More on the smoking paradox...
https://www.dailymai...oronavirus.html
Professor Francois Balloux, director of the genetics institute at University College London: "the evidence for a protective effect of smoking (or nicotine) against COVID-19 is bizarrely strong... actually far stronger than for any drug trialed at this stage"
Far stronger than for any drug trialed at this stage??? WTF!
"America's Centers for Disease Control of over 7,000 people who tested positive for coronavirus, found that just 1.3 per cent of them were smokers - against the 14 percent of all Americans that the CDC says smoke"
"Hospitals in China, the US, Germany and France have had hundreds of thousands of coronavirus patients but admitted disproportionately small numbers of smokers"
"Data from the Centers for Disease Control and Prevention (CDC) in the US showed that of around 7,000 COVID-19 patients, former smokers were more likely to be hospitalized or taken into intensive care than current smokers"
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The ACE2 issue is driving me to madness! It is known smoking increases ACE2 enzyme deployment:
https://www.medrxiv....3.18.20038455v1
"Current smoking also significantly increased ACE2 expression levels compared with never smokers"
The virus enters through the ACE2 RECEPTOR sites of lung cells, so more of these (ACE2 receptor sites) are bad, but the ACE2 enzyme itself is actually protective against inflammation and perhaps the "ground glass opacities" seen on CT that develop almost universally during the very early stages of COVID disease?
We've simply got to get to the bottom of this. What "mimic" might there be for smoking that might duplicate this "far stronger effect than any drug trialed to date"?
Please help me!
I think that the increase of ACE2 by smoking is the reason why smokers do better.
This recent article talks about the ACE2 paradox:
"Given ACE2 itself is the gateway of SARS-CoV-2 entry into cells, how can the reduction in ACE2 levels in older persons
and those with CVD predispose for greater COVID-19 severity? To address this paradox, they suggest it is plausible that
greater expression of ACE2 leads to higher predisposition to incur COVID-19, citing preliminary epidemiologic data from
South Korea, “where the most population-wide testing has taken place”
"But, they say that severity of disease is affected by the reduction in ACE2 levels that occurs with ageing and cardiovascular
disease, which causes an upregulation of angiotensin II proinflammatory pathway: The increase in ACE2 levels with ACEI/ARB
treatment is more likely to be corrective to these changes. This is exploited with SARS-CoV-2 binding to ACE2, further reducing
ACE2 cell surface expression, upregulating angiotensin II signalling in the lungs, and yielding acute lung injury."
https://cardiacrhyth...evere-covid-19/
So if this is correct then we would want to increase ACE2, even though it might predispose us to incur Covid 19, it would protect us
more against the damaging inflammation of the lungs that seems to cause the death in this virus.
It's kinda of a catch 22 situation...do you raise ACE2 and have a higher predisposition of incurring Covid 19 but at the same time
give your body more ACE2 to hopefully protect from the damage to the lungs....or do you lower your ACE2 expression in the hope
not to even catch it, but if you do then take the chance of having a worse outcome in the end.
Edited by lancebr, 16 April 2020 - 07:14 AM.