COVID-19 Never Killed Anybody

by Ted Noel MD

Before you get out the tar and feathers, note that I am a physician with experience in Expensive Care (Intensive Care) – the art of getting people who have both feet on the banana peel well – or spending as much money as possible on high tech expensive resources as possible before they assume room temperature. That’s all done in the Intensive Care Unit, for those of you not familiar with medical humor.

The US is treating the Wuhan Flu as if it is a single disease that has killed so many people that it will kill the rest of us if we open up the economy. They claim that because we are allegedly having a massive spike in new cases, we have to reverse actions to open up our society. At the very least, we have to put masks on everyone.

In other places I’ve discussed how masks do no good and can actually cause harm. Others have discussed how the actual data on mortality and case count are vastly inflated. But this completely misses a couple of very important points.

First, COVID-19 doesn’t kill people.

There. I’ve gone and said it again. There’s a very important reason for this conclusion. If all you get is the Wuhan Flu, you may get a bit sick, but you won’t even need to go to the hospital. You’ll get over it. That’s because you don’t get a “Cytokine Storm.”

In plain English, CS is a different disease process. It’s an uncontrolled release of signaling molecules that engage the immune system at ludicrous speed. A number of different infections can trigger it. An infection is needed before the Storm can start, but the Storm is a different process. Once it’s underway, it drives the train. We know that the risk of dying from CS following COVID-19 in Florida if you are under age 25 is 0.02%, but if you are over 85, it’s 24.5% (FL Dept of Health as of July 6).


That 1,225x difference in risk proves that something else is in play. The infection is necessary, but it’s not sufficient. CS requires something more than just infection such as COVID-19, SARS, or H5N1 flu. In general, age and infirmity are correlated with bad outcomes, but we don’t know in any detail what factor within those categories is needed. What we do know is that the interventions that work don’t have all that much to do with antiviral effects.

Multiple studies have shown that hydroxychloroquine works to reduce severity and duration of the infection complex (COVID + CS) if given in the earlier stages of the disease. We also know that HCQ has both antiviral and immune modulating effects. Which of its effects is important with COVID-19 is not entirely clear. But as we look further, studies have shown that dexamethasone, a common, inexpensive steroid, has beneficial effects, most likely by reducing CS. And new reports indicate that early administration of budesonide, an inhaled steroid that only gets to the lungs, can rapidly reverse the onset of CS.

The common feature of these treatments is an anti-inflammatory effect. HCQ is a mild anti-inflammatory, inhaled budesonide works the same way in the lung, and dexamethasone is a more potent systemic anti-inflammatory. If we add suggestive data that non-steroidal anti-inflammatories may reduce inflammatory symptoms of respiratory virus infections, we start to see a strongly suggestive picture that CS is the major culprit.

When we look at drugs with antiviral effects, the picture isn’t so clear. A search of PubMed reveals no strong candidates for therapy. Lay news reports have remdesivir reducing hospital stays, but detailed studies are still in the pipeline. In short, antivirals don’t seem to be all that useful in advanced COVID-19 cases. At the same time, viral load on admission does not seem to match outcome. But viral load does match inflammatory markers in critically ill patients.

Putting the viral load data together doesn’t tell us much. That suggests that antiviral therapy isn’t likely to be terribly helpful in the critically ill patient. And that seems to be what we’re seeing. The disease that kills people is CS, not COVID-19.

This tells us that we need to be concerned with CS, not Wuhan Flu. But CS can come from a number of infections, not just Wuhan Flu. And it seems to happen almost exclusively in the elderly and infirm. So a focus on stopping Wuhan Flu is misguided. We need lots of young people to get and recover from COVID-19 infection. Their immunity will help protect the rest of us. For them, COVID-19’s just the common cold. Or less. In Florida, under age 25 there have been exactly eight deaths related to COVID-19. That means that we need to re-open all schools ASAP. Even if those kids get infected, they’ll get over it, and they don’t often pass it on.

COVID-19 is not the problem. When it triggers CS, a potentially lethal problem develops. So we need to remember that there are people at high risk. They are the only people who should socially distance, isolate, or wear masks. And the only masks that actually work for them are N-95s. Those filter well as you breathe in, but let you breathe out through a valve. So they protect the wearer, but not those around. We should also actively monitor at-risk populations. With the early onset of symptoms, anti-inflammatory therapy seems likely to be beneficial, possibly averting the onset of CS.

Low risk activities (outdoors) by low risk populations should be completely opened up. Schools need to open up. And indoor activities should be resumed with Americans being allowed to assume the normal risks of daily life. Nothing in any lockdown has been beneficial. In New York we know it increased the number of people getting sick. Why do we want to repeat that?

Dr. Noel is a retired physician who is trained in Critical Care Medicine. He writes on medical and political issues.

Comments (0)

The Kick Them All Out Project