On vaccination.

On vaccination.

The shape of things determines what they can do. Or, as a molecular biologist would phrase it, “structure determines function.”

In most ways, forks and spoons are similar. They’re made from the same materials, they show up alongside each other in place settings. But a spoon has a curved, solid bowl – you’d use it for soup or ice cream. A fork has prongs and is better suited for stabbing.

In matters of self defense, I’d reach for the fork.

On a much smaller scale, the three-dimensional shapes of a protein determines what it can do.

Each molecule of hemoglobin has a spoon-like pocket that’s just the right size for carrying oxygen, while still allowing the oxygen to wriggle free wherever your cells need it. A developing fetus has hemoglobin that’s shaped differently – when the fetal hemoglobin grabs oxygen, it squeezes more tightly, causing oxygen to pass from a mother to her fetus.

Each “voltage-gated ion channel” in your neurons has a shape that lets it sense incoming electrical signals and pass them forward. Voltage-gated ion channels are like sliding doors. They occasionally open to let in a rush of salt. Because salts are electrically charged, this creates an electric current. The electrical current will cause the next set of doors to open.

Every protein is shaped differently, which lets each do a different job. But they’re all made from the same materials – a long chain of amino acids.

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Your DNA holds the instructions for every protein in your body.

Your DNA is like a big, fancy cookbook – it holds all the recipes, but you might not want to bring it into the kitchen. You wouldn’t want to spill something on it, or get it wet, or otherwise wreck it.

Instead of bringing your nice big cookbook into the kitchen, you might copy a single recipe onto an index card. That way, you can be as messy as you like – if you spill something, you can always write out a new index card later.

And your cells do the same thing. When it’s time to make proteins, your cells copy the recipes. The original cookbook is made from DNA; the index-card-like copies are made from RNA. Then the index cards are shipped out of the nucleus – the library at the center of your cells – into the cytoplasm – the bustling kitchen where proteins are made and do their work.

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When a protein is first made, it’s a long strand of amino acids. Imagine a long rope with assorted junk tied on every few inches. Look, here’s a swath of velcro! Here’s a magnet. Here’s another magnet. Here’s a big plastic knob. Here’s another magnet. Here’s another piece of velcro. And so on.

If you shake this long rope, jostling it the way that a molecule tumbling through our cells gets jostled, the magnets will eventually stick together, and the velcro bits will stick to together, and the big plastic knob will jut out because there’s not enough room for it to fit inside the jumble.

That’s what happens during protein folding. Some amino acids are good at being near water, and those often end up on the outside of the final shape. Some amino acids repel water – like the oil layer of an unshaken oil & vinegar salad dressing – and those often end up on the inside of the final shape.

Other amino acids glue the protein together. The amino acid cysteine will stick to other cysteines. Some amino acids have negatively-charged sidechains, some have positively-charged sidechains, and these attract each other like magnets.

Sounds easy enough!

Except, wait. If you had a long rope with dozens of magnets, dozens of patches of velcro, and then you shook it around … well, the magnets would stick to other magnets, but would they stick to the right magnets?

You might imagine that there are many ways the protein could fold. But there’s only a single final shape that would allow the protein to function correctly in a cell.

So your cells use little helpers to ensure that proteins fold correctly. Some of the helpers are called “molecular chaperones,” and they guard various parts of the long strand so that it won’t glom together incorrectly. Some helpers are called “glycosylation enzymes,” and these glue little bits and bobs to the surface of a protein, some of which seem to act like mailing addresses to send the protein to the right place in a cell, some of which change the way the protein folds.

Our cells have a bunch of ways to ensure that each protein folds into the right 3D shape. And even with all this help, something things go awry. Alzheimer’s disease is associated with amyloid plaques that form in the brain – these are big trash heaps of misfolded proteins. The Alzheimer’s protein is just very tricky to fold correctly, especially if there’s a bunch of the misfolded protein strewn about.

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Many human proteins can be made by bacteria. Humans and bacteria are relatives, after all – if you look back in our family trees, you’ll find that humans and bacteria shared a great-great-great-grandmother a mere three billion years ago.

The cookbooks in our cells are written in the same language. Bacteria can read all our recipes.

Which is great news for biochemists, because bacteria are really cheap to grow.

If you need a whole bunch of some human protein, you start by trying to make it in bacteria. First you copy down the recipe – which means using things called “restriction enzymes” to move a sequence of DNA into a plasmid, which is something like a bacterial index card – then you punch holes in some bacteria and let your instructions drift in for them to read.

The bacteria churn out copies of your human protein. Bacteria almost always make the right long rope of amino acids.

But human proteins sometimes fold into the wrong shapes inside bacteria. Bacteria don’t have all the same helper molecules that we do,.

If a protein doesn’t fold into the right shape, it won’t do the right things.

If you were working in a laboratory, and you found out that the protein you’d asked bacteria to make was getting folded wrong … well, you’d probably start to sigh a lot. Instead of making the correctly-folded human protein, your bacteria gave you useless goo.

Shucks.

But fear not!

Yeast can’t be grown as cheaply as bacteria, but they’re still reasonably inexpensive. And yeast are closer relatives – instead of three billion years ago, the most recent great-great-grandmother shared between humans and yeast lived about one billion years ago.

Yeast have a few of the same helper proteins that we do. Some human proteins that can’t be made in bacteria will fold correctly in yeast.

So, you take some yeast, genetically modify it to produce a human protein, then grow a whole bunch of it. This is called “fermentation.” It’s like you’re making beer, almost. Genetically modified beer.

Then you spin your beer inside a centrifuge. This collects all the solid stuff at the bottom of the flask. Then you’ll try to purify the protein that you want away from all the other gunk. Like the yeast itself, and all the proteins that yeast normally make.

If you’re lucky, the human protein you were after will have folded correctly!

If you’re unlucky, the protein will have folded wrong. Your yeast might produce a bunch of useless goo. And then you do more sighing.

There’s another option, but it’s expensive. You can make your human protein inside human cells.

Normally, human cells are hesitant to do too much growing and dividing and replicating. After all, the instructions in our DNA are supposed to produce a body that looks just so – two arms, two eyes, a smile. Once we have cells in the right places, cell division is just supposed to replace the parts of you that have worn out.

Dead skin cells steadily flake from our bodies. New cells constantly replace them.

But sometimes a cell gets too eager to grow. If its DNA loses certain instructions, like the “contact inhibition” that tells cells to stop growing when they get too crowded, a human cell might make many, many copies of itself.

Which is unhelpful. Potentially lethal. A cell that’s too eager to grow is cancer.

Although it’s really, really unhelpful to have cancer cells growing in your body, in a laboratory, cancer cells are prized. Cancer cells are so eager to grow that we might be able to raise them in petri dishes.

Maybe you’ve heard of HeLa cells – this is a cancer cell line that was taken from a Black woman’s body without her consent, and then this cell line was used to produce innumerable medical discoveries, including many that were patented and have brought in huge sums of money, and this woman’s family was not compensated at all, and they’ve suffered huge invasions of their privacy because a lot of their genetic information has been published, again without their consent …

HeLa cells are probably the easiest human cells to grow. And it’s possible to flood them with instructions to make a particular human protein. You can feel quite confident that your human protein will fold correctly.

But it’s way more expensive to grow HeLa cells than yeast. You have to grow them in a single layer in a petri dish. You have to feed them the blood of a baby calf. You have to be very careful while you work or else the cells will get contaminated with bacteria or yeast and die.

If you really must have a whole lot of a human protein, and you can’t make it in bacteria or yeast, then you can do it. But it’ll cost you.

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Vaccination is perhaps the safest, most effective thing that physicians do.

Your immune system quells disease, but it has to learn which shapes inside your body represent danger. Antibodies and immunological memory arise in a process like evolution – random genetic recombination until our defenses can bind to the surface of an intruder. By letting our immune system train in a relatively safe encounter, we boost our odds of later survival.

The molecular workings of our immune systems are still being studied, but the basic principles of inoculation were independently discovered centuries ago by scientists in Africa, India, and China. These scientists’ descendants practiced inoculation against smallpox for hundreds of years before their techniques were adapted by Edward Jenner to create his smallpox vaccine.

If you put a virus into somebody’s body, that person might get sick. So what you want is to put something that looks a lot like the virus into somebody’s body.

One way to make something that looks like the virus, but isn’t, is to take the actual virus and whack it with a hammer. You break it a little. Not so much that it’s unrecognizable, but enough so that it can’t work. Can’t make somebody sick. This is often done with “heat inactivation.”

Heat inactivation can be dangerous, though. If you cook a virus too long, it might fall apart and your immune system learns nothing. If you don’t cook a virus long enough, it might make you sick.

In some of the early smallpox vaccine trials, the “heat inactivated” viruses still made a lot of people very, very sick.

Fewer people got very sick than if they’d been exposed to smallpox virus naturally, but it feels different when you’re injecting something right into somebody’s arm.

We hold vaccines to high standards. Even when we’re vaccinating people against deadly diseases, we expect our vaccines to be very, very safe.

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It’s safer to vaccinate people with things that look like a virus but can’t possibly infect them.

This is why you might want to produce a whole bunch of some specific protein. Why you’d go through that whole rigamarole of testing protein folding in bacteria, yeast, and HeLa cells. Because you’re trying to make a bunch of protein that looks like a virus.

Each virus is a little protein shell. They’re basically delivery drones for nasty bits of genetic material.

If you can make pieces of this protein shell inside bacteria, or in yeast, and then inject those into people, then the people can’t possibly be infected. You’re not injecting people with a whole virus – the delivery drone with its awful recipes inside. Instead, you’re injecting people with just the propeller blades from the drone, or just its empty cargo hold.

These vaccine are missing the genetic material that allow viruses to make copies of themselves. Unlike with a heat inactivated virus, we can’t possibly contract the illness from these vaccines.

This is roughly the strategy used for the HPV vaccine that my father helped develop. Merck’s “Gardasil” uses viral proteins made by yeast, which is a fancy way of saying that Merck purifies part of the virus’s delivery drone away from big batches of genetically-modified beer.

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We have a lot of practice making vaccines from purified protein.

Even so, it’s a long, difficult, expensive process. You have to identify which part of the virus is often recognized by our immune systems. You have to find a way to produce a lot of this correctly-folded protein. You have to purify this protein away from everything else made by your bacteria or yeast or HeLa cells.

The Covid-19 vaccines bypass all that.

In a way, these are vaccines for lazy people. Instead of finding a way to make a whole bunch of viral protein, then purify it, then put it into somebody’s arm … well, what if we just asked the patient’s arm to make the viral protein on its own?

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Several of the Covid-19 vaccines are made with mRNA molecules.

These mRNA molecules are the index cards that we use for recipes in our cells’ kitchens, so the only trick is to deliver a bunch of mRNA with a recipe for part of the Covid-19 virus. Then our immune system can learn that anything with that particular shape is bad and ought to be destroyed.

After learning to recognize one part of the virus delivery drone, we’ll be able to stop the real thing.

We can’t vaccinate people by injecting just the mRNA, though, because our bodies have lots of ways to destroy RNA molecules. After all, you wouldn’t want to cook from the recipe from any old index card that you’d found in the street. Maybe somebody copied a recipe from The Anarchist Cookbook – you’d accidentally whip up a bomb instead of a delicious cake.

I used to share laboratory space with people who studied RNA, and they were intensely paranoid about cleaning. They’d always wear gloves, they’d wipe down every surface many times each day. Not to protect themselves, but to ensure that all the RNA-destroying enzymes that our bodies naturally produce wouldn’t ruin their experiments.

mRNA is finicky and unstable. And our bodies intentionally destroy stray recipes.

So to make a vaccine, you have to wrap the mRNA in a little envelope. That way, your cells might receive the recipe before it’s destroyed. In this case, the envelope is called a “lipid nanoparticle,” but you could also call a fat bubble. Not a bubble that’s rotund – a tiny sphere made of fat.

Fat bubbles are used throughout cells. When the neurons in your brain communicate, they burst open fat bubbles full of neurotransmitters and scatter the contents. When stuff found outside a cell needs to be destroyed, it’s bundled into fat bubbles and sent to a cellular trash factories called lysosomes.

For my Ph.D. thesis, I studied the postmarking system for fat bubbles. How fat bubbles get addressed in order to be sent to the right places.

Sure, I made my work sound fancier when I gave my thesis defense, but that’s really what I was doing.

Anyway, after we inject someone with an mRNA vaccine, the fat bubble with the mRNA gets bundled up and taken into some of their cells, and this tricks those cells into following the mRNA recipe and making a protein from the Covid-19 virus.

This mRNA recipe won’t teach the cells how to make a whole virus — that would be dangerous! That’s what happens during a Covid-19 infection – your cells get the virus’s whole damn cookbook and they make the entire delivery drone and more cookbooks to put inside and then these spread through your body and pull the same trick on more and more of your cells. A single unstopped delivery drone can trick your cells into building a whole fleet of them and infecting cells throughout your body.

Instead, the mRNA recipe we use for the vaccine has only a small portion of the Covid-19 genome, just enough for your cells to make part of the delivery drone and learn to recognize it as a threat.

And this recipe never visits the nucleus, which is the main library in your cells that holds your DNA, the master cookbook with recipes for every protein in your body. Your cells are tricked into following recipes scribbled onto the vaccine’s index cards, but your master cookbook remains unchanged. And, just like all the mRNA index cards that our bodies normally produce, the mRNA from the vaccine soon gets destroyed. All those stray index cards, chucked unceremoniously into the recycling bin.

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The Johnson & Johnson vaccine also tricks our cells into making a piece of the Covid-19 virus.

This vaccine uses a different virus’s delivery drone to send the recipe for a piece of Covid-19 into your cells. The vaccine’s delivery drone isn’t a real virus – the recipe it holds doesn’t include the instructions on how to make copies of itself. But the vaccine’s delivery drone looks an awful lot like a virus, which means it’s easier to work with than the mRNA vaccines.

Those little engineered fat bubbles are finicky. And mRNA is finicky. But the Johnson & Johnson vaccine uses a delivery drone that was optimized through natural selection out in the real world. It evolved to be stable enough to make us sick.

Now we can steal its design in an effort to keep people well.

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Lots of people received the Johnson & Johnson vaccine without incident, but we’ve temporarily stopped giving it to people. Blood clots are really scary.

You might want to read Alexandra Lahav’s excellent essay, “Medicine Is Made for Men.” Lahav describes the many ways in which a lack of diversity in science, technology, and engineering fields can cause harm.

Cars are designed to protect men: for many years, we used only crash test dummies that were shaped like men to determine whether cars were safe. In equivalent accidents, women are more likely to die, because, lo and behold, their bodies are often shaped differently.

Women are also more likely to be killed by medication. Safety testing often fails to account for women’s hormonal cycles, or complications from contraceptives, or differences in metabolism, or several other important features of women’s bodies.

White male bodies are considered to be human bodies, and any deviation is considered an abnormal case. Medication tested in white men can be approved for everyone; medication tested in Black patients was approved only for use in other Black patients.

Although more than half our population are women, their bodies are treated as bizarre.

For most people, the Johnson & Johnson vaccine is safe. But this is a sort of tragedy that occurs too often – causing harm to women because we’re inattentive to the unique features of their bodies.

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I haven’t been vaccinated yet, but I registered as soon as I was able – my first dose will be on April 26th. Although I’ve almost certainly already had Covid-19 before, and am unlikely to get severely ill the next time I contract it, I’m getting the vaccine to protect my friends and neighbors.

So should you.

On reinfection.

On reinfection.

If you’ve been reading about Covid-19 in the New York Times, you’ve probably learned that reinfection is very unlikely.

What you’ve learned is incorrect.

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Don’t get me wrong – I love the New York Times. Within the spectrum of United States politics, I am very far to the left. Anti-consumerist, prison abolitionist, environmentalist, feminist, climate activist, etc., etc. I fit into all those categories.

I’m also a scientist. I am staunchly pro-vaccine. I don’t like pesticides, but I’m a huge fan of GMO crops. (Honestly, I wish there was a category at the grocery store where you could pay to support genetically-modified organisms grown without environmental toxins – “organic” doesn’t have the nuance I’d like.)

So my goal here isn’t to rag on the New York Times. I’m including screenshots of their headlines only to give us a common frame of reference.

This is what the news is saying. And it’s wrong.

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It was going to be very difficult to demonstrate reinfection with Covid-19.

Why?

In general, reinfection with any virus will produce a milder illness the second time.

Most people’s first infection with Covid-19 is so mild that they don’t realize they have it – perhaps 80% of infections are “asymptomatic,” in which a person has been infected with the virus, is probably shedding the virus (thereby infecting other people), but feels totally fine. So, people’s second infection? Some percentage higher than 80% are likely to feel totally well, even though they might be shedding virus.

When people develop severe complications from Covid-19, the illness can linger for weeks or even months.

I don’t know for certain whether my family contracted Covid-19 in February, because there were no tests available here at the time. All I know is that we were two close contacts removed from someone who had just returned from China, that this close contact tested negative for influenza, that my family had been vaccinated for influenza, and that our symptoms precisely mirrored the common suite for Covid-19. But in any case, we felt horrible for about three weeks, and we experienced lingering fatigue with occasional coughing for about two months.

Lengthy recovery is so common that there’s a colloquial name for it: “long-haulers.” If we’re trying to identify whether someone was re-infected, we’d need to make sure that we weren’t looking at continued viral shedding during a lengthy recovery.

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To demonstrate that someone was re-infected with Covid-19, the following would have to happen:

  • A person gets tested for Covid-19 during their first infection.
  • The genome of the virus is sequenced after that first infection.
  • The person is re-infected.
  • The person happens to get a Covid-19 test during the second infection (even though it’s highly likely that this person feels well at the time).
  • The genome of the virus is sequenced after the second infection.
  • The genome of the virus that infected the person on the second occasion is noticeably different from the first (even though Covid-19 includes a proofreading enzyme that slows genetic drift).

That’s all very unlikely!

There are just so many coincidences involved – that you happen to get infected with an easily distinguishable virus the second time, that you happen to get a test the second time, that anyone took the (significant) trouble and expense to sequence both genomes.

And what I mean is, proving re-infection is very unlikely. Which is totally independent of the likelihood of re-infection itself.

And yet, even though it’s so unlikely we’d be able to prove that re-infection is occurring, we have.

We know, with 100% certainty, that people can be reinfected. We’ve documented it.

Given how unlikely it was that we’d be able to document reinfection, the fact that we’ve seen this at all indicates that it’s probably quite common. As you would expect based upon our bodies’ responses to other coronaviruses.

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Given that re-infection definitely occurs, and is probably quite common, why have you read that it’s unlikely?

The underlying probably is language usage. When my father – an infectious diseases specialist – talks about re-infection, he’s thinking about contracting severe symptoms during a second infection. Which is reasonable. He’s a medical doctor. He cares about helping sick people get better.

But when we’re thinking about how to respond, as a nation, to this pandemic, we’re thinking about the dynamics of transmission. We’re trying to answer questions like, “Can kids go to school without people dying?”

(Yup, they can! And should!)

From this perspective, we’re thinking about who is going to spread the virus, and where. We need to know whether a person who is protected from severe disease – either from prior recovery or vaccination – might shed viral particles. Will that individual register as a positive case on a PCR test? Will that individual get classmates or co-workers sick?

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Re-infections are probably the underlying cause of the current rise in cases in New York City.

70% or more of the population of New York City was infected with Covid-19 during April. That’s a huge percentage, well above what most researchers consider the “herd immunity threshold” for similar respiratory viruses.

For there to be another spike in cases now, many of those 70% would need to have lost their initial immunity. That’s also why you’d expect to see a higher “test positivity rate” – if many of the current cases are reinfections, then they’re likely to be milder. People with milder (or asymptomatic) infections are less likely to seek out a test.

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For general audiences, the phrasing I’d recommend is to say “Severe illness is unlikely during Covid-19 reinfections” as opposed to “Reinfection is unlikely.”

There have been a few cases of people’s second infection being more severe than the first, but these cases indeed appear to be quite rare.

But re-infection itself?

The fact that we’ve documented any instances of re-infection suggests that it’s quite common. Which we could have predicted from the beginning – indeed, I did. And that’s why I’ve been recommending – for months – policies very different from what we’ve done.

On predictions and a scientific response to calamity.

On predictions and a scientific response to calamity.

We’re fast approaching flu season, which is especially harrowing this year.

We, as a people, have struggled to respond to this calamity. We have a lot of scientific data about Covid-19 now, but science is never value-neutral. The way we design experiments reflects our biases; the way we report our findings, even more so.

For example, many people know the history of Edward Jenner inventing the world’s first vaccine. Fewer are aware of the long history of inoculation in Africa (essentially, low-tech vaccination) that preceded Jenner’s work.

So it’s worthwhile taking a moment to consider the current data on Covid-19.

Data alone can’t tell us what to do – the course of action we choose will reflect our values as a society. But the data may surprise a lot of people – which is strange considering how much we all feel that we know about Covid-19.

Indeed, we may realize that our response so far goes against our professed values.

Spoiler: I think we shouldn’t close in-person school.

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Since April, I’ve written several essays about Covid-19. In these, I’ve made a number of predictions. It’s worthwhile to consider how accurate these predictions have been.

This, after all, is what science is. We use data to make an informed prediction, and then we collect more data to evaluate how good our prediction was.

Without the second step – a reckoning with our success or failure – we’re just slinging bullshit.

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I predicted that our PCR tests were missing most Covid-19 infections, that people’s immunity was likely to be short-lived (lasting for months, not years), and that Covid-19 was less dangerous than seasonal influenza for young people.

These predictions have turned out to be correct.

In my essays, I’ve tried to unpack the implications of each of these. From the vantage of the present, with much more data at our disposal, I still stand by what I’ve written.

But gloating’s no fun. So I’d rather start with what I got wrong.

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My initial predictions about Covid-19 were terrible.

I didn’t articulate my beliefs at the time, but they can be inferred from my actions. In December, January, and February, I made absolutely no changes to my usual life. I didn’t recommend that travelers be quarantined. I didn’t care enough to even follow the news, aside from a cursory glance at the headlines.

While volunteering with the high school running team, I was jogging with a young man who was finishing up his EMT training.

“That new coronavirus is really scary,” he said. “There’s no immunity, and there’s no cure for it.”

I shrugged. I didn’t know anything about the new coronavirus. I talked with him about the 1918 influenza epidemic instead.

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I didn’t make any change in my life until mid-March. And even then, what did I do?

I called my brother and talked to him about the pizza restaurant – he needed a plan in case there was no in-person dining for a few months.

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My next set of predictions were off, but in the other direction – I estimated that Covid-19 was about four-fold more dangerous than seasonal influenza. The current best estimate from the CDC is that Covid-19 is about twice as dangerous, with an infection fatality ratio of 0.25%.

But seasonal influenza typically infects a tenth of our population, or less.

We’re unlikely to see a significant disruption in the transmission of Covid-19 (this is the concept of “herd immunity”) until about 50% of our population has immunity from it, whether from vaccination or recovery. Or possibly higher – in some densely populated areas, Covid-19 has spread until 70% (in NYC) or even 90% (in prisons) of people have contracted the disease.

Population density is hugely important for the dynamics of Covid-19’s spread, so it’s difficult to predict a nation-wide threshold for herd immunity. For a ballpark estimate, we could calculate what we’d see with a herd immunity threshold of about 40% in rural areas and 60% in urban areas.

Plugging in some numbers, 330 million people, 80% urban population, 0.25% IFR, 60% herd immunity threshold in urban areas, we’d anticipate 450,000 deaths.

That’s about half of what I predicted. And you know what? That’s awful.

Each of those 450,000 is a person. Someone with friends and family. And “slow the spread” doesn’t help them, it just stretches our grieving to encompass a whole year of tragedy instead of a horrific month of tragedy.

If we don’t have a safe, effective vaccine soon enough, the only way to save some of those 450,000 people is to shift the demographics of exposure.

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Based on the initial data, I concluded that the age demographics for Covid-19 risk were skewed more heavily toward elderly people than influenza risk.

I may have been wrong.

It’s difficult to directly compare the dangers of influenza to the dangers of Covid-19. Both are deadly diseases. Both result in hospitalizations and death. Both are more dangerous for elderly or immunocompromised people, but both also kill young, healthy people.

Typically, we use an antigen test for influenza and a PCR-based test for Covid-19. The PCR test is significantly more sensitive, so it’s easier to determine whether Covid-19 is involved a person’s death. If there are any viral particles in a sample, PCR will detect them. Whereas antigen tests have a much higher “false negative” rate.

Instead of using data from these tests, I looked at the total set of pneumonia deaths. Many different viruses can cause pneumonia symptoms, but the biggest culprits are influenza and, in 2020, Covid-19.

So I used these data to ask a simple question – in 2020, are the people dying of pneumonia disproportionately more elderly than in other years?

I expected that they would be. That is, after all, the prediction from my claims about Covid-19 demographic risks.

I was wrong.

In a normal year (I used the data from 2013, 2014, and 2015, three years with “mild” seasonal influenza), 130,000 people die of flu-like symptoms.

In 2020 (at the time I checked), 330,000 people have died of flu-like symptoms. Almost three times as many people as in a “normal” year.

For people under the age of 18, we’ve seen the same number of deaths (or fewer) in 2020 as in other years. The introduction of Covid-19 appears to have caused no increased risk for these people.

But for people of all other ages, there have been almost three times as many people dying of these symptoms in 2020 compared to other years.

In most years, one thousand people aged 25-34 die of these symptoms; in 2020, three thousand have died. In most years, two thousand people aged 35-44 die of these symptoms; in 2020, six thousand have died. This same ratio holds for all ages above eighteen.

Younger people are at much less risk of harm from Covid-19 than older people are. But, aside from children under the age of eighteen, they don’t seem to be exceptionally protected.

Of course, my predictions about the age skew of risk might be less incorrect than I’m claiming here. If people’s dramatically altered behavior in 2020 has changed the demographics of exposure as compared to other years – which is what we should be doing to save the most lives – then we could see numbers like this even if Covid-19 had the risk skew that I initially predicted.

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I predicted that four or more years would pass before we’d be able to vaccinate significant numbers of people against Covid-19.

I sure hope that I was wrong!

We now know that it should be relatively easy to confer immunity to Covid-19. Infection with other coronaviruses, including those that cause common colds, induce the production of protective antibodies. This may partly explain the low risk for children – because they get exposed to common-cold-causing coronaviruses so often, they may have high levels of protective antibodies all the time.

Several pharmaceutical companies have reported great results for their vaccine trials. Protection rates over 90%.

So the problem facing us now is manufacturing and distributing enough doses. But, honestly, that’s the sort of engineering problem that can easily be addressed by throwing money at it. Totally unlike the problem with HIV vaccines, which is that the basic science isn’t there – we just don’t know how to make a vaccine against HIV. No amount of money thrown at that problem would guarantee wide distribution of an effective vaccine.

We will still have to overcome the (unfortunately significant) hurdle of convincing people to be vaccinated.

For any individual, the risk of Covid-19 is about twice the risk of seasonal influenza. But huge numbers of people choose not to get a flu vaccine each year. In the past, the United States has had a vaccination rate of about 50%. Here’s hoping that this year will be different.

Covid-19 spreads so fast – and so silently, with many cases of infected people who feel fine but are still able to spread the virus – that it will almost certainly be a permanent resident of the world we live in. We’re unlikely to eradicate Covid-19.

Which means that elderly people will always be at risk of dying from Covid-19.

The only way to protect people whose bodies have gone through “age-related immunosenence” – the inevitable weakening of an immune system after a person passes the evolutionarily-determined natural human lifespan of about 75 years – will be to vaccinate everybody else.

Depending on how long vaccine-conferred immunity lasts, we may need to vaccinate people annually. I worry, though, that it will become increasingly difficult to persuade people to get a Covid-19 vaccine once the yearly death toll drops to influenza-like levels – 50,000 to 100,000 deaths per year in the United States.

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I wrote, repeatedly, that immunity to Covid-19 is likely to be short-lived. Immunity to other coronaviruses fades within a few months.

(Note: you may have seen articles in the New York Times suggesting that we’ll have long-lasting protection. They’re addressing a different question — after recovery, or vaccination, are you likely to become severely ill with Covid-19? And the answer is “probably not,” although it’s possible. When I discuss immunity here, I mean “after recovery, or vaccination, are you likely to be able to spread the virus after re-infection?” And the answer is almost certainly “yes, within months.”)

And I wrote about the interplay between short-lived immunity and the transmission dynamics of an extremely virulent, air-born virus.

This is what the Harvard public health team got so wrong. When we slow transmission enough that a virus is still circulating after people’s immunity wanes, they can get sick again.

For this person, the consequences aren’t so dire – an individual is likely to get less sick with each subsequent infection by a virus. But the implications for those who have not yet been exposed are horrible. The virus circulates forever, and people with naive immune systems are always in danger.

It’s the same dynamics as when European voyagers traveled to the Americas. Because the European people’s ancestors lived in unsanitary conditions surrounded by farm animals, they’d cultivated a whole host of zoogenic pathogens (like influenza and this new coronavirus). The Europeans got sick from these viruses often – they’d cough and sneeze, have a runny nose, some inflammation, a headache.

In the Americas, there were fewer endemic diseases. Year by year, people wouldn’t spend much time sick. Which sounds great, honestly – I would love to go a whole year without headaches.

But then the disgusting Europeans reached the Americas. The Europeans coughed and sneezed. The Americans died.

And then the Europeans set about murdering anyone who recovered. Today, descendants of the few survivors are made to feel like second-class citizens in their ancestral homelands.

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In a world with endemic diseases, people who have never been exposed will always be at risk.

That’s why predictions made in venues such as the August New York Times editorial claiming that a six- to eight-week lockdown would stop Covid-19 were so clearly false. They wrote:

Six to eight weeks. That’s how long some of the nation’s leading public health experts say it would take to finally get the United States’ coronavirus epidemic under control.

For proof, look at Germany. Or Thailand. Or France.

Obviously, this didn’t work – in the presence of an endemic pathogen, the lockdowns preserved a large pool of people with naive immune systems, and they allowed enough time to pass that people who’d been sick lost their initial immunity. After a few months of seeming calm, case numbers rose again. For proof, look at Germany. Or France.

Case numbers are currently low in Thailand, but a new outbreak could be seeded at any time.

And the same thing is currently happening in NYC. Seven months after the initial outbreak, immunity has waned; case numbers are rising; people with mild second infections might be spreading the virus to friends or neighbors who weren’t infected previously.

All of which is why I initially thought that universal mask orders were a bad idea.

We’ve known for over a hundred years that masks would slow the spread of a virus. The only question was whether slowing the spread of Covid-19 would cause more people to die of Covid-19.

And it would – if a vaccine was years away.

But we may have vaccines within a year. Which means that I may have been wrong. Again, the dynamics of Covid-19 transmission are still poorly understood – I’ll try to explain some of this below.

In any case, I’ve always complied with our mask orders. I wear a mask – in stores, at school pickup, any time I pass within six feet of people while jogging.

To address global problems like Covid-19 and climate change, we need global consensus. One renegade polluting wantonly, or spewing viral particles into the air, could endanger the whole world. This is precisely the sort of circumstance where personal freedom is less important than community consensus.

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The transmission dynamics of Covid-19 are extremely sensitive to environment. Whether you’re indoors or outdoors. How fast the air is moving. The population density. How close people are standing. Whether they’re wearing masks. Whether they’re shouting or speaking quietly.

Because there are so many variable, we don’t have good data. My father attended a lecture and a colleague (whom he admires) said, “Covid-19 is three-fold more infectious than seasonal influenza.” Which is bullshit – the transmission dynamics are different, so the relative infectivity depends on our behaviors. You can’t make a claim like this.

It’s difficult to measure precisely how well masks are slowing the spread of this virus.

But here’s a good estimate: according to Hsiang et al., the number of cases of Covid-19, left unchecked, might have increased exponentially at a rate of about 34% per day in the United States.

That’s fast. If about 1% of the population was infected, it could spread to everyone within a week or two. In NYC, Covid-19 appear to spread to over 70% of the population within about a month.

(To estimate the number of infections in New York City, I’m looking at the number of people who died and dividing by 0.004 – this is much higher than the infection fatality rate eventually reported by the CDC, but early in the epidemic, we were treating people with hydroxychloraquine, an unhelpful poison, and rushing to put people on ventilators. We now know that ventilation is so dangerous that it should only be used as a last resort, and that a much more effective therapy is to ask people to lie on their stomachs – “proning” makes it easier to get enough oxygen even when the virus has weakened a person’s lungs.)

Masks dramatically slow the rate of transmission.

A study conducted at a military college – where full-time mask-wearing and social distancing were strictly enforced – showed that the number of cases increased from 1% to 3% of the population over the course of two weeks.

So, some math! Solve by taking ten to the power of (log 3)/14, which gives an exponential growth rate of 8% per day. Five-fold slower than without masks.

But 8% per day is still fast.

Even though we might be able to vaccinate large numbers of people by the end of next year, that’s not soon enough. Most of us will have been sick with this – at least once – before then.

I don’t mean to sound like a broken record, but the biggest benefit of wearing masks isn’t that we slow the rate of spread for everyone — exponential growth of 8% is still fast — but that we’re better able to protect the people who need to be protected. Covid-19 is deadly, and we really don’t want high-risk people to be infected with it.

I’ve tried to walk you through the reasoning here — the actual science behind mask policies — but also, in case it wasn’t absolutely clear: please comply with your local mask policy.

You should wear a mask around people who aren’t in your (small) network of close contacts.

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I’m writing this essay the day after New York City announced the end of in-person classes for school children.

This policy is terrible.

A major problem with our response to Covid-19 is that there’s a time lag between our actions and the consequences. Human brains are bad at understanding laggy data. It’s not our fault. Our ancestors lived in a world where they’d throw a spear at an antelope, see the antelope die, and then eat it. Immediate cause and effect makes intuitive sense.

Delayed cause and effect is tricky.

If somebody hosts a party, there might be an increase in the number of people who get sick in the community over the next three weeks. Which causes an increase in the number of hospitalizations about two weeks after that. Which causes people to die about three weeks after that.

There’s a two-month gap between the party and the death. The connection is difficult for our brains to grasp.

As a direct consequence, we’ve got ass-hats and hypocrites attending parties for, say, their newly appointed Supreme Court justice.

But the problem with school closures is worse. There’s a thirty year gap between the school closure and the death. The connection is even more difficult to spot.

Even if you have relatively limited experience reading scientific research papers, I think you could make your way through this excellent article from Chistakis et al.

The authors link two sets of existing data: the correlation between school closures and low educational achievement, and the correlation between low educational achievement and premature death.

The public debate has pitted “school closures” against “lives saved,” or the education of children against the health of the community. Presenting the tradeoffs in this way obscures the very real health consequences of interrupted education.

These consequences are especially dire for young children.

The authors calculate that elementary school closures in the United States might have (already!) caused 5.5 million years of life lost.

Hsiang et al. found that school closures probably gave us no benefit in terms of reducing the number of Covid-19 cases, because children under 18 aren’t significant vectors for transmission (elementary-aged children even less so), but even if school closures had reduced the number of Covid-19 cases, closing schools would have caused more total years of life to be lost than saved.

The problem – from a political standpoint – is that Covid-19 kills older people, who vote, whereas school closures kill young people, who are intentionally disenfranchised.

And, personally, as someone with far-left political views, it’s sickening for me to see “my” political party adopt policies that are so destructive to children and disadvantaged people.

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So, here’s what the scientific data can tell us so far:

  • We will eventually have effective vaccines for Covid-19. Probably within a year.
  • Covid-19 spreads even with social distancing and masks, but the spread is slower.
  • You have no way of knowing the risk status of people in a stranger’s bubble. (Please, follow your local mask orders!)
  • Schools – especially elementary schools – don’t contribute much to the spread of Covid-19.
  • School closures shorten children’s lives (and that’s not even accounting for their quality of life over the coming decades).
  • An individual case of Covid-19 is about twice as dangerous as a case of seasonal influenza (which is scary!).
  • Underlying immunity (from prior disease and vaccination) to Covid-19 is much lower than for seasonal influenza, so there will be many more cases.
  • Most people’s immunity to Covid-19 probably lasts several months, after which a person can be re-infected and spread the virus again.

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So, those are some data. But data don’t tell us what to do. Only our values can do that.

Personally, I value the lives of children.

I wouldn’t close schools.

On sending kids to school.

On sending kids to school.

I was walking my eldest child toward our local elementary school when my phone rang.

We reached the door, shared a hug, and said goodbye. After I left, I called back – it was a friend of mine from college who now runs a cancer research laboratory and is an assistant professor at a medical school.

“Hey,” I said, “I was just dropping my kid off at school.”

“Whoa,” he said, “that’s brave.”

I was shocked by his remark. For most people under retirement age, a case of Covid-19 is less dangerous than a case of seasonal influenza.

“I’ve never heard of anybody needing a double lung transplant after a case of the flu,” my friend said.

But our ignorance doesn’t constitute safety. During this past flu season, several young, healthy people contracted such severe cases of influenza that they required double lung transplants. Here’s an article about a healthy 30-year-old Wyoming man nearly killed by influenza from December 2019, and another about a healthy 20-year-old Ohio woman from January 2020. And this was a rather mild flu season!

One of the doctors told me that she’s the poster child for why you get the flu shot because she didn’t get her flu shot,” said [the 20-year-old’s mother].

These stories were reported in local newspapers. Stories like this don’t make national news because we, as a people, think that it’s normal for 40,000 to 80,000 people to die of influenza every year. Every three to five years, we lose as many people as have died from Covid-19. And that’s with vaccination, with pre-existing immunity, with antivirals like Tamiflu.

Again, when I compare Covid-19 to influenza, I’m not trying to minimize the danger of Covid-19. It is dangerous. For elderly people, and for people with underlying health issues, Covid-19 is very dangerous. And, sure, all our available data suggest that Covid-19 is less dangerous than seasonal influenza for people under retirement age, but, guess what? That’s still pretty awful!

You should get a yearly flu shot!

A flu shot might save your life. And your flu shot will help save the lives of your at-risk friends and neighbors.

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For a while, I was worried because some of my remarks about Covid-19 sounded superficially similar to things said by the U.S. Republican party. Fox News – a virulent propaganda outlet – was publicizing the work of David Katz – a liberal medical doctor who volunteered in a Brooklyn E.R. during the Covid-19 epidemic and teaches at Yale’s school of public health.

The “problem” is that Katz disagrees with the narrative generally forwarded by the popular press. His reasoning, like mine, is based the relevant research data – he concludes that low-risk people should return to their regular lives.

You can see a nifty chart with his recommendations here. This is the sort of thing we’d be doing if we, as a people, wanted to “follow the science.”

And also, I’m no longer worried that people might mistake me for a right-wing ideologue. Because our president has once again staked claim to a ludicrous set of beliefs.

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Here’s a reasonable set of beliefs: we are weeks away from a safe, effective Covid-19 vaccine, so we should do everything we can to slow transmission and get the number of cases as low as possible!

Here’s another reasonable set of beliefs: Covid-19 is highly infectious, and we won’t have a vaccine for a long time. Most people will already be infected at least once before there’s a vaccine, so we should focus on protecting high-risk people while low-risk people return to their regular lives.

If you believe either of those sets of things, then you’re being totally reasonable! If you feel confident that we’ll have a vaccine soon, then, yes, delaying infections is the best strategy! I agree! And if you think that a vaccine will take a while, then, yes, we should end the shutdown! I agree!

There’s no right answer here – it comes down to our predictions about the future.

But there are definitely wrong answers. For instance, our current president claims that a vaccine is weeks away, and that we should return to our regular lives right now.

That’s nonsense. If we could get vaccinated before the election, then it’d make sense to close schools. To wait this out.

If a year or more will pass before people are vaccinated, then our efforts to delay the spread of infection will cause more harm than good. Not only will we be causing harm with the shutdown itself, but we’ll be increasing the death toll from Covid-19.

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On October 14th, the New York Times again ran a headline saying “Yes, you can be reinfected with the coronavirus. But it’s extremely unlikely.

This is incorrect.

When I’ve discussed Covid-19 with my father – a medical doctor specializing in infectious diseases, virology professor, vaccine developer with a background in epidemiology from his masters in public health – he also has often said to me that reinfection is unlikely. I kept explaining that he was wrong until I realized that we were talking about different things.

When my father uses the word “reinfection,” he means clearing the virus, catching it again, and becoming sicker than you were the first time. That’s unlikely (although obviously possible). This sort of reinfection happens often with influenza, but that’s because influenza mutates so rapidly. Covid-19 has a much more stable genome.

When I use the word “reinfection” – and I believe that this is also true when most laypeople use the word – I mean clearing the virus, catching it again, and becoming sick enough to shed the viral particles that will make other people sick.

This sense of the word “reinfection” describes something that happens all the time with other coronaviruses, and has been documented to occur with Covid-19 as well.

The more we slow the spread of Covid-19, the more total cases there will be. In and of itself, more cases aren’t a bad thing – most people’s reinfection will be milder than their first exposure. The dangerous aspect is that a person who is reinfected will have another period of viral shedding during which they might expose a high-risk friend or neighbor.

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If our goal is to reduce the strain on hospitals and reduce total mortality, we need to avoid exposing high-risk people. Obviously, we should be very careful around nursing home patients. We should provide nursing homes with the resources they need to deal with this, like extra testing, and preferably increased wages for nursing home workers to compensate them for all that extra testing.

It’s also a good idea to wear masks wherever low-risk and high-risk people mingle. The best system for grocery stores would be to hire low-risk shoppers to help deliver food to high-risk people, but, absent that system, the second-best option would be for everyone to wear masks in the grocery store.

Schools are another environment where a small number of high-risk teachers and a small number of students living with high-risk family members intermingle with a large number of low-risk classmates and colleagues.

Schools should be open – regions where schools closed have had the same rates of infection as regions where schools stayed open, and here in the U.S., teachers in districts with remote learning have had the same rates of infection as districts with in-person learning.

Education is essential, and most people in the building have very low risk.

A preponderance of data indicate that schools are safe. These data are readily accessible even for lay audiences – instead of reading research articles, you could read this lovely article in The Atlantic.

Well, I should rephrase.

We should’ve been quarantining international travelers back in December or January. At that time, a shutdown could have helped. By February, we were too late. This virus will become endemic to the human species. We screwed up.

But, given where we are now, students and teachers won’t experience much increased risk from Covid-19 if they attend in person, and schools aren’t likely to make the Covid-19 pandemic worse for the surrounding communities.

That doesn’t mean that schools are safe.

Schools aren’t safe: gun violence is a horrible problem. My spouse is a teacher – during her first year, a student brought weapons including a chainsaw and some pipe bombs to attack the school; during her fourth year, a student had amassed guns in his locker and was planning to attack the school.

Schools aren’t safe: we let kids play football, which is known to cause traumatic brain injury.

Schools aren’t safe: the high stress of grades, college admissions, and even socializing puts some kids at a devastatingly high risk for suicide. We as a nation haven’t always done a great job of prioritizing kids’ mental health.

And the world isn’t safe – as David Katz has written,

If inclined to panic over anything, let it be climate change Not the most wildly pessimistic assessment of the COVID pandemic places it even remotely in the same apocalyptic ballpark.

On threat.

On threat.

At the end of “Just Use Your Thinking Pump!”, a lovely essay that discusses the evolution (and perhaps undue elevation) of a particular set of practices now known as the scientific method, Jessica Riskin writes:

Covid-19 has presented the world with a couple of powerful ultimatums that are also strikingly relevant to our subject here. The virus has said, essentially, Halt your economies, reconnect science to a whole understanding of yourself and the world, or die.

With much economic activity slowed or stopped to save lives, let us hope governments find means to sustain their people through the crisis.

Meanwhile, with the din of “innovation” partially silenced, perhaps we can also use the time to think our way past science’s branding, to see science once again as integral to a whole, evolving understanding of ourselves and the world.

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True, the world has presented us with an ultimatum. We must halt our economies, reconnect science to a whole understanding of ourselves and our world, or die.

Riskin is a professor at Stanford. Her skies are blackened with soot. In the words of Greta Thunberg, “Our house is on fire.

For many years, we’ve measured the success of our economy in terms of growth. The idea that we can maintain perpetual growth is a delusion. It’s simple mathematics. If the amount of stuff we manufacture – telephones, televisions, air conditioners – rises by 3% each and every year, we’ll eventually reach stratospheric, absurd levels.

In the game “Universal Paperclips,” you’re put in control of a capitalist system that seeks perpetual growth. If you succeed, you’ll make a lot of paperclips! And you will destroy the planet.

Here in the real world, our reckless pursuit of growth has (as yet) wrought less harm, but we’ve driven many species to extinction, destroyed ancient forests, and are teetering at the precipice of cataclysmic climate change. All while producing rampant inequality with its attendant abundance of human misery.

We must reconnect science to a whole understanding of ourselves and the world, or die.

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We are in danger. But Covid-19 isn’t the major threat we’re facing.

I consider myself to be more cautious than average – I would never ride a bicycle without a helmet – and I’m especially cautious as regards global pandemic. Antibiotic resistance is about to be a horrific problem for us. Zoogenic diseases like Covid-19 will become much more common due to climate change and increased human population.

I’m flabbergasted that these impending calamities haven’t caused more people to choose to be vegan. It seems trivial – it’s just food – but a vegan diet is one of our best hopes for staving off antibiotic resistant plagues.

A vegan diet would have prevented Covid-19. Not that eating plants will somehow turbocharge your immune system – it won’t – but this pandemic originated from a meat market.

And a vegan diet will mitigate your contribution to climate change, which has the potential to cause the full extinction of the human race.

Make our planet uninhabitable? We all die. Make our planet even a little less habitable, which leads to violent unrest, culminating in warring nations that decide to use nukes? Yup, that’s another situation where we all die.

By way of contrast, if we had made no changes in our lives during the Covid-19 pandemic – no shutdown, no masks, no social distancing, no PCR tests, no contact tracing, no quarantines – 99.8% of our population would have survived.

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Indeed, we often discuss the Covid-19 crisis in a very imprecise way. We say that Covid-19 is causing disruptions to learning, that it’s causing domestic violence or evictions. On the front page of Sunday’s New York Times business section, the headline reads, “The Other Way that Covid Kills: Hunger.

Covid-19 is a serious disease. We need to do our best to avoid exposing high-risk people to this virus, and we should feel ashamed that we didn’t prioritize the development of coronavirus vaccines years ago.

But there’s a clear distinction between the harms caused by Covid-19 (hallucinogenic fevers, cardiac inflammation, lungs filling up with liquid until a person drowns, death) and the harms caused by our response to Covid-19 (domestic violence, educational disruption, starvation, reduced vaccination, delayed hospital visits, death).

Indeed, if the harms caused by our response to Covid-19 are worse than the harms caused by Covid-19 itself, we’re doing the wrong thing.

In that New York Times business article, Satbir Singh Jatain, a third-generation farmer in northern India, is quoted: “The lockdowns have destroyed farmers. Now, we have no money to buy seeds or pay for fuel. …. soon they will come for my land. There is nothing left for us.

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Covid-19 is awful. It’s a nasty disease. I’m fairly confident that I contracted it in February (before PCR tests were available in the United States), and my spouse says it’s the sickest she’s ever seen me.

Yes, I’d done something foolish – I was feeling a little ill but still ran a kilometer repeat workout with the high school varsity track team that I volunteer with. High intensity workouts are known to cause temporary immunosuppression, usually lasting from 3 to 72 hours.

My whole family got sick, but I fared far worse than the others.

It was horrible. I could barely breathe. Having been through that, it’s easy to understand how Covid-19 could kill so many people. I wouldn’t wish that experience on anyone.

And I have very low risk. I don’t smoke. I don’t have diabetes. I’m thirty-seven.

I wish it were possible to protect people from this.

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Obviously, we should have quarantined all international travelers beginning in December 2019. Actually, ten days probably would have been enough. We needed to diecitine all international travelers.

By February, we had probably allowed Covid-19 to spread too much to stop it.

By February, there were probably enough cases that there will always be a reservoir of this virus among the human species. 80% of people with Covid-19 feel totally fine and don’t realize they might be spreading it. By talking and breathing, they put viral particles into the air.

By the end of March, we were much, much too late. If you look at the numbers from New York City, it’s pretty clear that the preventative measures, once enacted, did little. Given that the case fatality rate is around 0.4%, there were probably about 6 million cases in New York City – most of the population.

Yes, it’s possible that New York City had a somewhat higher case fatality rate. The case fatality rate depends on population demographics and standard of care – the state of New York had an idiotic policy of shunting Covid-19 patients into nursing homes, while banning nursing homes from using Covid-19 PCR tests for these patients, and many New York doctors were prescribing hydroxychloroquine during these months, which increases mortality – but even if the case fatality rate in New York City was as high as 0.6%, a majority of residents have already cleared the virus by now.

The belated public health measures probably didn’t help. And these health measures have caused harm – kids’ schooling was disrupted. Wealthy people got to work from home; poor people lost their jobs. Or were deemed “essential” and had to work anyway, which is why the toll of Covid-19 has been so heavily concentrated among poor communities.

The pandemic won’t end until about half of all people have immunity, but a shutdown in which rich people get to isolate themselves while poor people go to work is a pretty shitty way to select which half of the population bears the burden of disease.

I am very liberal. And it’s painful to see that “my” political party has been advocating for policies that hurt poor people and children during the Covid-19 pandemic.

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Because we did not act soon enough, Covid-19 won’t end until an appreciable portion of the population has immunity – at the same time.

As predicted, immunity to Covid-19 lasts for a few months. Because our public health measures have caused the pandemic to last longer than individual immunity, there will be more infections than if we’d done nothing.

The shutdowns, in addition to causing harm on their own, will increase the total death toll of Covid-19.

Unless – yes, there is a small glimmer of hope here – unless we soon have a safe, effective vaccine that most people choose to get.

This seems unlikely, though. Making vaccines is difficult. And we already know that most people don’t get the influenza vaccine, even though, for younger people, influenza is more dangerous than Covid-19.

Look – this is shitty. I get an influenza vaccine every year. It’s not just for me – vaccination protects whole communities.

Economist Gregory Mankiw believes that we should pay people for getting a Covid-19 vaccine.

Yes, there are clear positive externalities to vaccination, but I think this sounds like a terrible idea. Ethically, it’s grim – the Covid-19 vaccines being tested now are a novel type, so they’re inherently more risky than other vaccines. By paying people to get vaccinated, we shift this burden of uncertainty onto poor communities.

We already do this, of course. Drug trials use paid “volunteers.” Especially phase 1 trials – in which drugs are given to people with no chance of medical benefit, only to see how severe the side effects are – the only enrollees are people so poor that the piddling amounts of money offered seem reasonable in exchange for scarfing an unknown, possibly poisonous medication.

Just because we already do an awful thing doesn’t mean we should make the problem worse.

And, as a practical matter, paying people to do the right thing often backfires.

In An Uncertain Glory, Jean Dreze and Amartya Sen write:

To illustrate, consider the recent introduction, in many Indian states, of schemes of cash incentives to curb sex-selective abortion. The schemes typically involve cash rewards for the registered birth of a girl child, and further rewards if the girl is vaccinated, sent to school, and so on, as she gets older.

These schemes can undoubtedly tilt economic incentives in favor of girl children. But a cash reward for the birth of a girl could also reinforce people’s tendency to think about family planning in economic terms, and also their perception, in the economic calculus of family planning, that girls are a burden (for which cash rewards are supposed to compensate).

Further, cash rewards are likely to affect people’s non-economic motives. For instance, they could reduce the social stigma attached to sex-selective abortion, by making it look like some sort of ‘fair deal’ — no girl, no cash.

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What happens if it takes a few years before there are sufficient doses of an effective vaccine that people trust enough to actually get?

Well, by then the pandemic will have run its course anyway. Masks reduce viral transmission, but they don’t cut transmission to zero. Even in places where everyone wears masks, Covid-19 is spreading, just slower.

I’ve been wearing one – I always liked the Mortal Kombat aesthetic. But I’ve been wearing one with the unfortunate knowledge that masks, by prolonging the pandemic, are increasing the death toll of Covid-19. Which is crummy. I’ve chosen to behave in a way that makes people feel better, even though the science doesn’t support it.

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We, as a people, are in an awful situation right now. Many of us are confronting the risk of death in ways that we have not previously.

In The Rise and Fall of American Growth, Robert Gordon writes:

More than 37 percent of deaths in 1900 were caused by infectious diseases, but by 1955, this had declined to less than 5 percent and to only 2 percent by 2009.

Of course, this trend will still hold true in 2020. In the United States, there have been about 200,000 Covid-19 deaths so far, out of 2,000,000 deaths total this year. Even during this pandemic, less than 1% of deaths are caused by Covid-19.

And I’m afraid. Poverty is a major risk factor for death of all causes in this country. Low educational attainment is another risk factor.

My kids am lucky to live in a school district that has mostly re-opened. But many children are not so fortunate. If we shutter schools, we will cause many more deaths – not this year, but down the road – than we could possibly prevent from Covid-19.

Indeed, school closures, by prolonging the pandemic (allowing people to be infected twice and spread the infection further), will increase the death toll from Covid-19.

School closures wouldn’t just cause harm for no benefit. School closures would increase the harm caused by Covid-19 and by everything else.

On apocalypse clocks.

On apocalypse clocks.

The world is complicated. There’s so much information out there, so much to know. And our brains are not made well for knowing much of it.

I can understand numbers like a dozen, a hundred. I can make a guess at the meaning of a thousand. Show me a big gumball machine and ask me to guess how many gumballs are in it, maybe I’ll guess a thousand, a few thousand.

But numbers like a million? A billion? A trillion? These numbers are important, I know. These numbers might be the population of cities, or of planets, or of solar systems. These numbers might be the ages of species or planets. These numbers might be how many stars are in the sky, or how many stars in the sky might harbor life.

These numbers don’t mean much to me.

I don’t think the problem is just my brain. I’m fairly good with numbers, relative to the average human. It’s been years since I’ve sat in a math class, but I can still do basic integrals and derivatives in my head.

Yet I can’t understand those big numbers. They don’t feel like anything to me.

So we make graphs. Charts. We try to represent information in ways that our meager human brains can grasp.

A good chart can be a revelation. Something that seemed senseless before is now made clear.

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An apocalypse is a revelation. The word “apocalypse” means lifting the veil – apo, off; kalyptein, conceal. To whisk away the cover and experience a sudden insight.

An illustration that depicts information well allows numbers to be felt.

Often, though, we illustrate information and we do it poorly.

The scientific method is gorgeous. Through guesswork, repetition, and analysis, we can learn about our world.

But science is never neutral. We impart our values by the questions we choose to ask, by the ways we choose to interpret the world’s ever-oblique answers.

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Geological time is often depicted as a clock. A huge quantity of time, compressed down into a 24-hour day. Often, this is done with the ostensible goal of showing the relative unimportance of humans.

Our planet has been here for a day, and humans appear only during the final two minutes!

Unfortunately, this way of depicting time actually overemphasizes the present. Why, after all, should the present moment in time seem so special that it resides at midnight on our clock?

The present feels special to us because we’re living in it. From a geological perspective, it’s just another moment.

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In Timefulness, geologist Marcia Bjornerud writes:

Geologic textbooks invariably point out (almost gleefully) that if the 4.5-billion-year story of the Earth is scaled to a 24-hour day, all of human history would transpire in the last fraction of a second before midnight.

But this is a wrongheaded, and even irresponsible, way to understand our place in Time. For one thing, it suggests a degree of insignificance and disempowerment that not only is psychologically alienating but also allows us to ignore the magnitude of our effects on the planet in that quarter second.

And it denies our deep roots and permanent entanglement with Earth’s history; our specific clan may not have shown up until just before the clock struck 12:00, but our extended family of living organisms has been around since at least 6 a.m.

Finally, the analogy implies, apocalyptically, that there is no future – what happens after midnight?

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Timefulness is a lovely book, but Bjornerud does not present a corrected clock.

And so I lay in bed, thinking. How could these numbers be shown in a way that helped me to understand our moment in time?

I wanted to fix the clock.

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The first midnight is easy – the birth of our sun. A swirling cloud of gas condenses, heating as gravity tugs the molecules into more and more collisions. Nuclear fusion begins.

Gravity tugs molecules inward, nuclear explosions push them outward. When these are balanced, our sun exists. Twelve o’clock.

Two minutes later, our planet is born. Metal and water and dust become a big rock that keeps swirling, turning, as it orbits the sun. It’s warmed, weakly, by light from the sun – our star shone dimly then, but shines brighter and brighter every day.

Our sun earns low interest – 0.9% each hundred million years, hotter, brighter. But wait long enough, and a low interest is enough.

Someday, shortly before it runs out of fuel, our sun will be blinding.

By 12:18 a.m., there is life on Earth. We’ve found fossils that many billions of years old.

And at 7:26 p.m., there will be no more life. Our sun will have become so bright that its blinding light evaporates all the oceans. The water will boil so hot that it will be flung into space. The Earth will be a rocky desert, coated perhaps in thick clouds of noxious gas.

Currently, it’s 10:58 a.m.

The dinosaurs appeared 35 minutes ago. 9.5 minutes ago, all of them died (except the ancestors of our birds).

Humans appeared 1 minute ago.

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So, we have 3.5 billion years remaining – another 8.5 hours on our clock – before we have to migrate to the stars.

Humans certainly can’t persist forever. Empty space is stretching. Eventually, the whole universe will be dark and cold, which each speck of matter impossibly far from every other.

But our kind could endure for a good, long while. Scaled to the 24-hour day representing the lifespan of our sun, we still have another 300 years before the universe goes dark.

So many stories could fit into that span of time.

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It’s 10:58 a.m., and life on Earth has until 7:26 p.m.

Humans crept down from trees, harnessed fire, invented writing, and built rockets all within a single minute. Life moves fast.

Quite likely, life from Earth will reach the stars.

But it needn’t be us.

The dinosaurs were cool. They didn’t make it.

We naked apes are pretty cool, too. I love our cave drawings, art museums, psychedelic street art. Our libraries. But we’ve also made prodigious mounds of trash. We’re pouring plumes of exhaust into the sky as we ship giant flatscreen televisions from place to place.

We burn a lot of fuel for the servers that host our websites.

We humans aren’t the first organisms to risk our own demise by pumping exhaust into the atmosphere. The industrial revolution was fueled by ancient plants – our engines burn old sunlight. But many microbes are happy to eat old sunlight, too. These microbes also pump carbon dioxide into the air. They’ve warmed our planet many times before – each time the permafrost thawed, microbes went to town, eating ancient carbon that had been locked up in the ice.

Foolish microbes. They made the Earth too hot and cooked themselves.

Then again, the microbes may have more modest goals than us humans. We’ve found no fossils suggesting that the microbes tried to build spaceships.

For our endeavors, we’ve benefited from a few thousand years of extremely stable, mild climate.

We still have 8.5 hours left to build some spaceships, but a thirty second hot squall at 10:59 a.m. would doom the entire project.

So much time stretches out in front of us. We could have a great day. We, in continuation of the minute of humans who preceded us, and continued by the seconds or minutes or hours of humans who will be born next.

We shouldn’t let our myopic focus on present growth fuck up the entire day.

Honestly? My children are four and six. I’d be so disappointed if I took them for a hike and they guzzled all their water, devoured all their snacks, within the first minute after we left our house.

On octopuses and family gatherings.

On octopuses and family gatherings.

Recently, a dear friend sent me an article from Scientific American about the blanket octopus.

She and I had been discussing unusual animal mating, because that’s what you do, right? Global pandemic hits and you share freaky trivia with your friends.

Miniscule male anglerfish will merge with the body of a female if they find her, feeding off her blood. Deadbeat male clinginess at its worst.

Blanket octopuses also have extreme sexual dimorphism – a female’s tentacles can span seven feet wide, whereas the males are smaller than an inch.

But, wait, there’s more! In a 1963 article for Science magazine, marine biologist Everet Jones speculated that blanket octopuses might use jellyfish stingers as weapons.

While on a research cruise, Jones installed a night-light station to investigate the local fish.

Among the frequent visitors to the submerged light were a number of immature female blanket octopuses. I dip-netted one of these from the water and lifted it by hand out of the net. I experienced sudden and severe pain and involuntarily threw the octopus back into the water.

To determine the mechanism responsible for this sensation, 10 or 12 small octopuses were captured and I purposely placed each one on the tender areas of my hands. The severe pain occurred each time, but careful observation indicated that I was not being bitten.

The pain and resulting inflammation, which lasted several days, resembled the stings of the Portuguese man-of-war jellyfish, which was quite abundant in the area.

tl;dr – “It really hurt! So I did it again.”

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My spouse teaches high school biology. An important part of her class is addressing misconceptions about what science is.

Every so often, newspapers will send a reporter to interview my father about his research. Each time, they ask him to put on a lab coat and pipette something:

I mean, look at that – clearly, SCIENCE is happening here.

But it’s important to realize that this isn’t always what science looks like. Most of the time, academic researchers aren’t wearing lab coats. And most of the time, science isn’t done in a laboratory.

Careful observation of the natural world. Repeated tests to discover, if I do this, what will happen next? There are important parts of science, and these were practiced by our ancestors for thousands of years, long before anyone had laboratories. Indigenous people around the world have known so much about their local varieties of medicinal plants, and that’s knowledge that can only be acquired through scientific practice.

A nine month old who keeps pushing blocks off the edge of the high chair tray to see, will this block fall down, too? That’s science!

And this octopus article, published in the world’s most prestigious research journal? The experiment was to scoop up octopuses by hand and see how much it hurt.

It hurt a lot.

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The article that I linked to earlier, the Scientific American blog post that my friend had sent me, includes a video clip at the bottom. Here’s a direct link to the video:

I should warn, you, though. The first section of the video shows a blanket octopus streaming gracefully through the ocean. She’s beautiful. But then the clip continues with footage of a huge school of fish.

Obviously, I was hoping that they’d show the octopus lurch forward, wielding those jellyfish stingers like electrified nun-chucks to incapacitate the fish. I mean, yes, I’m vegan. I don’t want the fish to die. But an octopus has to eat. And, if the octopus is going to practice wicked cool tool-using martial arts, then I obviously want to see it.

But I can’t. Our oceans are big, and deep, and dark. We’re still making new discoveries when we send cameras down there. So far, nobody has ever filmed a blanket octopus catching fish this way.

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Every time I learn something new about octopuses, I think about family reunions.

About twenty years ago, I attended a family reunion in upstate New York. My grandparents were celebrating their fiftieth wedding anniversary. Many people were there whom I’d never met before, and whom I haven’t seen since. But most of us shared ancestors, often four or five or even six generations back.

And we all shared ancestors at some point, even the people who’d married in. From the beginning of life on Earth until 150,000 years ago, you could draw a single lineage – _____ begat ______ who begat ______ – that leads up to every single human alive today. We have an ancestor in common who lived 150,000 years ago, and so every lineage that leads to her will be shared by us all.

There’s also an ancestor that all humans alive today share with all octopuses alive today. So we could host a family reunion for all of her descendants – we humans would be invited, and blanket octopuses would be, too.

I would love to meet a blanket octopus. They’re brilliant creatures. If we could find a way to communicate, I’m sure there’d be lots to talk about.

But there’s a problem. You see, not everyone invited to this family reunion would be a scintillating conversationalist.

That ancestor we share? Here’s a drawing of her from Jian Han et al.’s Nature article.

She was about the size of a grain of rice.

And, yes, some of her descendants are brilliant. Octopuses. Dolphins. Crows. Chimpanzees. Us.

But this family reunion would also include a bunch of worms, moles, snails, and bugs. A lot of bugs. Almost every animals would’ve been invited, excluding only jellyfish and sponges. Many of the guests would want to lay eggs in the potato salad.

So, sure, it’d be cool to get to meet up with the octopuses, our long-lost undersea cousins. But we might end up seated next to an earthworm instead.

I’m sure that worms are very nice. Charles Darwin was fascinated by the intelligence of earthworms. Still, it’s hard to have a conversation with somebody when you don’t have a lot of common interests.

On hydroxychloroquine, expertise, and the power of persuasion.

On hydroxychloroquine, expertise, and the power of persuasion.

Recently, a friend who works in the ER wrote to ask me about hydroxychloroquine.

Yes, I know. I was shocked, too. But my friend was sincere. Although most reputable news outlets have publicized that hydroxychloroquine doesn’t work against Covid-19, my friend read an article from Harvey Risch in Newsweek that seemed really compelling.

Risch has impeccable credentials – he’s an M.D. Ph.D. and a professor of epidemiology at Yale’s School of Public Health. And a lot of what he wrote for his July 23rd article is quite sensible:

Why has hydroxychloroquine been disregarded?

First, as all know, the medication has become highly politicized. For many, it is viewed as a marker of political identity, on both sides of the political spectrum. Nobody needs me to remind them that this is not how medicine should proceed.

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Medical data isn’t perfect, and confirmation bias is very real. So there’s a chance that medical doctors really could hoodwink themselves into discounting a helpful medication, the same way that so many medical doctors get suckered into overprescribing drugs after pharmaceutical companies bribe them with gifts. Yup, medical doctors are human, too.

I know that I’m so dismayed by our current president that I’m inclined to distrust hydroxychloroquine just because he says the drug is great.

So it was a shock for me to read Risch’s article. He wrote that there was data showing that hydroxychloroquine, when used in a combination therapy early during a high-risk person’s Covid-19 infection, could dramatically reduce the risk of serious complications. If more people took hydroxychloroquine, he wrote, fewer would die.

Risch acknowledges that hydroxychloroquine is dangerous – it might kill 1 out of each 10,000 people who take it – but Covid-19 is obviously dangerous, too – it kills 3 out of each 1,000 people who contract it:

In the future, I believe this misbegotten episode regarding hydroxychloroquine will be studied by sociologists of medicine as a classic example of how extra-scientific factors overrode clear-cut medical evidence.

But for now, reality demands a clear, scientific eye of the evidence and where it points. For the sake of high-risk patients, for the same of our parents and grandparents, for the sake of the unemployed, for our economy and for our polity, especially those disproportionately affected, we must start treating immediately.

Those are strong words. And, really, the Newsweek article felt persuasive to me. And so I looked up Risch’s research in the American Journal of Epidemiology, hoping to see the actual data in support of his claims.

I’m lucky, that way. I’m a scientist, so I don’t have to trust the words of a supposed expert. I’m an expert. I get to look at the data.

The data are much less compelling than Risch’s words.

Risch discusses the results of an uncontrolled study by Vladimir Zelenko, a medical doctor in Monroe, New York: “For example, among Connecticut cases 60 years of age or older, at present the mortality is 20%. Thus it would be ballpark to estimate that some 20% of the 1466 treated high-risk patients in the Zelenko cohort would have died without outpatient hydroxychloroquine plus antibiotic.

This is an egregiously inaccurate statement. The high death rate cited – 20 – is for older patients who test positive for Covid-19 and have such severe symptoms that they need to be hospitalized.

As described in the short statement released by Zelenko, he treated 405 people who visited his office complaining of mild cough, fever, headache, sore throat, or diarrhea. His patients were not given a Covid-19 test. Presumably, many were never infected with Covid-19.

It is not a surprise to see that a 60-year-old patient who takes hydroxychloroquine after developing a sore throat from seasonal allergies is less likely to die than a 60-year-old patient who is diagnosed with Covid-19 in the hospital.

Of Zelenko’s 405 patients, at least two 2 died. This is lower than the expected 1% mortality rate of high-risk patients who contract Covid-19. But this set of 405 patients included low-risk patients experiencing shortness of breath and high-risk patients experiencing mild headache, many of whom never had Covid-19.

Zelenko’s report is two pages long and written in extremely lucid prose. Risch either totally misread it, which is galling, or intentionally mis-described it, which is worse.

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So, why was Zelenko giving people hydroxychloroquine in the first place?

Well, I’d heard that an in vitro study – which means “inside a test tube or petri dish, not a person” – showed that hydroxychloroquine reduced Covid-19 viral replication. But I hadn’t read the original paper. So I looked it up.

It should have taken me less than a minute to find this paper. Unfortunately, people have been pretty sloppy with their references. I get it. Covid-19 is scary, and it’s urgent, so people are publishing faster than usual.

I assumed that I could pull up almost any paper on hydroxychloroquine and Covid-19 and quickly find the citation for the original study. Indeed, most purport to be citing it. But in this, the citation that ought to have pointed to that study instead sent me to a paper on the differentiation of lung stem cells, and in this, the relevant citation incorrectly points to a paper on the drug lopinavir.

Ugh. I mean, these bungled citations aren’t that big a deal for me, personally – just means I had to give up on piggybacking and instead search Pubmed. But it undermines trust when you can’t get the little things right.

Anyway, the earliest reference that I found was from Liu et al., their study “Hydroxychloroquine, a less toxic derivative of chloroquine, is effective at inhibiting SARS-CoV-2 infection in vitro.” And, yes, I’ll admit – I thought about putting in the wrong link just to mess with you. But, if I did that, would you still trust me about the rest of this?

Liu et al. used Vero cells – a cell line derived from a kidney cancer in African green monkeys – and for Figure 1, they measured both how much hydroxychloroquine it takes to kill cells (about 200 micromolar is a cytotoxic dose) and how much hydroxychloroquine it takes to inhibit viral infection (about a 10 micromolar dose).

Okay. To me, that’s already sounding a little spooky. The bigger the difference between an effective dose and a lethal dose, the safer you are.

That’s why a bunch of hippies died after The Teachings of Don Juan was published. That book touted jimsomweed as a psychedelic. Indeed, the plant contains a high concentration of scopolamine, which can give people nightmarish visions of flying. It’s a powerful hallucinogen. But the effective dose is quite close to the lethal dose – when curious kids try to get high off it, they’re flirting with death.

Everyone’s body is a little different from everyone else’s. Maybe a dose that’s safe for you would kill me. The odds of disaster are worse when the effective dose and lethal dose are similar.

So, Liu et al. saw cytotoxicity kick in at around 100 micromolar hydroxychloroquine, getting pretty high by 200 micromolar. And for their visual assay of viral infection, they bathed their Vero cells in 50 micromolar hydroxychloroquine.

To block viral entry, they were coming pretty close to just killing these cells with the drug.

And the problem is even worse inside a human body. You take a drug and it gets into your bloodstream. It’ll reach some concentration there. This is the concentration that matters most for toxicity.

But the drug will only be effective against Covid-19 when it reaches your lungs. When Marzolini et al. used mass spectrometry to measure how much of hydroxychloroquine was actually getting from a patient’s blood to their lungs, they found that it wasn’t at a high enough concentration to reproduce any effects seen in vitro.

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Indeed, a randomized clinical study showed that hydroxychloroquine fails as a post-exposure prophylaxis. The drug was given to people who were worried about exposure because they’d spent time with someone who tested positive for Covid-19. The drug didn’t help – these people contracted the infection at the same rate as people who were given a placebo.

A randomized clinical study also showed that hydroxychloroquine fails as a cure. People who visited a hospital and tested positive for Covid-19 but had mild symptoms were given the drug. Their disease was just as likely to progress as people who received a placebo.

Hydroxychloroquine doesn’t work, and it’s toxic.

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I was left wondering: why would Risch write these things? Why would he write that article for Newsweek? He’s clearly intelligent, and, from the tone of his writing, I feel confident that he wants to help people.

He might even believe wholeheartedly in the conclusion he’s presenting.

That’s generally true among scientists. Confirmation bias is insidious.

That paper from the team at Harvard? They did some modeling and argued that, if Covid-19 is seasonal, we will save most lives by periodically shutting down. But their model left out the waning immunity that would cause Covid-19 to be seasonal! Whoops. That’s why they reached the wrong conclusion.

Or the recent New York Times editorial from Iwasaki and Medzhitov, both professors of immunobiology at Yale, reassuring readers that they won’t get Covid-19 twice. Well, that’s not correct.

Some antigens confer immunity that lasts about as long as our lives. Most don’t. Influenza immunity lasts months, not years. The paper that Iwasaki and Medzhitov cited in their article, a study in which people were intentionally infected with a less dangerous coronavirus, found that immunity to that virus lasted months, not years.

Covid-19 immunity will not last forever. The relevant question isn’t whether you can be infected again, it’s how soon you can be re-infected. With the data we have so far, it’s reasonable to expect that the answer will be measured in months, not years.

There’s some good news – the second time you contract Covid-19, it’ll probably be less severe than the first. In addition to antibodies, your immune system has “T cell memory” to help you fight off subsequent infections. But, as is also described in the paper cited by Iwasaki and Medzhitov, even people who felt fine were shedding virus again the second time they were infected.

During the second infection, the research subjects were shedding viral particles for a shorter period of time. But, especially with Covid-19 – a virus that can be transmitted simply by talking – a person who sheds virus for a short time while feeling fine is probably more likely to transmit the disease than somebody who sheds virus for a whole week while feeling like garbage.

The person who feels like garbage will stay home. The person who feels fine won’t.

Still, though, I was left wondering – what underlying beliefs would sway Risch enough that he’d make these blunders?

Eventually, I decided to lump his motivation in with mine. Maybe that’s fair, maybe it’s not. Really, I have no idea what he was thinking, so this is just my best guess.

But I imagine that many of these people – Risch, Iwasaki, Medzhitov, John Ioannidis, David Katz, all of whom are very smart, and all of whom mean well – understand that the strategies we’re using against Covid-19 are both ineffectual and are causing harm.

No shutdown will eliminate Covid-19 – the best we can do is to delay it. And we can delay it only as long as we maintain the shutdown. Maybe that seems fine if you’re an older, wealthy person brimming with optimism about vaccine development, like Anthony Fauci who thinks we’ll have a working vaccine early next year, but it’s unconscionable if you think a working vaccine might be five or more years away.

I don’t think we should try to pause children’s development for five years.

Still, there’s no mathematical or logical way to prove what we should do. School closures definitely slow the spread of Covid-19. How do you balance the good of delaying an elderly person’s infection by three months (which is equivalent to a drug that extends a patient’s life by three months) with the harms we’re causing?

I know what I’d do, but other people have different priorities than me. And that’s okay!

I’d like to think, though, that I’m not trying to hoodwink anybody about the science in order to deceptively get them to do the thing I think is right.

Like, yes, I think schools should be open. I think we owe it to children. Right now, children are suffering, but this is our fault, the fault of grown-ups.

We have known for over a decade that we ought to make coronavirus vaccines – we didn’t devote enough resources to it, and now we don’t have one. We’ve known for decades that eating animals – both those sold in meat markets like in Wuhan and the ones raised in “concentrated animal feeding operations” throughout the U.S. – will create more zoogenic diseases, and we kept doing it. We know that a guaranteed basic income would’ve given people the resources they needed to self-isolate during an epidemic – we don’t have one. We know that guaranteed access to health care would keep our death rate down.

Climate change will make pandemics more frequent, in addition to making our world unliveable for future generations. And we haven’t taken action to stop it.

None of these failings are children’s fault. We, older people, have failed. We fucked up. And now we’re asking children to make sacrifices to dampen the impact of our mistake (although, again, it won’t work – it’ll just delay the eventual repercussions).

I think today’s children deserve a fair shot at a good life, and I think that school is an essential part of that.

But don’t let anybody try to convince you that it’s safe to re-open schools because hydroxychloroquine will stop Covid-19.

On empathy and the color red.

On empathy and the color red.

I can’t fly.

I try to feed my children every night, but I never vomit blood into their mouths.

When I try to hang upside down – like from monkey bars at a playground – I have to clench my muscles, and pretty soon I get dizzy. I couldn’t spend a whole day like that.

And, yes, sometimes I shout. Too often during the pandemic, I’ve shouted at my kids. But when I shout, I’m trying to make them stop hitting each other – I’m not trying to figure out where they are.

It’s pretty clear that I’m not a bat.

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Photograph by Anne Brooke, USFWS

Because I haven’t had these experiences, philosopher Thomas Nagel would argue that I can’t know how it feels to be a bat.

In so far as I can imagine [flitting through the dark, catching moths in my mouth], it tells me only what it would be like for me to behave as a bat behaves.

But that is not the question. I want to know what it is like for a bat to be a bat.

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Perhaps I can’t know what it feels like for a bat to be a bat. And yet, I can empathize with a bat. I can imagine how it might feel to be trapped in a small room while a gamboling, wiry-limbed orc-thing tried to swat me with a broom.

It would be terrifying!

And that act of imagination – of empathy – is enough for me to want to protect bats’ habitats. To make space for them in our world. Sure, you could argue that bats are helpful for us – they’re pollinators, they eat pesky bugs – but empathy lets us care about the well-being of bats for their own sake.

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Literature exercises our minds: when we read, invent, and share stories, we build our capacity for empathy, becoming more generally aware of the world outside our own skulls.

Writing can be a radical act of love. Especially when we write from a perspective that differs from our own. The poet Ai said that “Whoever wants to speak in my poems is allowed to speak, regardless of sex, race, creed, or color.” Her poems often unfurl from the perspective of violent men, and yet she treats her protagonists with respect and kindness. Ai gives them more than they deserve: “I don’t know if I embrace them, but I love them.

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That capacity for love, for empathy, will let us save the world. Although many of us haven’t personally experienced a lifetime of racist microaggressions or conflict with systemic oppression, we all need to understand how rotten it would feel. We need to understand that the pervasive stress seeps into a person’s bones, causing all manner of health problems. We need understand the urgency of building a world where all children feel safe.

And if we don’t understand – yet – maybe we need to read more.

Experiments suggest that reading any engaging literary fiction boosts our ability to empathize with others. Practice makes better: get outside your head for a while, it’ll be easier to do it again next time.

Of course, we’ll still need to make an effort to learn what others are going through. Thomas Nagel was able to ruminate so extensively about what it would feel like to live as a bat because we’ve learned about echolocation, about their feeding habits, about their family lives. If we want to be effective anti-racists, we need to learn about Black experiences in addition to developing our empathy more generally.

Luckily, there’s great literature with protagonists facing these struggles – maybe you could try How We Fight for Our Lives, Americanah, or The Sellout.

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As a bookish White person, it’s easy for me to empathize with the experiences of other bookish White people. In Search of Lost Time doesn’t tax my brain. Nor does White Noise. The characters in these books are a lot like me.

The cognitive distance between me and the protagonists of Americanah is bigger. Which is sad in and of itself – as high schoolers, these characters were playful, bookish, and trusting, no different from my friends or me. But then they were forced to endure hard times that I was sufficiently privileged to avoid. And so when I read about their lives, perched as I was atop my mountain of privilege, it was painful to watch Ifemelu and Obinze develop their self-protective emotional carapaces, armoring themselves against the injustice that ceaselessly buffets them.

Another reader might nod and think, I’ve been there. I had to exercise my imagination.

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In Being a Beast, Charles Foster describes his attempts to understand the lives of other animals. He spent time mimicking their behaviors – crawling naked across the dirt, eating worms, sleeping in an earthen burrow. He wanted a badger’s-eye view of the world.

Foster concluded that his project was a failure – other animals’ lives are just so different from ours.

And yet, as a direct consequence of his attempt at understanding, Foster changed his life. He began treating other animals with more kindness and respect. To me, this makes his project a success.

White people might never understand exactly how it feels to be Black in America. I’m sure I don’t. But we can all change the way we live. We can, for instance, resolve to spend more money on Black communities, and spend it on more services than just policing.

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Empathy is working when it forces us to act. After all, what we do matters more than what we purport to think.

It’s interesting to speculate what it would feel like to share another’s thoughts – in Robert Jackson Bennett’s Shorefall, the protagonists find a way to temporarily join minds. This overwhelming rush of empathy and love transforms them: “Every human being should feel obliged to try this once.

In the real world, we might never know exactly how the world feels to someone else. But Nagel wants to prove, with words, that he has understood another’s experience.

One might try, for example, to develop concepts that could be used to explain to a person blind from birth what it was like to see. One would reach a blank wall eventually, but it should be possible to devise a method of expressing in objective terms much more than we can at present, and with much greater precision.

The loose intermodal analogies – for example, “Red is like the sound of a trumpet” – which crop up in discussions of this subject are of little use. That should be clear to anyone who has both heard a trumpet and seen red.

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We associate red with many of our strongest emotions: anger, violence, love.

And we could tell many different “just so” stories to explain why we have these associations.

Like:

Red is an angry color because people’s faces flush red when they’re mad. Red blood flows when we’re hurt, or when we hurt another.

Or:

Red represents love because a red glow spreads over our partners’ necks and chests and earlobes as we kiss and caress and fumble together.

Or:

Red is mysterious because a red hue fills the sky at dawn and dusk, the liminal hours when we are closest to the spirit world.

These are all emergent associations – they’re unrelated to the original evolutionary incentive that let us see red. Each contributes to how we see red now, but none explains the underlying why.

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We humans are blue-green-red trichromatic – we can distinguish thousands of colors, but our brains do this by comparing the relative intensities of just three.

And we use the phrase “color blind” to describe the people and other animals who can’t distinguish red from green. But all humans are color blind – there are colors we can’t see. To us, a warm body looks identical to a cold wax replica. But their colors are different, as any bullfrog could tell you.

Photograph by Tim Mosenfelder, Getty Images

Our eyes lack the receptors – cone cells with a particular fold of opsin – that could distinguish infrared light from other wavelengths. We mistakenly assume these two singers have the same color skin.

When we look at flowers, we often fail to see the beautiful patterns that decorate their petals. These decorations are obvious to any bee, but we’re oblivious. Again, we’re missing the type of cone cells that would let us see. To fully appreciate flowers, we’d need receptors that distinguish ultraviolet light from blue.

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Most humans can see the color red because we’re descended from fruit eaters. To our bellies, a red berry is very different from a green berry. And so, over many generations, our ancestors who could see the difference were able to gather more nutritious berries than their neighbors. Because they had genes that let them see red, they were better able to survive, have children, and keep their children fed.

The genes for seeing red spread.

Now, several hundred thousand years later, this wavelength of light blares at us like a trumpet. Even though the our ancestors learned to cook food with fire, and switched from fruit gathering to hunting, and then built big grocery stores where the bright flashes of color are just advertisements for a new type of high-fructose-corn-syrup-flavored cereal, red still blares at us.

Once upon a time, we really needed to see ripe fruit. The color red became striking to us, wherever we saw it. And so we invented new associations – rage, or love – even though these are totally unrelated to the evolutionary pressures that gave us our red vision.

Similarly, empathy wasn’t “supposed” to let us build a better world. Evolution doesn’t care about fairness.

And yet. Even though I might never know exactly how it feels when you see the color red, I can still care how you’re treated. Maybe that’s enough.

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Header image: a greater short-nosed fruit bat, photograph by Anton 17.

On meditation and the birth of the universe.

On meditation and the birth of the universe.

This is part of a series of essays prepared to discuss in jail.

Our bodies are chaos engines. 

In our nearby environment, we produce order.  We form new memories.  We build things.  We might have sex and create new life.  From chaos, structure.

As we create local order, though, we radiate disorder into the universe. 

The laws of physics work equally well whether time is moving forward or backward.  The only reason we experience time as flowing forward is that the universe is progressing from order into chaos.

In the beginning, everything was homogeneous.  The same stuff was present everywhere.  Now, some regions of the universe are different from others.  One location contains our star; another location, our planet.  Each of our bodies is very different from the space around us.

This current arrangement is more disorderly than the early universe, but less so than what our universe will one day become.  Life is only possible during this intermediate time, when we are able to eat structure and excrete chaos. 

Hubble peers into a stellar nursery. Image courtesy of NASA Marshall Space Flight on Flickr.

Sunlight shines on our planet – a steady stream of high-energy photons all pointed in the same direction.  Sunshine is orderly.  But then plants eat sunshine and carbon dioxide to grow.  Animals eat the plants.  As we live, we radiate heat – low-energy photons that spill from our bodies in all directions.

The planet Earth, with all its life, acts like one big chaos engine.  We absorb photons from the sun, lower their energy, increase their number, and scatter them.

We’ll continue until we can’t.

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Our universe is mostly filled with empty space. 

But empty space does not stay empty.  Einstein’s famous equation, E equals M C squared, describes the chance that stuff will suddenly pop into existence.  This happens whenever a region of space gathers too much energy.

Empty space typically has a “vacuum energy” of one billionth of a joule per cubic meter.  An empty void the size of our planet would have about as much energy as a teaspoon of sugar.  Which doesn’t seem like much.  But even a billionth of a joule is thousands of times higher than the energy needed to summon electrons into being.

And there are times when a particular patch of vacuum has even more energy than that.

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According to the Heisenberg Uncertainty Principle, time and energy can’t be defined simultaneously.  Precision in time causes energy to spread – the energy becomes both lower and higher than you expected.

In practice, the vacuum energy of a particular region of space will seem to waver.  Energy is blurry, shimmering over time.

There are moments when even the smallest spaces have more than enough energy to create new particles.

Objects usually appear in pairs: a particle and its anti-particle.  Anti-matter is exactly like regular matter except that each particle has an opposite charge.  In our world, protons are positive and electrons are negative, but an anti-proton is negative and an anti-electron is positive.

If a particle and its anti-particle find each other, they explode.

When pairs of particles appear, they suck up energy.  Vacuum energy is stored inside them.  Then the particles waffle through space until they find and destroy each other.  Energy is returned to the void.

This constant exchange is like the universe breathing.  Inhale: the universe dims, a particle and anti-particle appear.  Exhale: they explode.

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Our universe is expanding.  Not only are stars and galaxies flying away from each other in space, but also empty space itself is growing.  The larger a patch of nothingness, the faster it will grow.  In a stroke of blandness, astronomers named the force powering this growth “dark energy.”

Long ago, our universe grew even faster than it does today.  Within each small fraction of a second, our universe doubled in size.  Tiny regions of space careened apart billions of times faster than the speed of light.

This sudden growth was extremely improbable.  For this process to begin, the energy of a small space had to be very, very large.  But the Heisenberg Uncertainty Principle claims that – if we wait long enough – energy can take on any possible value.  Before the big bang, our universe had a nearly infinite time to wait.

After that blip, our universe expanded so quickly because the vacuum of space was perched temporarily in a high-energy “metastable” state.  Technically balanced, but warily.  Like a pencil standing on its tip.  Left alone, it might stay there forever, but the smallest breath of air would cause this pencil to teeter and fall.

Similarly, a tiny nudge caused our universe to tumble back to its expected energy.  A truly stable vacuum.  The world we know today was born – still growing, but slowly.

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During the time of rapid expansion, empty vacuum had so much energy that particles stampeded into existence.  The world churned with particles, all so hot that they zipped through space at nearly the speed of light. 

For some inexplicable reason, for every billion pairs of matter and anti-matter, one extra particle of matter appeared.  When matter and anti-matter began to find each other and explode, this billionth extra bit remained.

This small surplus formed all of stars in the sky.  The planets.  Ourselves.

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Meditation is like blinking.  You close your eyes, time passes, then you open your eyes again.  Meditation is like a blink where more time passes.

But more is different.

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Our early universe was filled with the smallest possible particles.  Quarks, electrons, and photons.  Because their energy was so high, they moved too fast to join together.  Their brilliant glow filled the sky, obscuring our view of anything that had happened before.

As our universe expanded, it cooled.  Particles slowed down.  Three quarks and an electron can join to form an atom of hydrogen.  Two hydrogen atoms can join to form hydrogen gas.  And as you combine more and more particles together, your creations can be very different from a hot glowing gas.  You can form molecules, cells, animals, societies.

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When a cloud of gas is big enough, its own gravity can pull everything inward.  The cloud becomes more and more dense until nuclear fusion begins, releasing energy just like a nuclear bomb.  These explosions keep the cloud from shrinking further.

The cloud has become a star.

Nuclear fusion occurs because atoms in the center of the cloud are squooshed too close together.  They merge: a few small atoms become one big atom.  If you compared their weights – four hydrogens at the start, one helium at the finish – you’d find that a tiny speck of matter had disappeared.  And so, according to E equals M C squared, it released a blinding burst of energy.

The largest hydrogen bomb detonated on Earth was 50 megatons – the Kuz’kina Mat tested in Russia in October, 1961.  It produced a mushroom cloud ten times the height of Mount Everest.  This test explosion destroyed houses hundreds of miles away.

The fireball of Tsar Bomba, the Kuz’kina Mat.

Every second, our sun produces twenty billion times more energy than this largest Earth-side blast.

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Eventually, our sun will run out of fuel.  Our sun shines because it turns hydrogen into helium, but it is too light to compress helium into any heavier atoms.  Our sun has burned for about four billion years, and it will probably survive for another five billion more.  Then the steady inferno of nuclear explosions will end.

When a star exhausts its fuel, gravity finally overcomes the resistance of the internal explosions.  The star shrinks.  It might crumple into nothingness, becoming a black hole.  Or it might go supernova – recoiling like a compressed spring that slips from your hand – and scatter its heavy atoms across the universe.

Planets are formed from the stray viscera of early stars.

Supernova remains. Image by NASA’s Chandra X-Ray Observatory and the European Space Agency’s XMM-Newton.

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Our universe began with only hydrogen gas.  Every type of heavier atom – carbon, oxygen, iron, plutonium – was made by nuclear explosions inside the early stars.

When a condensing cloud contains both hydrogen gas and particulates of heavy atoms, the heavy atoms create clumps that sweep through the cloud far from its center.  Satellites, orbiting the star.  Planets.

Nothing more complicated than atoms can form inside stars.  It’s too hot – the belly of our sun is over twenty million degrees.  Molecules would be instantly torn apart.  But planets – even broiling, meteor-bombarded planets – are peaceful places compared to stars.

Molecules are long chains of atoms.  Like atoms, molecules are made from combinations of quarks and electrons.  The material is the same – but there’s more of it.

More is different.

Some atoms have an effect on our bodies.  If you inhale high concentrations of oxygen – an atom with eight protons – you’ll feel euphoric and dizzy.  If you drink water laced with lithium – an atom with three protons – your brain might become more stable.

But the physiological effects of atoms are crude compared to molecules.  String fifty-three atoms together in just the right shape – a combination of two oxygens, twenty-one carbons, and thirty hydrogens – and you’ll have tetrahydrocannibol.  String forty-nine atoms together in just the right shape – one oxygen, three nitrogens, twenty carbons, and twenty-five hydrogens – and you’ll have lysergic acid diethylamide.

The effects of these molecules are very different from the effects of their constituent parts.  You’d never predict what THC feels like after inhaling a mix of oxygen, carbon, and hydrogen gas.

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An amino acid is comparable in scale to THC or LSD, but our bodies aren’t really made of amino acids.  We’re built from proteins – anywhere from a few dozen to tens of thousands of amino acids linked together.  Proteins are so large that they fold into complex three-dimensional shapes.  THC has its effect because some proteins in your brain are shaped like catcher’s mitts, and the cannibinoid nestles snuggly in the pocket of the glove.

Molecules the size of proteins can make copies of themselves.  The first life-like molecules on Earth were long strands of ribonucleic acid – RNA.  A strand of RNA can replicate as it floats through water.  RNA acts as a catalyst – it speeds up the reactions that form other molecules, including more RNA.

Eventually, some strands of RNA isolated themselves inside bubbles of soap.  Then the RNA could horde – when a particular sequence of RNA catalyzed reactions, no other RNA would benefit from the molecules it made.  The earliest cells were bubbles that could make more bubbles.

Cells can swim.  They eat.  They live and die.  Even single-celled bacteria have sex: they glom together, build small channels linking their insides to each other, and swap DNA.

But with more cells, you can make creatures like us.

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Consciousness is an emergent property.  With a sufficient number of neuron cells connected to each other, a brain is able to think and plan and feel.  In humans, 90 billion neuron cells direct the movements of a 30-trillion-cell meat machine.

Humans are such dexterous clever creatures that we were able to discover the origin of our universe.  We’ve dissected ourselves so thoroughly that we’ve seen the workings of cells, molecules, atoms, and subatomic particles.

But a single human animal, in isolation, never could have learned that much.

Individual humans are clever, but to form a culture complex enough to study particle physics, you need more humans.  Grouped together, we are qualitatively different.  The wooden technologies of Robinson Crusoe, trapped on a desert island, bear little resemblance to the vaulted core of a particle accelerator.

English writing uses just 26 letters, but these can be combined to form several hundred thousand different words, and these can be combined to form an infinite number of different ideas.

More is different.  The alphabet alone couldn’t give anyone insight into the story of your life.

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Meditation is like a blink where more time passes, but the effect is very different.

Many religions praise the value of meditation, especially in their origin stories.  Before Jesus began his ministry, he meditated for 40 days in the Judaean Desert – his mind’s eye saw all the world’s kingdoms prostrate before him, but he rejected that power in order to spread a philosophy of love and charity. 

Before Buddha began his ministry, he meditated for 49 days beneath the Bodhi tree – he saw a path unfurl, a journey that would let travelers escape our world’s cycle of suffering. 

Before Odin began his ministry, he meditated for 9 days while hanging from a branch of Yggdrasil, the world tree – Odin felt that he died, was reborn, and could see the secret language of the universe shimmering beneath him. 

The god Shiva meditated in graveyards, smearing himself with crematory ash.

At its extreme, meditation is purportedly psychedelic.  Meditation can induce brain states that are indistinguishable from LSD trips when visualized by MRI.  Meditation isolates the brain from its surroundings, and isolation can trigger hallucination.

Researchers have found that meditation can boost our moods, attentiveness, cognitive flexibility, and creativity.  Our brains are plastic – changeable.  We can alter the way we experience the world.  Many of our thoughts are the result of habit.  Meditation helps us change those habits.  Any condition that is rooted in our brain – like depression, insomnia, chronic pain, or addiction – can be helped with meditation.

To meditate, we have to sit, close our eyes, and attempt not to think.  This is strikingly difficult.  Our brains want to be engaged.  After a few minutes, most people experience a nagging sense that we’re wasting time.

But meditation gives our minds a chance to re-organize.  To structure ourselves.  And structure is the property that allows more of something to become different.  Squirrels don’t form complex societies – a population of a hundred squirrels will behave similarly to a population of a million or a billion.  Humans form complex webs of social interactions – as our numbers grew through history, societies changed in dramatic ways.

Before there was structure, our entire universe was a hot soup of quarks and electrons, screaming through the sky.  Here on Earth, these same particles can be organized into rocks, or chemicals, or squirrels, or us.  How we compose ourselves is everything.

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The easiest form of meditation uses mantras – this is sometimes called “transcendental meditation” by self-appointed gurus who charge people thousands of dollars to participate in retreats.  Each attendee is given a “personalized” mantra, a short word or phrase to intone silently with every breath.  The instructors dole mantras based on a chart, and each is Sanskrit.  They’re meaningless syllables to anyone who doesn’t speak the language.

Any two-syllable word or phrase should work equally well, but you’re best off carving something uplifting into your brain.  “Make peace” or “all one” sound trite but are probably more beneficial than “more hate.”  The Sanskrit phrase “sat nam” is a popular choice, which translates as “truth name” or more colloquially as “to know the true nature of things.”

The particular mantra you choose matters less than the habit – whichever phrase you choose, you should use it for every practice.  Because meditation involves sitting motionless for longer than we’re typically accustomed, most people begin by briefly stretching.  Then sit comfortably.  Close your eyes.  As you breathe in, silently think the first syllable of your chosen phrase.  As you breathe out, think the second.

Repeating a mantra helps to crowd out other thoughts, as well as distractions from your environment.  Your mind might wander – if you catch yourself, just try to get back to repeating your chosen phrase.  No one does it perfectly, but practice makes better.  When a meditation instructor’s students worried that their practice wasn’t good enough, he told them that “even on a shallow dive, you still get wet.”

In a quiet space, you might take a breath every three to six seconds.  In a noisy room, you might need to breathe every second, thinking the mantra faster to block out external sound.  The phrase is a tool to temporarily isolate your mind from the world.

Most scientific studies recommend you meditate for twenty minutes at a time, once or twice a day, each and every day.  It’s not easy to carve out this much time from our daily routines.  Still, some is better than nothing.  Glance at a clock before you close your eyes, and again after you open them.  Eventually, your mind will begin to recognize the passage of time.  After a few weeks of practice, your body might adopt the approximate rhythm of twenty minutes.

Although meditation often feels pointless during the first week of practice, there’s a difference between dabbling and a habit.  Routine meditation leads to benefits that a single experience won’t.

More is different.