As I predicted in my last journal, protests are beginning around the US demanding that the country get back to work. With lines of cars at food banks sometimes miles long and the essentially complete collapse of the job market, this is certainly understandable. At the same time, if we open the economy incorrectly, there is going to be another wave of COVID-19 infections. Even so, there are probably ways to go about this without endangering a broad swath of the population.
Before I get into that, I want to briefly address two questions that I am being asked on a regular basis. ‘What do the visitors have to say about this,’ and ‘why don’t they help us?’
In the privacy of my own life, I am more deeply connected with this enigmatic presence than I ever have been before, and I feel sure that some of what I will say here comes from that source. What, though, I cannot say for sure. As to why they won’t intervene, I explain why such interruptions in the flow of events is always unlikely and usually impossible in my book A New World, particularly in Chapter 6.
So what do we need to do to get back to work safely, and how can we best proceed to protect ourselves against the virus when we do get it? And if we go back to work in May, as I think most of us will, then there will be a second wave of infections, just as is occurring in Singapore and Japan. I don’t see any choice but to take this risk. If we don’t, fundamental aspects of our economy are going to collapse, most dangerously the structure of the food supply chain, and that must not be allowed to happen.
The first question that has not been answered is, how lethal is the virus? This should have been determined early, but so far no country has carried out the kind of epidemiological studies necessary to generate this sort of statistical insight.
Some recent evidence suggests that vastly more people may have had it than we realize. A recent study in Santa Clara, California, for example, suggests that there may be a remarkable 50 to 80 percent more cases than has been thought. This would mean that, because the virus is so much more widespread, it is therefore less lethal.
If true, then this means that an entirely different and much less economically damaging mitigation strategy is suggested: 1, most people can safely get back to work; 2, vulnerable populations, which have already for the most part been clearly identified, should continue on lockdown. But it is absolutely critical to know for certain that we are right about this before proceeding, otherwise we could end up with an uncontrollable disaster.
As matters stand, we have to get back to work or experience an economic catastrophe beyond anything that has been known in modern history, and which will be in many ways unrecoverable.
If we are going to regain control of the situation, we are going to need to obtain some clear information about who is too vulnerable to risk exposure and who can reasonably take the risk.
We already know which populations are more vulnerable: first, the elderly, especially those with chronic illnesses like diabetes, coronary disease and high blood pressure. There is a possibility that the blood pressure vulnerability is increased by the use of ACE-inhibitors and angiotensin 2 receptor blockers. This is because, while they block ACE proteins that lead to high blood pressure, they also increase ACE-2 protein levels, and it is these proteins that COVID-19 attaches to. Until it is clear that these two classes of drug are not exacerbating this disease, it would seem prudent to move these patients to other drugs whenever possible. In the case of diabetes, it is known that high blood sugar interferes with the body’s ability to fight infection, so the problem is likely to be more serious for people with uncontrolled or poorly controlled diabetes than those with well controlled disease. With regard to coronary disease, the additional stress on the heart caused by the body’s need to fight the virus is what causes increased mortality among these people. In addition, COVID-19 triggers inflammation of the heart muscle.
The second population that appears more vulnerable is males, but it’s not clear that there is an underlying genetic cause for this. In fact, the studies that identified this factor were mostly conducted in China, where many more men smoke than women. Because smoking causes constant low-level inflammation in the lungs, being a smoker is a major risk factor. Also, men, in general, suffer from higher rates of obesity and other known risk factors than women.
These things are also true among blacks and Latinos, who have higher COVID-19 morbidity, largely, apparently, because of more obesity, diabetes and inability to sequester themselves or obtain household supplies like disinfectants, originally because of poverty, and now because they are not generally available at all.
When COVID-19 kills, it does so because it breaks the body’s immune system, causing it to go into overdrive. The lungs then become inflamed and filled with fluid, and the victim drowns in their own mucus production. Because of the way coronaviruses mutate, is may prove more difficult than we are hoping to create an effective vaccine for this virus. This would be for the same reason that it is hard to create a vaccine that is effective against the rhinoviruses that cause most colds.
While a vaccine is likely to eventually be found, it is also likely to be strain specific like the flu vaccine, and to require frequent updating. However, it is possible that drugs that prevent the immune system from overreacting might be effective in aiding recovery from COVID-19, and should become a standard treatment protocol, especially in vulnerable populations.
This means that anti-inflammatory drugs should be subject to careful and objective study. They should not be politicized. Unfortunately, just that has happened with hydrochloroquine, which is used routinely to treat two inflammatory diseases, lupus and rheumatoid arthritis. There are a few limited studies that suggest that it might be efficacious against other diseases that cause excessive inflammation, in particular COVID-19. But because of the politicization, the situation has become very confused, with some media outlets claiming that it is a cure and others that it is useless and even poisonous. There is clear reason to test this drug properly, and it is to be hoped that that is done.
There is some evidence that it was active against SARS-COVID-1, and did prevent its replication, at least in laboratory settings. However, even if it does not prevent the replication of COVID-19, its anti-inflammatory effects should be subjected to clinical trials to find out if they reduce the inflammation associated with the virus. This means that there should not only be trials of the drug on seriously ill patients but also on early presenters in p0pulation groups known to be vulnerable. Similarly, the Macrolide antibiotic family should be subjected to clinical trials, in part because of their anti-inflammatory effects, but also because they have efficacy against secondary bacterial infections that are a common result of viral pneumonias.
As with any viral pneumonia, once the lungs become irritated by coughing and inflammation, they become susceptible to secondary bacterial pneumonias. The Macrolides, like Erythormyiacin, have two effects: first, they kill most of the bacterias that cause bacterial pneumonia; second, they have an anti-inflammatory effect. There is only one case being reported of a Macrolide being effective, but because of the logic of why this might be true and the widespread availability of the drug class, trials would seem to be in order. But like hydrocholoroquine, early presenters in vulnerable populations need to be trialled as well as more seriously ill patients.
Other anti-inflammatories need to be studied as well, but non-steroidal anti-inflammatories (Aleve, Advil, etc.) should not be among them because they suppress an enzyme that the body needs to fight off viruses such as COVD-19.
Obviously, anti-virals should also be studied, but I’m not going to discuss that because there are already many studies and trials under way.
The bottom line is that we need to quickly determine whether or not COVID-19 is more widespread and therefore less lethal than previously thought. This can be done most quickly by doing concentrated general-population testing in high population density areas, specifically big cities. By this, I don’t mean just testing of people who show symptoms, but testing of everybody, both for the disease and especially for the antibodies that show whether or not they have had it.
Until we do this, we are essentially flying blind. Instituting general population testing in our ten largest cities could give us a viable management tool in a matter of weeks. What is lacking is a realization on the part of our epidemiological leadership of the importance of doing this. Hopefully, that will change, and soon.
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