abandonconflict
Well-Known Member
My point with that argument was specific to Danes. The part about oxidative stress is relavant to that due to the fact that relevant comorbidities may occur at lower rates in the population of Denmark. Since all we have to go on are confirmed cases, Denmark or any country may simply have fewer or more people in its population with such comorbidities which would cause clinically apparent infection. Yes, part of my point is that the reproductive rate is unknown. I suggest that it is very high and that seroprevalence is also already very high and that those most susceptible are becoming infected through community spread that is well beyond control. Some populations are younger and fitter and have lower rates of coronary disease than others. My argument is that instead of the R0, we should be looking at the prevalence of comorbidities to explain case growth, particularly in such places where the rate of infection isn't known.
It is coming out in studies that much of the death and many of the cases showing clinically apparent infection (everywhere) are related to the coronary damage being done by the virus. Much more so than the lungs. Even in many patients showing pulmonary distress, it is often found that there is enough functional lung tissue to deliver oxygen and that ventilators often aren't saving people. It's a whole interesting debate on its own but it's true that the latest medical findings indicate this. I would highly recommend following the latest medical findings. They do in fact suggest that it's primarily a circulatory disease. It's still not 100% understood. Only one in five of those who have critical cases have no apparent underlying cardiopulmonary condition or diabetes.
I'm indeed arguing, "what if that's why?". And yes, a premise here is that we really don't know the infection rate.
. I hope no rules were broken