You have no doubt heard the news that as universities reconvene students on campuses around the country, there are flares in COVID case counts.
The inclination to return universities to lock down and disperse the students back home in response to this is predictable, and about as nuanced as a knee jerk reflex, give or take the knee.
As we explore this matter, let’s apply just one assumption: that we cannot count on having a highly effective, perfectly safe, universally distributed, uniformly accepted vaccine against COVID19 by this time tomorrow- and perhaps, not for quite some time. A recent pause in a major vaccine trial reminds us how challenging the obstacle course to fast-track vaccine production can be.
Given that, we have four- and exactly four- courses through the pandemic between now and “then,” whenever then happens to be. They are summarized in the table below.
We can have high or low case counts (this presupposes that our testing is sufficient to correspond reasonably well with the actual occurrence of cases, so high case counts mean a high number of incident cases; low case counts mean the opposite); and high or low casualty counts. A casualty of COVID is any bad outcome: hospitalization, severe illness, lasting complication (I will return to this one), or death. A “case” not causing a “casualty” is an infection that comes and goes, imposing no discernible or lasting harm of any consequence.
In the immortal words of one of the cultural icons of my childhood: that’s all, folks. There is no fifth alternative.
So, what does each possible outcome of these four signify? Let’s take them one at a time.
Cell A, high case counts with high casualties, is famously now equated with the Swedish model. The virus spreads without any lockdown, and the toll of infection... is the toll. The jury is still out on Sweden’s approach, but it does seem clear that they could have had their cases and prevented their casualties, too, had they better protected the vulnerable- the elderly, chronically ill, and in particular, nursing home residents- right from the start.
Cell D, low case counts with low casualty counts- represents the more severe versions of societal lockdown. Among the better illustrations is New Zealand. The problem with this “hide away from the virus, wait for it to go away or a vaccine to arrive” approach is that the entire population remains vulnerable to infection at any time. This as astutely pointed out very early in the pandemic, is the famous “just flatten the curve” policy that does far more to change timing and dates than it does to change outcomes. New Zealand is now living this- experiencing small flares each time the population pokes out into the world. They are stuck living this way- lockdown maintained, or lockdown recurring- indefinitely.
Cell B isn’t worth talking about; it’s the unmitigated disaster of the group. A low overall case count with a high casualty count would occur if those most vulnerable to COVID catastrophes got the infection preferentially, while those who could most safely weather the infection- did not. This would be…spread concentrated among, say, nursing home residents, with the rest of the population protected. The very opposite of total harm minimization, and vertical (risk stratified) interdiction turned upside down, this scenario is not particularly plausible, and especially undesirable.
Finally, then, there is Cell C. From the start I have favored this as the best of “bad options.” Why only “bad” options? Because the one good option…is not having a pandemic in the first place! That, too, was possible- but only before our dietary habits started introducing animal viruses into the human population so routinely. Our incursions into the ecosystems of other creatures, carrying forks and knives, make zoonotic pandemics inevitable. Once we have one, and a virus has taken up shop in human bodies…Cell C is as good as it gets.
Cell C is, in effect, what I have advocated from the beginning: total harm minimization by means of risk-stratified interdiction. Those who can most safely abide exposure get exposed, and generally have a mild infection, or no apparent infection at all. Those most prone to bad outcomes- are meticulously protected from exposure until herd immunity is achieved.
Yes, I know: talk of herd immunity is blasphemy! But it should not be.
The reason it seems heretical - in addition to our polarized, opinionated, tweet-first-and-think-after-if-ever inclinations- is that herd immunity should be a product of Cell C, while we (in the United States) are living in Cell A. We did not protect the vulnerable, and have nearly 195,000 deaths attributed to COVID as a result. Most of our families have been touched personally by this unnecessary carnage; mine certainly has. No wonder there is a visceral antipathy to “herd immunity” with so high a toll on flagrant display.
But there is no such toll in Cell C- and although we have lived in Cell A until now, that does not preclude a pivot to Cell C for the remainder of the COVID experience.
What’s happening on colleges points in that very direction. We are, in fact, testing massively more now than we were at the start of the pandemic- and that’s a good thing; it should certainly continue. Even now, we are- if anything- testing too little (or too haphazardly), certainly not too much.
But, let’s be clear: we can only find cases when we look for them. We are looking for them more assiduously now, and finding them- even when they are very mild, or entirely asymptomatic- as they tend often to be in young, healthy people. The very people, in other words, who tend to gather on college campuses.
Some select precautions make sense even when low risk people mingle with other low risk people; sensible use of distancing or masks can reduce exposure doses, augmenting the likelihood of the mildest possible bout. But in general, the virus circulating among young people and fostering immunity without causing distress- is a good thing. This is Cell C: lots of mild cases, few if any harms, and the fast track to herd immunity that gives all the rest of us our lives back, too- because the virus stops circulating.
If that sounds implausible to you- perhaps because you have been living in a Cell A nightmare and can no longer see beyond its boundary- then look at this map of the United States and note the condition of the Northeast, where I live. We locked down too late here, and had the famous overload of New York City hospitals – where I made my own, brief clinical contributions as a volunteer- as a consequence. But the virus spread widely here, and the result is what one would expect: population level immunity takes over, and viral transmission rates start falling toward zero. The pandemic looks to be all but over here.
The case for non-heretical, Cell C-variety herd immunity is much fortified by the recent report out of Iceland, focus of my prior column, indicating COVID infection fatality rates in those under age 70 rather comparable to seasonal flu. But the news may be better still.
There is a recent suggestion- and yes, I find it plausible- that the mortality toll of COVID may have been inadvertently misrepresented by an order of magnitude in the early going. In other words, the notion may have taken hold early in the pandemic that this virus is ten times more lethal than it actually is. I invite you to dig further into that matter as the spirit moves you. The argument implies that had this error not been made, lockdown would never have been a consideration in the first place. For now, that is conjecture amidst the consternation of our on-going difficulties, so we really cannot know for sure.
What is clear at this point is that the actual mortality risk is a fraction of a percent among all infected, currently estimated at 0.3%; and a much smaller fraction of a percent, currently estimated at 0.1%, among those under the age of 70. As I noted recently, since we know that many achieve immunity without measurable IgG, these numbers are quite likely to be too high. Let’s be clear: these numbers can be too high, but they are very unlikely to be too low. Why? Because we can overlook cases of infection without symptoms, and immunity without antibodies, but we don’t tend to overlook hospitalization or death. In other words, we will reliably find every “bad” case of COVID, but remain prone to overlook many of the mild cases.
This means that the “numerator”- hospitalizations, deaths- will be fully populated, but the denominator- total infections- almost certainly will not be. If the infection fatality rate is D/I, where D is deaths and we don’t miss any of those; and I is infections, and we miss many of those- our rate will be too high by whatever degree “I” is incomplete.
What this means is that we can know the worst-case scenario for COVID deaths, but are unlikely – absent a massive testing effort- to know the best-case end of the range. But whatever that is, the actual toll is somewhere in that range, and obviously- not worse than the worst-case scenario.
That means COVID truly is no greater threat to generally healthy college students than seasonal flu, and apparently- less of a threat. That comparison, too, has devolved into heresy- but again, that’s because we have hoped for Cell C while living in Cell A; and because we have monumentally misgauged the infection fatality rate (IFR).
The now quite vast and remarkably consistent global data indicating an overall IFR of 0.3% or less does nothing at all to attenuate the tragedy of untimely loss many of our families have suffered. In response to that, I have nothing but my condolences to offer. But it does invite us to revisit the “American denominator.” The “official” perspective is that the U.S. has had nearly 200,000 deaths out of about 6.5 million known infections; but this is not right. The deaths are reliable, the infection count is far from it. We can instead “reverse engineer” our denominator.
A death toll of 200,000 is 0.3% of what? This is simple algebra (sorry!). The answer is, X = 67 million, with rounding. That is one out of every five Americans.
But we also know that infection rates are actually much higher than antibodies reveal, due to “immunological dark matter,” or immunity without routinely measured antibodies. If we conservatively use this knowledge to double the infection rate – then well over 130 million Americans have already been through a COVID infection, most without knowing it.
And once again, Cell C looks a lot less like heresy. The experience all around us suggests that the vast majority of those infected never even know it happened.
This extends to the fraught matter of visceral complications of COVID, now much in the news. I share the concern that lasting complications of all varieties should be included in the “casualty” counts; any long-term complication of COVID constitutes a bad outcome. And yes, there is evidence of cardiac inflammation in some young, healthy people who had apparently mild infection.
Here again, the “rightful” denominator is massively reassuring. We have not, to my knowledge, seen any spike in cardiovascular crises among young, formerly healthy people in the United States. If 65 million or more of us have had COVID; if even mild infection tends to inflame our vital organs; and if that poses a threat of acute medical crises- we should have seen a clear spike in such presentations. To the best of my knowledge (and I am working diligently to keep up with all COVID-related data of consequence), we simply have not. The penchant for drama invites us to worry a lot about such complications; the sobriety of epidemiology offers a quite reassuring: not so much.
One other noteworthy consideration on that topic: we do not routinely assess for cardiac or other vital organ inflammation after other common infections. Such inflammation is probably fairly common. I say this based on 30 years of clinical experience. I have seen it take months, even a year or longer, for formerly healthy people to recover fully from what we would deem a “garden variety” bout of pneumococcal pneumonia, or E. coli pyelonephritis (kidney infection). I have seen cardiac inflammation- myocarditis- from a very wide variety of causes. We even know that transient, cardiac dysfunction can occur with any severe stress, physical and/or psychological.
That does not make COVID complications less important- but it does remind us of the importance of context, and our predilection for distorting the unique harms of this contagion that has commanded our fixed attention and anxiety these long months.
Between here and the end of the pandemic, we need low casualty counts- but given that, we do not need low case counts. Rather the contrary, until that uniquely perfect vaccine materializes- we actually require high case counts to help put an end to this nightmare. If there is high viral circulation on college campuses, but hardly anyone is getting sick, the right response is not to disperse the students back home. The right response is to keep them right where they are, make sure vulnerable populations do not mingle with them until the viral flare burns out- and observe closely for any untoward changes. Flares on college campuses may be a way to give young adults their lives back, while letting them help end the pandemic for themselves and the rest of us, too.
Lastly: the extremely low risk of COVID to generally healthy college students is not zero risk. If enough young people get infected, someone is going to get hurt. I don’t want this to happen, and if/when it does, it will be a tragedy. But here, too, we need sense and context. Every year, some number of young, healthy college students die of alcohol intoxication, and from the puerile sadisms of “hazings.” We work to reduce such tragedies to as near zero as possible, but we do not shut down the nation’s universities as that effort continues without ever succeeding to perfection. COVID can, and should, be managed like other such threats. The only requirement for being at non-zero risk of being harmed or killed by something today is…being alive today.
Colleges are hinting at the promise of Cell C- and a more proximal and reliable end to our pandemic nightmare than the quite uncertain timelines of vaccine development. We seem to have a hard time accepting the view from the confines of our Cell A experience. To see that there is still a better way through the rest of this will require the primacy of sense over dogma, and a willingness to differentiate Epidemiology 101 from Drama 101. Thus far, we lack much evidence in favor of such heretical hopes.
David L. Katz, MD, MPH, FACPM, FACP, FACLM, is the Founding Director (1998) of Yale University’s Yale-Griffin Prevention Research Center, and former President of the American College of Lifestyle Medicine. He has published roughly 200 scientific articles and textbook chapters, and 15 books to date, including multiple editions of leading textbooks in both preventive medicine, and nutrition. He has made important contributions in the areas of lifestyle interventions for health promotion; nutrient profiling; behavior modification; holistic care; and evidence-based medicine. David earned his BA degree from Dartmouth College (1984); his MD from the Albert Einstein College of Medicine (1988); and his MPH from the Yale University School of Public Health (1993). He completed sequential residency training in Internal Medicine, and Preventive Medicine/Public Health. He is a two-time diplomate of the American Board of Internal Medicine, and a board-certified specialist in Preventive Medicine/Public Health. He has received two Honorary Doctorates.