Sooner or later, mild or severe

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Suppose that I could visit a fortune teller and get an answer to two questions.

Will I get the virus sooner, or will I get it later?

Will my case be mild, or will it be severe?

Here is how I would react to each of these possibilities:

Sooner Later
Mild Happiest Almost as happy
Severe Most unhappy Quite unhappy

I am assuming that if I get a mild case, then this will have no adverse long-term effects and that I will be immune going forward. These assumptions may not be 100 percent correct, but as long as they are most likely true I would stick to these rankings.

If you agree with me so far, then we have a framework for understanding the thinking of Johan Giesecke of Sweden. Many thanks to commenter John Alcorn for the pointer.

1. Lockdown policy was originally sold as a way of moving from left to right, that is from sooner to later. That is what was meant by “flattening the curve.” If I am going to get a severe case, then the lockdown makes me slightly better off. If I am going to get a mild case, it actually makes me slightly worse off, because I would rather get immunity sooner than later.

2. What I most care about is not getting a severe case. If I am going to get a severe case, then I would rather get it later, because I hope that by that point there is better treatment available.

All of the criteria that policy makers are using to decide on “re-opening,” whether they are models or trends in data, say something about sooner or later, which I hardly care about. They say nothing about mild or severe, which is what I most care about. When they use the terms “scientific” or “data-driven” to describe their thought process, I call Baloney Sandwich. Their science and their data don’t address the important issue.

Most of what we know about mild vs. severe concerns demographic categories. For example, very old people are particularly likely to get severe cases. We want to keep the virus out of nursing homes.

For young people, the risk of getting a severe case is not zero. But should they be treating the risk as more significant, say, than the risk of driving on the highway? Of course, everyone is in the dark because of the Unknown Denominator. Even if we know how many young people have died, we have no good estimate of how many young people have had the virus.

The most important question is what we can do to make it more likely to get a mild case than a severe case. If our health experts wanted to actually be useful, they would undertake to give us guidance on that. We could start by undertaking studies designed to pin down the Unknown Denominator. It would be most helpful to pin it down by demographic group, so that we could know something about the risk that each of us faces with respect to getting a severe case. Beyond that, perhaps government could conduct studies of clusters of people who have gotten severe illness to understand how they contracted the disease.

Some of us believe a hypothesis that viral load matters for mild vs. severe. If that is correct, then individuals can make better choices by avoiding spending a lot of time in enclosed spaces near other people. Also, they can help themselves by wearing masks, and they can help others by wearing masks whenever they are in public places. So subsidies for masks and laws requiring face covering in public places could be appropriate.

I wish that as a society we could switch emphasis away from the sooner or later axis. The emphasis on sooner or later gives inordinate power to government officials and the public health “experts” to control out lives, without ever getting at what matters.

35 thoughts on “Sooner or later, mild or severe”

  2. Mild vs. severe is not exogenous.

    If everyone gets sick sooner (or later, in theory), we outstrip our treatment capacity and more mild cases become severe cases. The evidence suggests the treatments we have are more effective when applied early and and so that the amount of virus we get contaminated with could affect the severity of the case.

    Also, secondary mortality rises as well. People who need other medical services can’t get them and start dying.

    And later gives us more time to work out how best to keep mild cases from becoming severe.

  3. MikeDC – healthcare doesn’t make mild cases into severe or vice versa. It makes severe cases into lethal, or not.

    • Could you support that assertion?

      The evidence I’ve seen is suggestive that early treatment (hydrocloroquinine+ Z-Pack, Remdesivir, etc) lowers the chance that a mild case becomes a severe case.

      So the ideal would be to flood the market with these drugs and as much as possible treat every symptomatic case with a cheap prophylactic response. This would seem to:

      1. Reduce the number of mild cases that later become severe cases.
      2. Reduce the duration (and therefore cost) of cases even if they never become severe.
      3. (Assumption and illustrative example) reduce the number of new cases, because if today’s mild case is resolved in 7 days instead of 14, that’s 7 fewer days in which the virus might spread.

      • Ah yes, an antibiotic does wonders for a virus. Never understood this assertion, my feeling is all placebo affect.

      • Remdesivir is an IV drug so you cannot go to your local pharmacy for it. There is no evidence to date that hydroxychloroquine + azithromycin work after one has contracted SARS-CoV-2. There are several large-scale trials set up to look at whether hydroxychloroquine alone is protective. there are documented really bad side effects with that combination of drugs (sudden death from cardiac arrythmias and unless you have a recent EKG showing your QT interval is normal, don’t even think about taking them. If you flood the market with these drugs, there is no way on earth that any decent clinical trial on a drug that has a good chance of working can be done.

  5. I’ve watched the video twice with my jaw dropped both times. Thank you Sweden for having the cojones to try something different.

    • Let Sweden be Sweden and let’s see where the chips fall out 6-12 months from now.

      Your approach to the virus is well known and has near monopoly status throughout the western world. Let’s allow another approach to proceed.

    • You’re comparing apples to oranges; the hypothesis is that the initial viral load (i.e. the number of viruses that the infectee initially comes into contact with) matters. The virus will obviously replicate in any infection to a much higher viral load, but starting from a lower baseline is thought to give the body’s immune system some extra time to come up to speed, resulting in a less threatening disease.

    • This isn’t evidence against the theory. Their tests in both legs were snapshots in time for all infected found, it tells us nothing about the initial viral load for each of the positives- only that there was no statistical difference between symptomatic and asymptomatic. For all we know, the asyptomatic were in day 10 of their infection, and the symptomatic were in day 5, and the real difference between the two groups is that the former were on the downside and the latter on the upside of viral load.

      • Sure, like I said, modest, but the fact that viral load seems irrelevant to progression is disturbing.

        • They don’t test for immune response- probably the key factor in symptomatic vs aysymptomatic.

          • Look, I was on team viral load, and pitched an absolute hissy for that reason when the nursing home tried to give my covid+ dad a covid+ roommate (he was in a single). I’m just saying, this has caused me to moderately revise my priors.

    • If the question is about variolation, this study doesn’t help much at all.

      There are two “viral load theories”.

      The first (I) is the “viral load kinetics” theory of symptom severity. That is, correcting for medical profiles, how ill you are at any moment is related to many many virus particles are in your body. But there are two sub-theories. (I.a) is that this applies to everyone, “most people with high viral load will have high symptoms”, and (I.b) is “Only if someone gets symptoms, then there is a correlation.”

      The past studies on MERS, SARS, and H1N1 (with unfortunately small n’s, selection bias for hospitalization) only provides support for (I.b). For cv19, this study provide strong evidence against (I.a). Lots of people go all the way through an infection with high viral loads, but they don’t feel a thing, but they still shed and spread.

      The second theory (II) behind the variolation proposal is that severity of symptoms depends on viral load compared to the time since the immune system response began. There are two sub-theories here too. (II.a) relies on the assumption of (I.a) and says that the reason is because the immune system was able to get started early enough to keep viral load down. (II.b) says that viral load during an infection is unaffected by timing, but something about the immune system not starting off so far behind from the start of the infection significantly reduces the severity of symptoms. That is “symptoms” somehow comes from “how overwhelmed the immune system feels, given the virus got an exponential head start.”

      Again, this study provides good evidence against (I.a), but doesn’t tell us anything about (II.b).

      I think about (II.b) this way. Let’s say your country can double mask production every month. Suddenly, demand for masks starts increasing exponentially. If you notice this and go into alarm mode very early, you can start doubling supply in line with demand, and keep pace, so the ‘price’ (i.e. symptoms) doesn’t go up. If you notice this a month too late, then despite all your efforts and the face you are increasing exponentially, you still cannot keep up with demand, and the price stays super high, like a fever.

      The idea behind variolation is “artificially kick off mask demand doubling, but from a base low enough so that mask supply production doubling will keep pace. The price will stay low.”

      Now, that study does provide some very modest evidence against (II.b), because it’s possible that kids get high exposed to high loads, and still don’t get any symptoms. But we already know that very few kids get sick at all from this, so for kids, initial viral loads don’t matter, probably because their young immune systems are so able to deal with this particular virus, that any exposure in the range of ordinary human contact is still below their ability to handle it without issue.

      Here was an interesting sentence from that study:

      “No infections were detected in either survey in 234 tested children ranging from 0 to 10 years, despite some of them living in the same household as infected people.”

      Unfortunately no antibody tests on those kids, so we don’t know if the kids had it first and had stopped shedding a while ago. If they didn’t get it first, they were getting lots of exposure, but their young immune systems knocked it out early.

      Also: “Subject 2 had contacts with four infected relatives who did not have any symptoms at the time of contact. … Subject 5 reported meeting an asymptomatic infected individual before the lockdown; Subject 7 did not report any contact with positive individuals and Subject 8 shared the same flat with two asymptomatic relatives. Notably, all asymptomatic individuals never developed symptoms, in the interval between the first and the second survey, and high proportion of them cleared the infection.”

      Pretty strong evidence that the asymptomatic are spreaders.

  7. I think that you want policies that make sense only if:
    1. An adequate testing program were in place, and
    2. If we had plenty of personal protective equipment.

    We’ve got to solve those problems before our option is anything other than quarantine.

    • The protective equipment is probably the more important of the two, because we need healthcare workers not to get sick so that they can treat patients (and not spread the disease to uninfected patients).

  8. One practical application of the less severe, sooner theory is to reopen schools on the theory that children and young adults will have less severe cases and thereby increase herd immunity. However, this assumes children are more likely to be exposed in a school setting. Not necessarily true. Looking at Denmark’s reopening with its ritual hourly hand washing and distancing as well as outdoor play, children may not necessarily be more likely at all to get exposure. Some might argue that students are losing something educationally, however, the vast majority of studies show that teachers strikes have no impact at all on educational attainment, see for example: https://scholar.google.com/scholar?hl=en&as_sdt=0%2C21&q=student+achievement+public+school+strikes&oq=student+achievement+public+school+strike#d=gs_qabs&u=%23p%3DIUOgFea2-xMJ

    And in some cases strikes improve outcomes. One really can’t be sure if the school shutdowns are a net gain or net loss in terms of student achievement. The other argument for reopening schools quickly is to free up parents of young children who might have jobs or who miss the babysitting function of schools. Against this though, we have to weigh the benefits: many local hospitals have set up offsite covid testing and treatment sites in closed university and school facilities like sports arenas. And many colleges are now allowing COVID patients to quarantine in dormitories.

    It would be a shame to rush back to the old way of doing things when we have a once in a lifetime opportunity to reimagine educational processes and replace the expensive factory farm education model with improved, less rigid, adaptable and more effective and efficient models outside the control of the corrupt teachers unions.

  9. This incredibly useful article by a medical professional at The Federalist suggests how one might prevent one’s infection from progressing to severe: https://thefederalist.com/2020/04/19/what-i-learned-from-nursing-my-husband-through-covid-19/ Lot of great ideas for preparing for when your turn comes.

    I would add to this a little additional prophylaxis: supplement with D3 and zinc. Since everyone assures me that the quinine in tonic is not helpful, I also have a daily gin and tonic with the juice of half a lime, on the theory that the quinine will actually improve the effectiveness of the zinc: no random controlled double blind research but I am still alive.

    • this is not the case. there are a number of preprints that I have read showing huge heterogeneity in antibody response.

  11. Most respiratory illnesses are milder in the summer. I suggest trying to get sick I June through August.

    • Yes, and polio was more prevalent during the summer than winter months during the pre-vaccine era.

      • Polio is totally different, not respiratory, it’s a gut infection that moves up nerves causing muscle paralysis. Fecal-oral transmission in contaminated water supplies, which is why it spread in summer, and why they started requiring lots of chlorine in pools.

        • As a general statement, yes, but there are tragic exceptions. We had three parents of adjacent homes who all contracted polio during the summer of 1953 (I was 7 at the time). None of them were regular swimmers and the mode of transmission in that cohort is still a mystery as the other three spouses and nine children were unaffected.

  12. Aren’t we setting aside some extremely likely scenarios?

    A). Not getting the virus at all because of herd immunity choking R below 1 and extinguishing the disease?

    B). Not getting the virus at all because of a vaccine?

    These are both likely and both argue for not getting the CV early.

    • Very true. We don’t understand it enough to know the version that we would get. I would opt for B please

      • It is not practical for everyone to stay home waiting for a vaccine. You would run out of food if everyone did that. Think through your opinions before posting them.

        • May I suggest thinking on the margin.

          None of the scenarios involve everyone staying at home and starving to death. That would indeed be pretty silly. The lockdowns involve non essential people staying at home (delaying) and the essential going out in the workforce and risking immediate exposure.

          My point, respectfully, is that it makes sense for the vulnerable — and possibly most of us — to be in the delay group for three reasons.

          1). Medical capacity, treatment and learning will improve, possibly significantly
          2). Herd immunity will be created by those getting earlier exposure.
          3). Vaccine, eventually.

    • The only way herd immunity happens is if hundreds of millions of people get, then recover from, the virus.

      • You are thinking in black and white terms.

        In reality the way to beat the virus is to get R under 1. Anything we do to reduce spread including isolation, sneezing in elbow, wearing masks, social distancing, hand washing etc, etc lowers R. So too does building herd immunity, especially among the super spreaders and those never conforming to the mitigation practices above.

        Over time, what is required is getting the young and healthy (99.9% survival rate with no underlying major risk factors) to develop a degree of immunity while those most at risk maximize their separation from the herd. Every percentage increase in the immunity level of the young and super spreaders decreases R.

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