté!
A very good session in my view, I liked it, a lot. Many will benefit from listening to it. Thank you @lindisfel .
 
Off topic a bit I know but it seems the reports about ibuprofen were wrong although NHS are still recommending we take paracetamol rather than ibuprofen.
Some years ago I was in hospital with Pneumonia and a bloke in next bed had been rushed in with internal bleeding that almost killed him. He was taking maximum doses of ibuprofen for some other condition he had. So, the consultant kept him on ibuprofen but gave him some stomach ulcer tablets omeprazole that he would need to take at the same time for the rest of his life. Ibuprofen is dangerous stuff if taken constantly (IMHO).
 
My take on it is that so far we are talking about how people with high levels of ACE-2 receptors may be at higher risk of getting infected, but it does not explain why SARS-COV-2 migrates to system shutdown in some identified at risk groups.

It would indeed be a problem if the common 'pril meds actually increased the number of ACE-2 receptors, but there seems to be no evidence of that happening either way. The limited evidence so far only considers plasma born free ACE-2 so does not record the cell takeup as receptors, which is what the inhibitor aspect of a 'pril is about. So we do not know yet if a 'pril is a good guy or a bad guy, or just simply a goodbye in this worrisome time.
 
This whole system has exercised me the last six or so years since I found out I had Conn's syndrome with very low renin and very high aldosterone...20x what it should be due to a 30mm adrenal tumour producing aldosterone uncontrolled output.
D.
 
My take on it is that so far we are talking about how people with high levels of ACE-2 receptors may be at higher risk of getting infected, but it does not explain why SARS-COV-2 migrates to system shutdown in some identified at risk groups.

It would indeed be a problem if the common 'pril meds actually increased the number of ACE-2 receptors, but there seems to be no evidence of that happening either way. The limited evidence so far only considers plasma born free ACE-2 so does not record the cell takeup as receptors, which is what the inhibitor aspect of a 'pril is about. So we do not know yet if a 'pril is a good guy or a bad guy, or just simply a goodbye in this worrisome time.

Thank you. That was clear.
 
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