In April, I wrote several essays and articles about our collective response to Covid-19.
I was worried – and am still worried, honestly – that we weren’t making the best choices.
It’s hard not to feel cynical about the reasons why we’ve failed. For instance, our president seems more concerned about minimizing the visibility of disaster than addressing the disaster itself. We didn’t respond until this virus had spread for months, and even now our response has become politicized.
Also, the best plans now would include a stratified response based on risk factor. Much more than seasonal influenza, the risk of serious complications from Covid-19 increases with age. Because we didn’t act until the virus was widespread, eighty-year-olds should be receiving very different recommendations from forty- and fifty-year-olds.
Our national response is being led by an eighty-year-old physician, though, and he might be biased against imposing exceptional burdens on members of his own generation (even when their lives are at stake) and may be less sensitive to the harms that his recommendations have caused younger people.
I’m aware that this sounds prejudiced against older folks. That’s not my intent.
I care about saving lives.
Indeed, throughout April, I was arguing that our limited Covid-19 PCR testing capacity shouldn’t be used at hospitals. These tests were providing useful epidemiological data, but in most cases the results weren’t relevant for treatment. The best therapies for Covid-19 are supportive care – anti-inflammatories, inhalers, rest – delivered as early as possible, before a patient has begun to struggle for breath and further damage their lungs. Medical doctors provided this same care whether a Covid-19 test came back positive or negative.
(Or, they should have. Many patients were simply sent home and told to come back if they felt short of breath. Because they didn’t receive treatment early enough, some of these patients then died.)
Instead, our limited testing capacity should have been used at nursing homes. We should have been testing everyone before they went through the doors of a nursing home, because people in nursing homes are the most vulnerable to this virus.
I realize that it’s an imposition to make people get tested before going in, either for care or to work – even with real-time reverse-transcription PCR, you have to wait about two hours to see the results. But the inconvenience seems worthwhile, because it would save lives.
From March 25 until May 10 – at the same time that I was arguing that our limited Covid-19 tests be used at nursing homes instead of hospitals – the state of New York had a policy stating that nursing homes were prohibited from testing people for Covid-19.
I really dislike the phrase “asymptomatic transmission” – it’s both confusing and inaccurate, because viral shedding is itself a symptom – but we knew early on that Covid-19 could be spread by people who felt fine. That’s why we should have been using PCR tests before letting people into nursing homes.
But in New York, nursing homes were “prohibited from requiring a hospitalized resident who is determined medically stable to be tested for COVID-19 prior to admission or readmission.”
Not only do nursing homes have the highest concentration of vulnerable people, they also have far fewer resources than hospitals with which to keep people safe. Nursing home budgets are smaller. Hallways are narrower. Air circulation is worse. The workers lack protective gear and training in sterile procedure. Nursing home workers are horrendously underpaid.
The low wages of nursing home workers aren’t just unethical, they’re dangerous. A recent study found that higher pay for nursing home workers led to significantly better health outcomes for residents.
This study’s result as described in the New York Times – “if every county increased its minimum wage by 10 percent, there could be 15,000 fewer deaths in nursing homes each year” – is obviously false. But even though the math doesn’t work out, raising the minimum wage is the right thing to do.
If we raised the minimum wage, we probably would have a few years in which fewer people died in nursing homes. But then we’d see just as many deaths.
Humans can’t live forever. With our current quality of care, maybe nursing home residents die at an average age of 85. If we raise the minimum wage, we’ll get better care, and then nursing home residents might die at an average age of 87. After two years, we’d reach a new equilibrium and the death rate would be unchanged from before.
But the raw number here – how many people die each year – isn’t our biggest concern. We want people to be happy, and an increase in the minimum wage would improve lives: both nursing home residents and workers. Which I’m sure that study’s lead author, economist Kristina Ruffini, also believes. The only problem is that things like “happiness” or “quality of life” are hard to quantify.
Especially when you’re dealing with an opposition party that argues that collective action can never improve the world, you have to focus on quantifiable data. Happiness is squishy. A death is unassailable.
Indeed, that’s partly why we’ve gotten our response to Covid-19 wrong. Some things are harder to measure than others. It’s easy to track the number of deaths caused by Covid-19. (Or at least, it should be – our president is still understating the numbers.)
It’s much harder to track the lives lost to fear, to domestic violence, and to despair (no link for this one – suddenly Fox News cares about “deaths of despair,” only because they dislike the shutdown even more than they dislike poor people). It’s hard to put a number on the value of 60 million young people’s education.
But we can’t discount the parts of our lives that are hard to measure – often, they’re the most important.
My family had spring break travel plans for before the shutdown.
We canceled them.
At the time, we feared for our safety. My spouse said to me, “You caught the flu twice this year, even after you were vaccinated, and the second time was the sickest I’ve ever seen you. I’m really worried about what will happen if you catch this new thing, too.”
She wanted me to cancel my poetry classes in the local jail. My father, an infectious diseases doctor and professor of immunology, thought I should still go in to teach. “If somebody’s in there coughing up a lung, you should recommend he skip class next week,” my father told me.
But I was spooked. I felt glad when the jail put out a press release saying they’d no longer allow volunteers to come in – I didn’t want to choose between helping the incarcerated men and protecting my family.
My spouse is a high school science teacher. She felt glad that her biology classroom has over a dozen sinks. During the final week of school, she asked all her students to wash their hands for 20 seconds as soon as they walked into the room.
My spouse and I are both scientists, but it wasn’t until a week into the shutdown that I began to read research papers about Covid-19. Until then, we had gotten all our information from the newspaper. And the news was terrifying. Huge numbers of people were dying in Italy. Our imbecilic president claimed that Covid-19 was no big deal, making me speculate that this disease was even more dangerous than I’d thought.
Later, I finally went through the data from Italy and from the Diamond Princess cruise ship. These data – alongside the assumption that viral exposure should be roughly similar across age groups, if not higher for school children and young people who are out and about in the world – showed my family that our personal risk was probably quite low.
Still, we stayed inside. We were worried about harming others.
When I saw photographs of beaches packed with revelers, I felt furious. Did those selfish young people not realize that their choices could cause more people to die?
So it was shocking for me to learn that those selfish young people were actually doing the thing that would save most lives.
If we, as a people, had acted earlier, we could have prevented all these deaths. In January, it would have been enough to impose a brief quarantine after all international travel. In February, it would have been enough to use our current strategy of business closures, PCR testing, and contact tracing. In March, we were too late. The best we could do then – the best we can do now – was to slow the spread of infections.
Unfortunately, slowing the spread of infections will cause more people to die.
There’s an obvious short-term benefit to slowing the spread of infections – if too many people became critically ill at the same time, our hospitals would be overwhelmed, and we’d be unable to offer treatment to everyone who wanted it. We’d run out of ventilators.
This problem is exacerbated by the fact that we, as a people, are terrible about talking about death. There’s no consensus about what constitutes a good life – what more would have to happen for you to feel ready to die?
Personally, I don’t want to die. As my mind stopped, I’d feel regret that I wouldn’t get to see my children become self-sufficient adults. But I’d like to think that I could feel proud that I’ve done so much to set them on the right path. Since my twenties, I’ve put forth a constant effort to live ethically, and I’d like to imagine that my work – my writing, teaching, and research – has improved other people’s lives.
I’ve also gotten to see and do a lot of wonderful things. I’ve been privileged to visit four countries. I visited St. Louis’s City Museum when one of my kids was old enough to gleefully play. I have a bundle of some two dozen love letters that several wonderful people sent me.
I’ve had a good life. I’d like for it to continue, but I’ve already had a good life.
Many medical doctors, who have seen how awful it can be for patients when everything is done to try to save a life, have “do not resuscitate” orders. My spouse and I keep our living wills in an accessible space in our home. But a majority of laypeople want dramatic, painful measures to be taken in the attempt to save their lives.
Still. Even without our reluctance to discuss death, there would be a short-term benefit to slowing the spread of infections. The American healthcare system is terrible, and was already strained to the breaking point. We weren’t – and aren’t – ready to handle a huge influx of sick patients.
But the short-term benefit of slowing the spread of Covid-19 comes at a major cost.
The shutdown itself hurts people. The deaths caused by increased joblessness, food insecurity, educational disruption, domestic violence, and loneliness (“loneliness and social isolation can be as damaging to health as smoking 15 cigarettes a day”) are more difficult to measure than the deaths caused by Covid-19. We won’t have a PCR test to diagnose which people were killed by the shutdown.
Those deaths won’t all come at once. But those deaths are no less real, and no less tragic, than the immediate horror of a person drowning from viral-induced fluid buildup in their lungs.
And, perhaps more damning, if the shutdown ends before there’s a vaccine, the shutdown will cause more people to die of Covid-19.
Without a vaccine, slowing the spread of Covid-19 has a short-term benefit of reducing the rate of hospital admissions, at the long-term cost of increasing the total number of Covid-19 cases.
All immunity fades – sometimes after decades, sometimes after months. Doesn’t matter whether you have immunity from recovery or from vaccination – eventually, your immunity will disappear. And, for a new disease, we have no way of predicting when. Nobody knows why some antigens, like the tetanus vaccine, trigger such long-lasting immunity, while other antigens, such as the flu vaccine or the influenza virus itself, trigger such brief protection.
We don’t know how long immunity to Covid-19 will last. For some coronaviruses, immunity fades within a year. For others, like SARS, immunity lasts longer.
The World Health Organization has warned, repeatedly, that immunity to Covid-19 might be brief. But the WHO seems unaware of the implications of this warning.
The shorter the duration of a person’s immunity, the more dangerous the shutdown. If our shutdown causes the Covid-19 epidemic to last longer than the duration of individual immunity, there will be more total infections – and thus more deaths – before we reach herd immunity.
This is, after all, exactly how a one-time “novel zoogenic disease” like influenza became a permanent parasite on our species, killing tens of thousands of people in the United States each year. Long ago, transmission was slowed to the point that the virus could circulate indefinitely. Influenza has been with us ever since.
That’s the glaring flaw in the recent Harvard Science paper recommending social distancing until 2022 – in their key figure, they do not incorporate a loss of immunity. Depending on the interplay between the rate of spread and the duration of immunity, their recommendation can cause this epidemic to never end.
And, if the shutdown ends before we have a vaccine, the lost immunity represents an increased death toll to Covid-19. Even neglecting all the other harms, we’ll have killed more people than if we’d done nothing.
This sounds terrifying. And it is. But the small glimmer of good news is that people’s second infections will probably be less severe. If you survive Covid-19 the first time you contract it, you have a good chance of surviving subsequent infections. But prolonging the epidemic will still cause more deaths, because herd immunity works by disrupting transmission. Even though an individual is less likely to die during a second infection, that person can still spread the virus. Indeed, people are more likely to spread the virus during subsequent infections, because they’re more likely to feel healthy while shedding infectious particles.
This calculation would be very different if people could be vaccinated.
Obviously, vaccination would be the best way to end this epidemic. In order to reach herd immunity by a sufficient number of people recovering, there would have to be a huge percentage of our population infected. Nobody knows how many infections it would take, but many researchers guess a number around 60% to 70% of our population.
Even if Covid-19 were no more dangerous than seasonal influenza (and our data so far suggest that it’s actually about four-fold moredangerous than most years’ seasonal influenza), that would mean 200,000 deaths. A horrifying number.
But there’s no vaccine. Lots of people are working on making a vaccine. We have Covid-19 vaccines that work well in monkeys. But that doesn’t necessarily mean anything in terms of human protection. We’ve made many HIV vaccines that work well in monkeys – some of these increase the chance that humans will contract HIV.
It should be easier to make a vaccine against this coronavirus than against HIV. When making a vaccine, you want your target to mutate as little as possible. You want it to maintain a set structure, because antibodies need to recognize the shape of external features of the virus in order to protect you. HIV mutates so fast that its shape changes, like a villain constantly donning a new disguise. But the virus that causes Covid-19 includes a proofreading enzyme, so it’ll switch disguises less.
Still, “easier to make a vaccine against than HIV” is not the most encouraging news. Certain pharmaceutical companies have issued optimistic press briefings suggesting that they’ll be able to develop a vaccine in 18 months, but we should feel dubious. These press briefings are probably intended to bolster the companies’ stock prices, not give the general public an accurate understanding of vaccine development.
Realistically, a Covid-19 vaccine is probably at least four years away. And it’s possible – unlikely, but possible – that we’ll never develop a safe, effective vaccine for this.
If we end the shutdown at any time before there is a vaccine, the shutdown will increase the number of people who die of Covid-19. The longer the shutdown, the higher the toll. And a vaccine is probably years away.
The combination of those two ideas should give you pause.
If we’re going to end the shutdown before we have a vaccine, we should end it now.
For a vaccine to end the Covid-19 epidemic, enough people will need to choose to be vaccinated for us to reach herd immunity.
Unfortunately, many people in the United States distrust the well-established efficacy and safety of vaccines. It’s worth comparing Covid-19 to seasonal influenza. On a population level, Covid-19 seems to be about four-fold more dangerous than seasonal influenza. But this average risk obscures some important data – the risk of Covid-19 is distributed less evenly than the risk of influenza.
With influenza, healthy young people have a smaller risk of death than elderly people or people with pre-existing medical conditions. But some healthy young people die from seasonal influenza. In the United States, several thousand people between the ages of 18 and 45 die of influenza every year.
And yet, many people choose not to be vaccinated against influenza. The population-wide vaccination rate in the United States is only 40%, too low to provide herd immunity.
Compared to influenza, Covid-19 seems to have less risk for healthy young people. Yes, healthy young people die of Covid-19. With influenza, about 10% of deaths are people between the ages of 18 and 45. With Covid-19, about 2% of deaths are people in this age group.
I’m not arguing that Covid-19 isn’t dangerous. When I compare Covid-19 to seasonal influenza, I’m simply comparing two diseases that are both deadly.
The influenza vaccine saves lives. The data are indisputable.
But people don’t choose to get it! That’s why I think it’s unfortunately very likely that people whose personal risk from Covid-19 is lower than their risk from influenza will forgo vaccination. Even if we had access to 300 million doses of a safe, effective vaccine today, I doubt that enough people would get vaccinated to reach herd immunity.
Obviously, I’d love to be wrong about this. Vaccination saves lives.
Please, dear reader, get a flu vaccine each year. And, if we develop a safe, effective Covid-19 vaccine, you should get that too.
We don’t have a vaccine. The shutdown is causing harm – the shutdown is even increasing the total number of people who will eventually die of Covid-19.
Is there anything we can do?
Luckily, yes. We do have another way to save lives. We can change the demographics of exposure.
Our understanding of Covid-19 still has major gaps. We need to do more research into the role of interleukin 6 in our bodies’ response to this disease – a lot of the healthy young people who’ve become critically ill with Covid-19 experienced excessive inflammation that further damaged their lungs.
But we already know that advanced age, smoking status, obesity and Type 2 diabetes are major risk factors for complications from Covid-19. Based on the data we have so far, it seems like a low-risk person might have somewhere between a hundredth or a thousandth the chance of becoming critically ill with Covid-19 as compared to an at-risk person. With influenza, a low-risk person might have between a tenth and a hundredth the chance of becoming critically ill.
The risk of Covid-19 is more concentrated on a small segment of the population than the risk of influenza.
To save lives, and to keep our hospitals from being overwhelmed, we want to do everything possible to avoid exposing at-risk people to this virus.
But when healthy young people take extraordinary measures to avoid getting sick with Covid-19 – like the shutdown, social distancing, and wearing masks – they increase the relative burden of disease that falls on at-risk people. We should be prioritizing the protection of at-risk people, and we aren’t.
Because this epidemic will not end until we reach the population-wide threshold for herd immunity, someone has to get sick. We’d rather it be someone who is likely to recover.
Tragically, we already have data suggesting that a partial shutdown can transfer the burden of infection from one group to another. In the United States, our shutdown was partial from the beginning. People with white-collar jobs switched to working remotely, but cashiers, bus drivers, janitors, people in food prep, and nurses have kept working. In part because Black and brown people are over-represented in these forms of employment, they’ve been over-represented among Covid-19 deaths.
There is absolutely no reason to think that poor people would be more likely to safely recover from Covid-19 – indeed, due to air pollution, stress, sleep deprivation, limited access to good nutrition, and limited access to health care, we should suspect that poor people will be less likely to recover – but, during the shutdown, we’ve shifted the burden of disease onto their shoulders.
This is horrible. Both unethical and ineffective. And, really, an unsurprising outcome, given the way our country often operates.
If we want to save lives, we need for healthy younger people to use their immune systems to protect us. The data we have so far indicates that the shutdown should end now — for them.
It will feel unfair if healthy younger people get to return to work and to their regular lives before others.
And the logistics won’t be easy. We’ll still need to make accommodations for people to work from home. Stores will have to maintain morning hours for at-risk shoppers, and be thoroughly cleaned each night.
If school buildings were open, some teachers couldn’t be there – they might need substitutes for months – and neither could some students, who might switch to e-learning to protect at-risk family.
We’ll need to provide enough monetary and other resources that at-risk people can endure a few more months of self-isolation. Which is horrible. We all know, now that we’ve all been doing this for a while, that what we’re asking at-risk people to endure is horrible. But the payoff is that we’ll be saving lives.
Indeed, the people who self-isolate will have lowest risk. We’ll be saving their lives.
And no one should feel forced, for financial reasons or otherwise, to take on more risk than they feel comfortable with. That’s why accommodations will be so important. I personally would feel shabby if I took extreme measures to protect myself, knowing that my risk is so much lower than other people’s, but you can’t look at someone in a mask and know their medical history, much less whom they might be protecting at home.
All told, this plan isn’t good. I’m not trying to convince you that this is good. I’m just saying that, because we bungled things in January, this is the best we have.
The scientific method is the best way to investigate the world.
Do you want to know how something works? Start by making a guess, consider the implications of your guess, and then take action. Muck something up and see if it responds the way you expect it to. If not, make a new guess and repeat the whole process.
This is slow and arduous, however. If your goal is not to understand the world, but rather to convince other people that you do, the scientific method is a bad bet. Instead you should muck something up, see how it responds, and then make your guess. When you know the outcome in advance, you can appear to be much more clever.
A large proportion of biomedical science publications are inaccurate because researchers follow the second strategy. Given our incentives, this is reasonable. Yes, it’s nice to be right. It’d be cool to understand all the nuances of how cells work, for instance. But it’s more urgent to build a career.
Both labs I worked in at Stanford cheerfully published bad science. Unfortunately, it would be nearly impossible for an outsider to notice the flaws because primary data aren’t published.
A colleague of mine obtained data by varying several parameters simultaneously, but then graphed his findings against only one of these. As it happens, his observations were caused by the variable he left out of his charts. Whoops!
(Nobel laureate Arieh Warshel quickly responded that my colleague’s conclusions probably weren’t correct. Unfortunately, Warshel’s argument was based on unrealistic simulations – in his model, a key molecule spins in unnatural ways. This next sentence is pretty wonky, so feel free to skip it, but … to show the error in my colleague’s paper, Warshel should have modeled multiple molecules entering the enzyme active site, not molecules entering backward. Whoops!)
Another colleague of mine published his findings about unusual behavior from a human protein. But then his collaborator realized that they’d accidentally purified and studied a similarly-sized bacterial protein, and were attempting to map its location in cells with an antibody that didn’t work. Whoops!
No apologies or corrections were ever given. They rarely are, especially not from researchers at our nation’s fanciest universities. When somebody with impressive credentials claims a thing is true, people often feel ready to believe.
Indeed, for my own thesis work, we wanted to test whether two proteins are in the same place inside cells. You can do this by staining with light-up antibodies for each. If one antibody is green and the other is red, you’ll know how often the proteins are in the same place based on how much yellow light you see.
Before conducting the experiment, I wrote a computer program that would assess the data. My program could identify various cellular structures and check the fraction that were each color.
As it happened, I didn’t get the results we wanted. My data suggested that our guess was wrong.
But we couldn’t publish that. And so my advisor told me to count again, by hand, claiming that I should be counting things of a different size. And then she continued to revise her instructions until we could plausibly claim that we’d seen what we expected. We made a graph and published the paper.
This is crummy. It’s falsehood with the veneer of truth. But it’s also tragically routine.
One of these nightmares is driven by the perverse incentives facing early neurosurgeons. Perhaps you noticed, above, that an essential step of the scientific method involves mucking things up. You can’t tell whether your guesses are correct until you perform an experiment. Dittrich provides a lovely summary of this idea:
The broken illuminate the unbroken.
An underdeveloped dwarf with misfiring adrenal glands might shine a light on the functional purpose of these glands. An impulsive man with rod-obliterated frontal lobes [Phineas Gage] might provide clues to what intact frontal lobes do.
This history of modern brain science has been particularly reliant on broken brains, and almost every significant step forward in our understanding of cerebral localization – that is, discovering what functions rely on which parts of the brain – has relied on breakthroughs provided by the study of individuals who lacked some portion of their gray matter.
. . .
While the therapeutic value of the lobotomy remained murky, its scientific potential was clear: Human beings were no longer off-limits as test subjects in brain-lesioning experiments. This was a fundamental shift. Broken men like Phineas Gage and Monsieur Tan may have always illuminated the unbroken, but in the past they had always become broken by accident. No longer. By the middle of the twentieth century, the breaking of human brains was intentional, premeditated, clinical.
Dittrich was dismayed to learn that his own grandfather had participated in this sort of research, intentionally wrecking at least one human brain in order to study the effects of his meddling.
Lacking a specific target in a specific hemisphere of Henry’s medial temporal lobes, my grandfather had decided to destroy both.
This decision was the riskiest possible one for Henry. Whatever the functions of the medial temporal lobe structures were – and, again, nobody at the time had any idea what they were – my grandfather would be eliminating them. The risks to Henry were as inarguable as they were unimaginable.
The risks to my grandfather, on the other hand, were not.
At that moment, the riskiest possible option for his patient was the one with the most potential rewards for him.
By destroying part of a brain, Dittrich’s grandfather could create a valuable research subject. Yes, there was a chance of curing the patient – Henry agreed to surgery because he was suffering from epileptic seizures. But Henry didn’t understand what the proposed “cure” would be. This cure was very likely to be devastating.
At other times, devastation was the intent. During an interview with one of his grandfather’s former colleagues, Dittrich is told that his grandmother was strapped to the operating table as well.
“It was a different era,” he said. “And he did what at the time he thought was okay: He lobotomized his wife. And she became much more tractable. And so he succeeded in getting what he wanted: a tractable wife.”
Compared to slicing up a brain so that its bearer might better conform to our society’s misogynistic expectations of female behavior, a bit of scientific fraud probably doesn’t sound so bad. Which is a shame. I love science. I’ve written previously about the manifold virtues of the scientific method. And we need truth to save the world.
Which is precisely why those who purport to search for truth need to live clean. In the cut-throat world of modern academia, they often don’t.
Dittrich investigated the rest of Henry’s life: after part of his brain was destroyed, Henry became a famous study subject. He unwittingly enabled the career of a striving scientist, Suzanne Corkin.
Dittrich writes that
Unlike Teuber’s patients, most of the research subjects Corkin had worked with were not “accidents of nature” [a bullet to the brain, for instance] but instead the willful products of surgery, and one of them, Patient H.M., was already clearly among the most important lesion patients in history. There was a word that scientists had begun using to describe him. They called him pure. The purity in question didn’t have anything to do with morals or hygiene. It was entirely anatomical. My grandfather’s resection had produced a living, breathing test subject whose lesioned brain provided an opportunity to probe the neurological underpinnings of memory in unprecedented ways. The unlikelihood that a patient like Henry could ever have come to be without an act of surgery was important.
. . .
By hiring Corkin, Teuber was acquiring not only a first-rate scientist practiced in his beloved lesion method but also by extension the world’s premier lesion patient.
. . .
According to [Howard] Eichenbaum, [a colleague at MIT,] Corkin’s fierceness as a gatekeeper was understandable. After all, he said, “her career is based on having that exclusive access.”
Because Corkin had (coercively) gained exclusive access to this patient, most of her claims about the workings of memory would be difficult to contradict. No one could conduct the experiments needed to rebut her.
Which makes me very skeptical of her claims.
Like most scientists, Corkin stumbled across occasional data that seemed to contradict the models she’d built her career around. And so she reacted in the same was as the professors I’ve worked with: she hid the data.
Dittrich: Right. And what’s going to happen to the files themselves?
She paused for several seconds.
Dittrich: Shredded? Why would they be shredded?
Corkin: Nobody’s gonna look at them.
Dittrich: Really? I can’t imagine shredding the files of the most important research subject in history. Why would you do that?
. . .
Corkin: Well, the things that aren’t published are, you know, experiments that just didn’t … [another long pause] go right.