“When children draw on walls, reject daily baths, or leave the house wearing no pants and a tutu, caretakers may reasonably doubt their capacity for rational decision-making.”
“However, recent evidence suggests that even very young children possess sophisticated decision-making capabilities …”
The authors conducted an experiment: a marshmallow was set in front of a small child; the child was told that if they waited to eat it, they’d be given two marshmallows instead; the child was left alone in the room with the marshmallow for up to fifteen minutes.
This is a common experiment – variants have been conducted since the 1970s. In Kidd, Palmeri, & Aslin’s 2013 version, each child was first shown that the researcher offering marshmallows was either reliable or unreliable. At the beginning of each child’s encounter with the researcher, the researcher provided mediocre art supplies and promised that, if the child waited, the researcher would bring something better. Then the researcher either fulfilled that promise (bringing fresh markers or cool stickers!), or came back offering only apologies and saying that the child should just use the mediocre supplies that had been in the room all along. The wait had been for naught!
During the subsequent marshmallow test, children were asked to trust this same researcher to fulfill a promise, even after being shown that the researcher wasn’t reliable.
The children who’d been disappointed were less likely to wait.
Actually, it’s not just “knock knock” jokes – none of the jokes that children tell are funny.
And yet, parents feign excitement. We smile, maybe even laugh.
My kids are two years apart. When they were six and four, my younger child would often watch and listen and then tell the exact same joke to me.
I’d do my best to respond in the exact same way. As though surely I couldn’t know – no child wants for you to actually try to guess the answer when they tell a joke.
“I don’t know, where does a cow go for entertainment?”
Eventually a child will experience disillusionment from the world; it needn’t come from a caretaker.
At the end of Kidd, Palmeri, & Aslin’s marshmallow experiment,every child was given evidence that the researchers were unreliable. No matter if the child had waited to eat the marshmallow or had scarfed it right away, each child was given three additional marshmallows.
No child’s expectations were met. And the children who’d decided that waiting was pointless had their beliefs reinforced.
In the great scheme of things, giving children a few extra marshmallows doesn’t cause much harm. Although it’s curious that this group of researchers would intentionally undermine children’s trust in scientists.
At the local high school, the boys’ bathroom adjacent to the cafeteria doesn’t have soap. Empty plastic shells are affixed to the wall where soap dispensers used to be.
There’s a soap dispenser in the hallway outside the bathroom. If someone wanted to wash their hands properly, they’d have to turn on a sink, get their hands wet, walk outside, use the dispenser, then walk back into the bathroom to rinse the soap off. Few students do.
The administration removed the dispensers because some students were stealing them, and, at least once, somebody urinated into the soap pouch – these students needed devious licks to boast about on social. Similar incidents happened all around the country.
The problem, several high school seniors insisted to me, is that schools were closed for a while during the pandemic, which meant that current sophomores and juniors didn’t get bullied enough during middle school.
Obviously, their theory is ridiculous – “more bullying” is never a good solution to the world’s problems. But I find it fascinating that this would be the students’ first hypothesis. That the underlying problem isn’t that children were forcibly isolated during a crucial phase of their development, nor that we’ve inundated children’s lives with addictive, psychologically manipulative smartphone apps. No, the real problem is that these young people weren’t bullied enough!
By middle school, nearly all students will have experienced the disillusionment of having a knock knock joke batted away without a “Who’s there?” in response – I believe most middle school humor still revolves around sex, sarcasm, and dead baby jokes.
But I find it difficult to believe that young people – whose lives transitioned from in-person interactions with people their own age to transpiring almost entirely on the internet – would’ve experienced significantly less bullying during the pandemic. The internet is a nightmare!
The best audience for a child’s knock knock joke is another child – maybe, just maybe, a child might think it’s funny to hear the turnabout from “Boo who?” to “Oh, what’s wrong, are you hurt?”
The interaction is personal, localized, and impermanent.
And when the disillusionment comes – a friend not saying “Who’s there?” – the moment is brief and private.
How much worse might it feel to have your moments of embarrassment linger in full view?
Personally, I’m embarrassed about the world we’re building for young people.
When I was a child, my parents gave me a toy walrus to sleep with. While cuddling this walrus, I’d twist my fingers through a small looped tag on its back, until one day I knotted the tag so thoroughly that I cut off my circulation. I screamed; my finger turned blue; my parents rushed in and wanted to cut off the tag.
“No!” I apparently screamed. “The soft tag is the best part!”
I continued to refuse their help until they offered a compromise, merely slicing the loop in half so we could save my throbbing finger and prevent any future calamity.
I continued to sleep with that toy walrus until I was midway through high school. As I fell asleep, my parents would sometimes peer inside my bedroom and see me lying there, eyes closed, breath slow, my fingers gently stroking that soft tag.
Yes, kids with autism are sometimes quite particular about sensory stimulation. But I am not alone! Baby monkeys also love soft fabric.
So do their mothers.
After biologist Margaret Livingstone published a research essay, “Triggers for Mother Love,” animal welfare activists and many other scientists were appalled. In the essay, Livingstone casually discusses traumatic ongoing experiments in which hours-old baby monkeys are removed from their mothers. The babies are then raised in environments where they never glimpse anything that resembles a face, either because they’re kept in solitary confinement and fed by masked technicians or because the babies’ eyes are sutured shut.
After the babies are removed from their mothers, Livingstone offers the mothers soft toys. And the mothers appear to bond with these soft toys. When one particular baby was returned to its mother several hours later, Livingstone writes that:
“The mother looked back and forth between the toy she was holding and the wiggling, squeaking infant, and eventually moved to the back of her enclosure with the toy, leaving the lively infant on the shelf.”
Although I dislike this ongoing research, and don’t believe that it should continue, I find Livingstone’s essay to be generally compassionate.
Livingstone discusses parenting advice from the early twentieth century – too much touch or physical affection will make your child weak! – that probably stunted the emotional development of large numbers of children. Livingstone expresses gratitude that the 1950s-era research of Harry Harlow – the first scientist to explore using soft toys to replace a severed maternal bond – revealed how toxic these recommendations really were.
Harlow’s research may have improved the lives of many human children.
Harlow’s research intentionally inflicted severe trauma on research animals.
To show that the aftereffects of trauma can linger throughout an animal’s life, Harlow used devices that he named “The Rape Rack” and “The Pit of Despair” to harm monkeys (whom he did not name).
Harlow did not justify these acts by denigrating the animals. Indeed, in Voracious Science and Vulnerable Animals, research-scientist-turned-animal-activist John Gluck describes working with Harlow as both a student and then professorial collaborator, and believes that Harlow was notable at the time for his respect for monkeys. But this was not enough. Gluck writes that:
“The accepted all-encompassing single ethical principle was simple: if considerations of risk and significant harm blocked the use of human subjects, using animals as experimental surrogates was automatically justified.”
“Harlow showed that monkeys could be emotionally destroyed when opportunities for maternal and peer attachment were withheld. He argued that affectionate relationships in monkeys were worthy of terms like love.”
“In his work on learning in monkeys … [he offered] abundant evidence that monkeys develop and evaluate hypotheses during attempts to develop a solution.”
“Everything that Harlow learned from his research declared that monkeys are self-conscious, emotionally complex, intentional, and capable of substantial levels of suffering.”
For my own scientific research, I purchased cow’s brains from slaughterhouses. I used antibodies that were made in the bodies of rabbits and mice who lived (poorly) inside industrial facilities. For my spouse’s scientific research, she killed male frogs to take their sperm.
We’re both vegan.
I’d like to believe that we’d find alternative ways to address those same research questions if we were to repeat those projects today. But that’s hypothetical – at the time, we used animals.
And I certainly believe that there are other ways for Livingstone to study, for instance, the developmental ramifications of autistic children rarely making eye contact with the people around them – without blinding baby monkeys. I believe that Livingstone could study the physiological cues for bonding without removing mothers’ babies (especially since Harlow’s work, from the better part of a century ago, already showed how damaging this methodology would be).
Personally, I don’t think the potential gains from these experiments are worth their moral costs.
But also I recognize that, as a person living in the modern world, I’ve benefited from Harlow’s research. I’ve benefited from the research using mice, hamsters, and monkeys that led to the Covid-19 vaccines. I’ve benefited from innumerable experiments that caused harm.
Livingstone’s particular research might not result in any benefits – a lot of scientific research doesn’t – but unfortunately we can’t know in advance what knowledge will be useful and won’t won’t.
And if there’s any benefit, then I will benefit from this, too. It’s very hard to avoid being helped by knowledge that’s out there in the world.
To my mind, this means I have to atone – to find ways to compensate for some of the suffering that’s been afflicted on my behalf – but reparations are never perfect. And no one can force you to recognize a moral debt.
You will have to decide what any of this means to you.
Recently my spouse & I reviewed Jennifer Raff’s Origin: A Genetic History of the Americas for the American Biology Teacher magazine (in brief: Raff’s book is lovely, you should read it! I’ll include a link to our review once it’s published!), which deftly balances twin goals of disseminating scientific findings and honoring traditional knowledge.
By the time European immigrants reached the Americas, many of the people living here told stories suggesting that their ancestors had always inhabited these lands. This is not literally true. We have very good evidence that all human species – including Homo sapiens, Homo neaderthalensis, and Homo denisovans among possible others – first lived in Africa. Their descendants then migrated around the globe over a period of a few hundred thousand years.
As best we know, no lasting population of humans reached the Americas until about twenty thousand years ago (by which time most human species had gone extinct – only Homo sapiens remained).
During the most recent ice age, a few thousand humans lived in an isolated, Texas-sized grassland called Beringia for perhaps a few thousand years. They were cut off from other humans to the west and an entire continent to the east by glacial ice sheets. By about twenty thousand years ago, though, some members of this group ventured south by boat and established new homes along the shoreline.
By about ten thousand years ago, and perhaps earlier, descendants of these travelers reached the southern tip of South America, the eastern seaboard of North America, and everywhere between. This spread was likely quite rapid (from the perspective of an evolutionary biologist) based on the diversity of local languages that had developed by the time Europeans arrived, about five hundred years ago.
So, by the time Europeans arrived, some groups of people had probably been living in place for nearly 10,000 years. This is not “always” from a scientific perspective, which judges our planet to be over 4,000,000,000 years old. But this is “always” when in conversation with an immigrant who believes the planet to be about 4,000 years old. Compared with Isaac Newton’s interpretation of Genesis, the First People had been living here long before God created Adam and Eve.
If “In the beginning …” marks the beginning of time, then, yes, their people had always lived here.
I found myself reflecting on the balance between scientific & traditional knowledge while reading Gabriel Andrade’s essay, “How ‘Indigenous Ways of Knowing’ Works in Venezuela.” Andrade describes his interactions with students who hold the traditional belief in partible paternity: that semen is the stuff of life from which human babies are formed, and so every cis-man who ejaculates during penetrative sex with a pregnant person becomes a father to the child.
I appreciate partible paternity because, although this belief is often framed in misogynistic language – inaccurately grandiose claims about the role of semen in fetal development, often while ignoring the huge contribution of a pregnant person’s body – the belief makes the world better. People who are or might become pregnant are given more freedom. Other parents, typically men, are encouraged to help many children.
Replacing belief in partible paternity with a scientifically “correct” understanding of reproduction would probably make the world worse – people who might become pregnant would be permitted less freedom, and potential parents might cease to aid children whom they didn’t know to be their own genetic offspring.
Also, the traditional knowledge – belief in partible paternity – might be correct.
Obviously, there’s a question of relationships – what makes someone a parent? But I also mean something more biological — a human child actually can have three or more genetic contributors among their parents.
Presumably you know the scientific version of human reproduction. To wit: a single sperm cell merges with a single egg cell. This egg rapidly changes to exclude all the other sperm cells surrounding it, then implants in the uterine lining. Over the next nine months, this pluripotent cell divides repeatedly to form the entire body of a child. The resulting child has exactly two parents. Every cell in the child’s body has the same 3 billion base pair long genome.
No scientist believes in this simplified version. For instance, every time a cell divides, the entire genome must be copied – each time, this process will create a few mistakes. By the time a human child is ready to be born, their cells will have divided so many times that the genome of a cell in the hand is different from the genome of a cell in the liver or in the brain.
In Unique, David Linden writes that:
Until recently, reading someone’s DNA required a goodly amount of it: you’d take a blood draw or a cheek swab and pool the DNA from many cells before loading it into the sequencing machine.
However, in recent years it has become possible to read the complete sequence of DNA, all three billion or so nucleotides, from individual cells, such as a single skin cell or neuron. With this technique in hand, Christopher Walsh and his coworkers at Boston Children’s Hopsital and Harvard Medical School isolated thirty-six individual neurons from three healthy postmortem human brains and then determined the complete genetic sequence for each of them.
This revealed that no two neurons had exactly the same DNA sequence. In fact, each neuron harbored, on average, about 1,500 single-nucleotide mutations. That’s 1,500 nucleotides out of a total of three billion in the entire genome – a very low rate, but those mutations can have important consequences. For example, one was in a gene that instructs the production of an ion channel protein that’s crucial for electrical signaling in neurons. If this mutation were present in a group of neurons, instead of just one, it could cause epilepsy.
No human has a genome: we are composite creatures.
Most scientists do believe that all these unique individual genomes inside your cells were composed by combining genetic information from your two parents and then layering on novel mutations. But we don’t know how often this is false.
Pluripotent (“able to form many things”) cells from a developing human embryo / fetus / baby can travel throughout a pregnant person’s body. This is quite common – most people with XX chromosomes who have given birth to people with XY chromosomes will have cells with Y chromosomes in their brains. During the gestation of twins, the twins often swap cells (and therefore genomes).
At the time of birth, most humans aren’t twins, but many of us do start that way. There’s only a one in fifty chance of twin birth following a dizygotic pregnancy (the fertilization of two or more eggs cells released during a single ovulation). Usually what happens next is a merger or absorption of one set of these cells by another, resulting in a single child. When this occurs, different regions of a person’s body end up with distinct genetic lineages, but it’s difficult to identify. Before the advent of genetic sequencing, you might notice only if there was a difference in eye, skin, or hair color from one part of a person’s body to the next. Even now, you’ll only notice if you sequence full genomes from several regions of a person’s body and find that they’re distinct.
For a person to have more than two genetic contributors, there would have to be a dizygotic pregnancy in which sperm cells from unique individuals merged with the two eggs.
In the United States, where the dominant culture is such that people who are trying to get pregnant are exhorted not to mate with multiple individuals, studies conducted in the 1990s found that at least one set of every few hundred twins had separate fathers (termed “heteropaternal superfecundication”). In these cases, the children almost certainly had genomes derived from the genetic contributions of three separate people (although each individual cell in the children’s bodies would have a genome derived from only two genetic contributors).
So, we actually know that partible paternity is real. Because it’s so difficult to notice, our current estimates are probably lower bounds. If 1:400 were the rate among live twins, probably that many dizygotic pregnancies in the United States also result from three or more genetic contributors. Probably this frequency is higher in cultures that celebrate rather than castigate this practice.
Honestly, I could be persuaded that estimates ranging anywhere from 1:20 to 1:4,000 were reasonable for the frequency that individuals from these cultures have three or more genetic contributors.** We just don’t know.
I agree with Gabriel Andrade that we’d like for medical students who grew up believing in partible paternity to benefit from our scientific understanding of genetics and inheritance – this scientific knowledge will help them help their patients. But I also believe that, even in this extreme case, the traditional knowledge should be respected. It’s not as inaccurate as we might reflexively believe!
The scientific uncertainty I’ve described above doesn’t quite match the traditional knowledge, though. A person can only receive genetic inheritance from, ahem, mating events that happen during ovulation, whereas partible paternity belief systems also treat everyone who has sex with the pregnant person over the next few months as a parent, too.
But there’s a big difference between contributing genes and being a parent. In Our Transgenic Future: Spider Goats, Genetic Modification, and the Will to Change Nature, Lisa Jean Moore discusses the many parents who have helped raise the three children she conceived through artificial insemination. Even after Moore’s romantic relationships with some of these people ended, they remained parents to her children. The parental bond, like all human relationships, is created by the relationship itself.
This should go without saying, but: foster families are families. Adopted families are families. Families are families.
Partible paternity is a belief that makes itself real.
** A note on the math: Dizygotic fertilization appears to account for 1:10 human births, and in each of these cases there is probably at least some degree of chimerism in the resulting child. My upper estimate for the frequency that individuals have three or more genetic contributors, 1:20, would be if sperm from multiple individuals had exactly equal probabilities of fertilizing each of the two egg cells. My lower estimate of 1:4,000 would be if dizygotic fertilization from multiple individuals had the same odds as the 1:400 that fraternal twin pairs in the U.S. have distinct primary genetic contributors. Presumably a culture that actively pursues partible paternity would have a higher rate than this, but we don’t know for sure. And in any case, these are large numbers! Up to 5% of people from these cultures might actually have three or more genetic contributors, which is both biologically relevant and something that we’d be likely to overlook if we ignored the traditional Indigenous knowledge about partible paternity.
header image from Zappy’s Technology Solution on flickr
The Supreme Court is considering whether to overturn the standing decisions from Roe v. Wade (1973) and Planned Parenthood v. Casey (1992). The majority opinions in those cases guaranteed … um, actually, quite little?
Soon, those opinions might guarantee even less!
Justice Sonia Sotomayor is worried that the Supreme Court might lose its aura of legitimacy.
Justice Sotomayor said, “Will this institution survive the stench that [overturning Roe v. Wade would create] in the public perception that the Constitution and its readings are just political acts? I don’t see how it is possible.”
This is actually a major reason why Roe v. Wade wasn’t overturned previously. In a recent essay on Planned Parenthood v. Casey, ACLU legal director David Cole writes that “As the three then-recently Republican-appointed justices … warned in 1992, overruling Roe would do ‘profound and unnecessary damage to the Court’s legitimacy and to the Nation’s commitment to the rule of law.’ That is only more true today.”
And, look: I’m pro-choice. I would prefer for anti-abortion laws like those recently enacted in Texas and Mississippi to be revoked.
But also: the idea that our Supreme Court might lose some of its power makes me quite pleased!
In our country, there are ostensibly three equal branches of government to balance each other.
Which sounds like a nifty design! Barstools often have three legs because any three points define a plane (unless they’re all on the same line), so three-legged stools are rarely tippy. Quite helpful when the sitter might be tipsy!
But something’s gone wrong with our government.
The recently-ritualized filibusterer system of our legislative branch that allows any proposal to be passively smothered, often by senators who represent fewer people than live in single neighborhoods of major cities. The post-9/11 domestic spying and drone strike assassinations from our executive branch. These are strange aberrations!
The worst offender, though, is probably our judiciary. Over many years, our Supreme Court justices have steadily commandeered more power, and the system is untenable.
Unfortunately, our Supreme Court justices are incompetent.
This isn’t really their fault!
And I happen to think that several of them are clever, kind-hearted people. I really liked when Justice Sotomayor’s minority opinion for Utah v. Strieff included a reading list to help people who hadn’t noticed the lingering ramifications of institutional racism in our country.
That was grand!
But for our Supreme Court justices to form meaningful opinions about the whole range of cases that come before them, they should understand computers, artificial intelligence, psychology, sociology, economics, biology, medicine … and, they don’t.
To be nominated for a seat on the Supreme Court, a person instead needs to have specialized in our country’s adversarial system of law. Which means, due to time constraints, that they probably won’t have an adequate understanding of many vital subjects.
Worse, the one subject that they did specialize in – adversarial law – isn’t even helpful! Immersion in this style of thought probably makes people less suited to serve on the Supreme Court. As law professor Sarah A. Seo wrote in a recent essay on public defenders, “Adversarialism is not inherent to justice – it’s simply one way of administering it.”
Even if the adversarial arguments mattered – if, for instance, we lived in an alternate universe where the judges were such flexibly-minded people that they allowed themselves to be persuaded in court, that we couldn’t predict how they were going to vote well before any arguments had been presented – the idea of “justice” arising from competition instead of justice by collaboration is a foolish way to run a country.
Often, people refer to Roe v. Wade in shorthand, suggesting that the decision guarantees a right to privacy, perhaps, or more specifically a right to abortion.
Instead, the majority opinion for Roe v. Wade says that “Though the State cannot override [the right to privacy, including a woman’s qualified right to terminate her pregnancy], it has legitimate interests in protecting both the pregnant woman’s health and the potentiality of human life, each of which interests grows and reaches a ‘compelling’ point at various stages of the woman’s approach to term.”
There are two conflicting rights, and the majority opinion is proposing a guideline for their balance. This is quite common. We balance people’s privacy against the state’s interest in preventing crime. We balance manufacturers’ desire to pollute with other people’s desire to breathe clean air or drink clean water.
In Roe v. Wade, the justices were balancing women’s bodily autonomy against the state’s interest in protecting the health of possible future citizens.
The justices concluded that: “For the stage subsequent to [fetal] viability the State, in promoting its interest in the potentiality of human life, may, if it chooses, regulate, and even proscribe, abortion except where necessary, in appropriate medical judgment, for the preservation of the life or health of the mother.”
When conservative commentators describe Roe v. Wade as a terrible ruling, I’m inclined to agree with them.
Yes, the three new Supreme Court justices – the stolen seat, the attempted rapist, & the hypocritical election’s-eve appointment – would like to overturn Roe v. Wade. But they hardly even need to! The existing opinion already does so little to protect women’s rights!
A large section of the ruling for Roe v. Wade discusses ancient attitudes toward abortion.
This discussion is markedly incomplete. Supreme Court justices simply don’t know enough to make their rulings! And there’s not a great solution to this, since very few possible groupings of nine people would include enough expertise to handle all the cases on a year’s Supreme Court docket.
Abortion has long been a common practice – healers and midwives in many cultures knew which local plants were arbotifacients. And any discussion of ancient attitudes toward abortion should also discuss infanticide.
Infanticide was common during recorded history. Based on studies of surviving hunter-gatherer cultures, we also have reason to suspect that infanticide was even more common in our species’s prehistory. In relatively recent times, if a baby was carried to term and then given up for adoption – perhaps left upon the doorstep or a church or monastery – there was significant risk of death. Amid high childhood mortality, a baby separated from the mother would face especially grim odds.
Compared to other primates, human mothers form emotional bonds to a child relatively late in development. Among our evolutionary cousins, it’s rare for a mother to allow any individual (not the baby’s father, not her own mother, not her other children) to even touch her baby. A full year might pass before the mother could bear the sight of her baby in another caregiver’s arms.
There are huge benefits that human mothers are less protective – shared child-rearing cements trust between adults, allows for our babies to be born earlier in biological development (essential given the size of our brains!), and leads to more attentive lifetime care.
Plus, this evolutionary history has made human babies so cute! Our offspring wouldn’t giggle and coo – behaviors that delight a potential caregiver – if they relied only upon irrevocable maternal love in order to survive. Chimpanzees are born cute – in their first few moments, they need to delight their mothers – but their tendency to giggle or mirror facial expressions fades within the first week or so. Unlike human babies, they aren’t constantly prepared to woo a new adult.
But human delay in attachment also made abortion and infanticide more acceptable to our species. In many hunter-gatherer societies, any child who could not be cared for would be abandoned. Other great apes are actually far more likely to care for a developmentally-disabled child than are human hunter gatherers.
In many societies, personhood wasn’t attained until age five or six, at which time a naming ceremony would be held. It was considered bad luck to name a child sooner, or to feel too attached before that date.
Of course, most families probably still did feel attached. There can be a stark difference between private affection and public nonchalance, a play act to ward off bad luck.
In terms of the rights at stake in Roe v. Wade, though, all these historical considerations are mostly irrelevant. Yes, that’s the science – findings from nature. But nature isn’t good or bad. Nature isn’t ethical. The natural world simply is, whereas ethics demands that we think about how the world should be. Reading the majority opinion for Roe v. Wade, it seems like these topics were introduced only to make the conclusion seem scientific or better reasoned.
In the end, the majority opinion is based solely on medical technology: the State can ban abortion at the age when a baby could survive outside a woman’s body.
Not would. And certainly not will.
“For the stage subsequent to viability the State … may proscribe abortion … “
In an age when being a good parent means being as attentive as possible even before birth, we want better access to the babies growing inside pregnant women, better ways of measuring them and putting them under surveillance, so we can do the best for them even before they enter the world. Women’s bodies are almost getting in the way.
Ultrasound images show how much female bodies are already seen as vestigial in reproductive medicine.
“I’ve been arguing for years, don’t show pictures of fucking developing fetuses unless you show the entire woman’s body,” [says Soraya Chemaly.]
“I understand people getting pregnant and being excited, but I’m the terrible feminist killjoy; I’m like, ‘Oh, that’s nice, why don’t we just make it bigger?’ Ultrasound was very deliberately developed to show the fetus as though it were a planet in a void, in a vacuum, in a container, in a jar. A wallpaper of blackness around it. It completely erases the woman whose body is generative.”
For a human baby to be born, a parent must make an enormous gift. Feeding and protecting and creating the gestating fetus over many months.
Currently, there’s no other way.
Currently, it’s impossible to combine a sperm cell and an egg cell in the laboratory, create an embryo, then provide the necessary nutrients and environment for that embryo to develop into a fetus, a baby, a child.
This would be a challenging project!
But not impossible.
Researchers will eventually be able to create a viable human child this way.
An act that would, per Roe v. Wade, instantly erase women’s rights.
Maybe this experiment would cost hundreds of millions of dollars. So what? For Supreme Court rulings, cost is irrelevant. They’ve made this clear in their decisions for many recent cases.
Our Supreme Court decided that anonymously-chartered corporations have as much right to free speech as individuals – as though they weren’t already privileged with more speech, since wealth can be used to purchase expensive advertisements, think tanks, unscrupulous academics.
Our Supreme Court decided that the police can legitimately spy on you with any technologies that are publicly available, even if these technologies – like infrared cameras to visualize your body through the walls of your home, or telescoping lenses to peer into your windows from a distance, or a steady helicopter to linger overhead and watch you from unexpected angles – are far outside the budgets (and therefore expectations) of most private citizens.
It’s quite convenient that the justices so often fail to notice people’s wealth! (Or lack thereof.) Abortion laws were never really intended to target wealthy people, anyway. Wealthy people could either travel out of state or pay off a doctor to certify that an abortion met “appropriate medical judgment for the preservation of the life or health of the mother.”
If researchers spent hundreds of millions of dollars to nurture one embryo into a viable human baby – in a laboratory anywhere around the world – then the principle of fetal viability cited in Roe v. Wade would allow states to outlaw all abortion. Even though the material facts of women’s lives would be unchanged.
This is, after all, the problem with trying to slap scientific justifications onto a philosophical argument. Whether or not women should have bodily autonomy is a philosophical question. I think that they should. Our steadily increasing technological prowess shouldn’t change that.
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.
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.
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.
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.
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.
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.
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.
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?
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.
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.
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.
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.
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.
I live in a college town. Last week, students returned.
Yesterday’s paper explains that dire punishment awaits the students who attended a Wednesday night party. In bold letters atop the front page, “IU plans to suspend students over party.”
In the decade that I’ve lived here, many parties have led to sexual assaults, racist hate speech, and violence. The offending students were rarely punished. But this party was egregious because “there were about 100 people there.”
IU officials “have seen a photo … that shows a large group of young people standing close together outside a house at night, many of them not wearing masks.”
I’ve seen the images – someone filmed a video while driving by. There they are – a group of young people, standing outside.
Science magazine recently interviewed biologist Dana Hawley about social distancing in the animal kingdom.
When spiny lobsters are sick, their urine smells different. Healthy lobsters will flee the shared den. Leaving is dangerous, since the lobsters will be exposed to predators until they find a new home, but staying would be dangerous, too – they might get sick. To survive, lobsters have to balance all the risks they face.
My favorite example of social distancing in the animal kingdom wasn’t discussed. When an ant is infected with the cordyceps fungus, it becomes a sleeper agent. Jennifer Lu writes in National Geographic that “as in zombie lore, there’s an incubation period where infected ants appear perfectly normal and go about their business undetected by the rest of the colony.”
Then the fungus spreads through the ants body, secreting mind control chemicals. Eventually, the fungus will command the infected ant to climb to a high place. A fruiting body bursts from the ant’s head and rains spores over the colony.
Infection is almost always lethal.
If an ant notices that a colony member has been infected, the healthy ant will carry the infected ant away from the colony and hurl it from a cliff.
The herd immunity threshold isn’t an inherent property of a virus – it depends upon our environment and behaviors. In prisons, we’ve seen Covid-19 spread until nearly 90% of people were infected. In parts of New York City where many essential workers live in crowded housing, Covid-19 spread until 50% of people were infected.
In a culture where everyone kissed a sacred statue in the center of town each morning, the herd immunity threshold would be higher. If people wear masks while interacting with strangers, the herd immunity threshold will be lower.
In a world that maintains a reservoir of the virus, though, someone who hasn’t yet been exposed will always be at risk.
The New York Times recently discussed some of the challenges that colleges face when trying to reopen during the epidemic.
Most schools ban … socializing outside “social pods” – the small groups of students that some colleges are assigning students to, usually based on their dorms.
Most administrators seem to believe that a rule banning sex is unrealistic, and are quietly hoping that students will use common sense and refrain from, say, having it with people outside their pod.
In 2012, The Huffington Post published a list of the “Top 10 sex tips for college freshmen.” Their fourth piece of advice (#1 and #2 were condoms, #3 was not having sex while drunk) is to avoid having sex with people who live too close to you. “Students in other dorms = fair game. Students in same dorm = proceed with caution.”
I had a big group of friends for my first two years of college. After a breakup, I lost most of those friends.
This is crummy, but it would be much worse if I’d lost my friendships with the only people whom the administrators allowed me to spend time with.
We can slow the spread of Covid-19, but slowing the spread won’t prevent deaths, not unless we can stave off infection until there is a highly effective vaccine. That might take years. We might never have a highly effective vaccine – our influenza vaccines range in efficacy from about 20% to 80%, and we have much more experience making these.
Our only way to reduce the eventual number of deaths is to shift the demographics of exposure. If we reach the herd immunity threshold without many vulnerable people being exposed, we’ll save lives.
A college would best protect vulnerable students and faculty by allowing the students who are going to socialize to host dense parties for a few weeks before mingling with others. This would allow the virus to spread and be cleared before there was a risk of transferring infections to vulnerable people.
I’d draft a waiver. Are you planning to socialize this semester? If so, come do it now! By doing so, you will increase your risk of contracting Covid-19. This is a serious disease – it’s possible for young, healthy people to die from it. But, look, if you’re gonna socialize eventually, please just get it over with so that you don’t endanger other people.
With this plan, some young people might die of Covid-19. But some young people will die of Covid-19 even if everyone practices social distancing – slowing the spread of infections doesn’t save lives, it delays deaths. And fewer young people would die of Covid-19 than die of influenza each year.
When confronting cordyceps, which is almost always fatal, ants throw sick colony members off cliffs.
When ants confront less lethal fungal infections, they protect the colony by shifting the demographics of exposure and by ramping up to the herd immunity threshold as quickly as possible.
Malagocka et al. discuss demographics in their review article, “Social immunity behavior among ants infected by specialist and generalist fungi.”
Outside-nest foragers, who have the highest risks of acquiring pathogens from the environment, have limited access to the brood area with the most valuable groups, and are recruited from older individuals, who are less valuable from the colony survival perspective.
Konrad et al. discuss intentional exposure in their research article, “Social transfer of pathogenic fungus promotes active immunization in ant colonies.”
When worker ants encounter an infected colony member, they intentionally inoculate themselves. “Social immunization leads to faster elimination of the disease and lower death rates.”
It feels disquieting for me to defend the behavior of frat guys. Personally, I’d like to see the whole fraternity system abolished. And in March, when we knew less about Covid-19, I was appalled that people went out partying over spring break. But I was wrong. Perhaps inadvertently, those young people were behaving in the way that would save most lives.
the nurse called back and told us to use bleach on anything we touch, she said wash everything in hot water, insisted we won’t treat you if you’re asymptomatic, we won’t, and made us an appointment anyway. so we waited and waited with the dog-eared magazines and recall posters
It’s horrible to face the end. It’s almost worse to know that the things you fear are harmless to others. All the asymptomatic cases are like a slap in the face to those whose friends and family have died.
Braun et al. recently published a study in Nature showing that a large number of people who’ve never encountered Covid-19 may already have significant immunity. Parts of the Covid-19 virus are similar to the viruses that cause common colds, and exposure to those viruses might provide the immunity that lets people recover without ever feeling sick.
I believe we should be doing more to protect young people. Gun control, ending farm subsidies, fighting climate change. Enacting privacy laws to reign in the surveillance capitalists. Breaking up monopolies. Providing good careers despite automation. Making sure that everyone has clean air to breathe and clean water to drink. Getting nutritious food into our nation’s many food deserts. Providing equitable access to health care.
But, punishing young people for socializing?
We’re not making them safer. And we’re not making ourselves safer, either.
Seriously, I know we humans are selfish, but we have to be able to handle an epidemic better than ants.
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.”
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.
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.
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 Naturearticle.
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.
2: “We know that the current shutdown is either delaying or preventing deaths due to Covid-19.”
To date, the data suggests that the virus has only reached saturation inside a few closed environments, such as prisons. In Italy, both the timecourse of mortality and the results of antibody studies suggest that infections were still rising at the time of their lockdown.
Among the passengers of the Diamond Princess cruise ship, deaths peaked 21 days after infections peaked – if the virus had already reached saturation in Italy, we’d expect to see deaths peak sooner than 21 days after the lockdown began. They did not.
So, again, this much is clear: worldwide, there was a significant new cause of death. When we look at mortality data, we see the curves suddenly rise in many locations. Some researchers, such as John Ioannidis, have speculated that Covid-19 causes death primarily in people with low life expectancy, in which case we would expect to see these mortality curves drop to lower-than-average levels after the epidemic ends. But even then, it’s unprecedented to see a number of deaths that would usually occur over the course of a year all within a matter of weeks.
Covid-19 is killing people, and the shutdown is either delaying or preventing people’s death from Covid-19.
For the shutdown to actually prevent death, one of the following needs to happen:
1.) We create a vaccine, allowing our population to reach 70% immunity without as many people contracting the illness.
2.) We take action to change which segment of the population is exposed to the virus, allowing us to reach 70% immunity without as many at-risk people being exposed.
See #3 and #4, below.
3: “Ending this epidemic with a vaccine would be ideal.”
Vaccination is great science. Both my spouse and I love teaching about vaccines, in part because teaching the history of vaccine use is a good component of anti-racist science class.
Developing vaccines often takes a long time. I’ve read predictions of a year or two; my father, an infectious disease doctor, epidemiologist, research physician who runs vaccine trials, and co-developer of Merck’s HPV vaccine, guesses that it will take about five years.
And then, for the vaccine to end this epidemic, enough people will need to choose to be vaccinated that we reach approximately 70% immunity.
The reason it’s worthwhile to compare Covid-19 to seasonal influenza is that a vaccine will only end the epidemic if enough people choose to get it. Many people’s personal risk from Covid-19 is lower than their risk from seasonal influenza. Will those people choose to be vaccinated?
Obviously, I would be thrilled if the answer were “yes.” I’d love to live in a nation where people’s sense of altruism and civic duty compelled them to get vaccinated. My family is up-to-date on all of ours.
But many privileged families in the United States have elected to be freeloaders, declining the (well tested, quite safe) measles vaccine with the expectation that other people’s immunity will keep them safe. And, despite the well-documented dangers of influenza, only 40% of our population gets each year’s influenza vaccine.
A vaccine with low efficacy will still offer better protection when more people get it. If a higher percentage of our population were vaccinated against influenza, then influenza transmission would drop, and so each person’s immunity, whether high or low, would be less likely to be challenged.
The influenza vaccine saves lives. In Italy, where fewer people choose to get vaccinated against influenza (about 15% compared to our 40% of the population), the death rate from influenza is higher. Although it’s worth noting that this comparison is complicated by the fact that our health care system is so bad, with poor people especially having limited access to health care. In the United States, people between the ages of 18 and 49 comprise a higher proportion of influenza deaths than anywhere in Europe. Either our obesity epidemic or limited access to health care is probably to blame; possibly a combination of both.
In summary, for this plan to help us save lives, we will need to develop an effective vaccine, and then people will have to get it.
I am quite confident that we can eventually develop a vaccine against Covid-19. The virus includes a proofreading enzyme, so it should mutate more slowly than most RNA viruses. We don’t know how long it will take, but we can do it.
I am unfortunately pessimistic that people will choose to get the vaccine. And, unfortunately, when a low-risk person chooses to forgo vaccination, they’re not just putting themselves in harm’s way, they are endangering others. Most vaccines elicit a weaker immune response in elderly or immunocompromised recipients – exactly the group most at risk from Covid-19 – which is why we spend so much time harping about herd immunity.
4: “Ending the shutdown while requesting that at-risk people continue to self-isolate would save lives.“
This plan has major downsides, too. Because we didn’t take action soon enough, every plan we have now is bad.
Low-risk people can still die of Covid-19. Even if they don’t die, Covid-19 can cause permanent health effects. Covid-19 reduces your ability to get oxygen to your body and brain. Even a “mild” case can leave your breathing labored for weeks – you’re not getting enough oxygen. Your muscles will ache. Your thoughts will be sluggish.
With a more severe case, people can be looking at heart damage. Renal failure. It would be cruel to look at all these long-term consequences and blithely call them “recovery.”
If our health care system were better, we’d treat people sooner. The earlier you intervene, helping to boost people’s oxygen levels, the better outcome you’ll have. There’s a great editorial from medical doctor Richard Levitan recommending that people monitor their health with a pulse oximeter during this epidemic.
If you notice your oxygen levels declining, get help right away. Early intervention can prevent organ damage. And you’ll be helping everyone else, too – the sooner you intervene, the less medical care you will need.
Because medical debt can derail lives, many people in this country delay treatment as long as possible, hoping that their problems will go away naturally. That’s why people are often so sick when they show up at the ER. I imagine that this is yet another reason – alongside air pollution, food deserts, sleep loss, and persistent stress exacerbated by racism – that poor communities have had such a high proportion of people with severe cases of Covid-19.
And I imagine – although we don’t yet have enough data to know – that financial insecurity caused by the shutdown is making this worse. It’s a rotten situation: you have a segment of population that has to continue working during the shutdown, which means they now have the highest likelihood to be exposed to the virus, and they’re now under more financial strain, which might increase the chance that they’ll delay treatment.
We know that early treatment saves lives, and not everyone is sufficiently privileged to access that.
All this sounds awful. And it is. But, if we took action to shift exposure away from high risk groups, the likelihood that any individual suffers severe consequences is lower.
And there is another caveat with this plan – some people may be at high risk of complications for Covid-19 and not even realize it. In the United States, a lot of people either have type 2 diabetes or are pre-diabetic and don’t yet realize. These people have elevated risk. Both smoking and airpollution elevate risk, but people don’t always know which airborn pollutants they’ve been exposed to. (Which, again, is why it’s particularly awful that our administration is weakening air quality standards during this epidemic.)
Even if we recommended continued self-isolation for only those people who know themselves to have high risk from Covid-19, though, we would be saving lives. The more we can protect people in this group from being exposed to the virus – not just now, but ever – the more lives we will save.
We won’t be able to do this perfectly. It’ll be a logistical nightmare trying to do it at all. People at high risk from Covid-19 needs goods and services just like everybody else. We might have to give daily Covid-19 PCR tests to anyone visiting their homes, like doctors, dentists, and even delivery workers.
At that point, the false negative rate from Covid-19 PCR tests becomes a much bigger problem – currently, these false negatives reduce the quality of our data (but who cares?) and delay treatment (which can be deadly). A false negative that causes inadvertent exposure could cost lives.
Some people will be unable to work, either because they or a close relative has high risk of Covid-19. Some children will be unable to go to school. We will need a plan to help these people.
We will have to work very hard to keep people safe even after the shutdown ends for some.
But, again, if everyone does the same thing, then the demographics of people infected with Covid-19 will reflect our population demographics. We can save lives by skewing the demographics of the subset of our population that is exposed to Covid-19 to include more low-risk individuals, which will require that we stratify our recommendations by risk (at least as well as we can assess it).
5: “Why is it urgent to end the shutdown soon?“
1.) By delaying Covid-19 deaths, we run to risk of causing more total people to die of Covid-19.
2.) The shutdown itself is causing harm.
See #6 and #7, below.
6: “Why might more people die of Covid-19 just because we are slowing the spread of the virus?“
[EDIT: I wrote a more careful explanation of the takeaways of the Harvard study. That’s here if you would like to take a look!]
This is due to the interplay between duration of immunity and duration of the epidemic. At one point in time, seasonal influenza was a novel zoogenic disease. Human behavior allowed the influenza virus to become a perpetual burden on our species. No one wants for humans to still be dying of Covid-19 in ten or twenty years. (Luckily, because the virus that causes Covid-19 seems to mutate more slowly than influenza, it should be easier to design a single vaccine that protects people.)
In the Harvard model, we can see that there are many scenarios in which a single, finite shutdown leads to more deaths from Covid-19 than if we’d done nothing. Note the scenarios for which the colored cumulative incidence curves (shown on the right) exceed the black line representing how many critical cases we’d have if we had done nothing.
Furthermore, their model does not account for people’s immunity potentially waning over time. Currently, we do not know how long people’s immunity to Covid-19 will last. We won’t know whether people’s immunity will last at least a year until a year from now. There’s no way to test this preemptively.
If we could all go into stasis and simply not move for about a month, there’d be no new cases of Covid-19, and this virus would be gone forever. But people still need to eat during the shutdown. Many people are still working. So the virus is still spreading, and we have simply slowed the rate of transmission.
This seems good, because we’re slowing the rate at which people enter the hospital, but it’s actually bad if we’re increasing the number of people who will eventually enter the hospital.
Based on our research with other coronaviruses, we expect that re-infection will cause a person to experience symptoms less severe than their first case of Covid-19. But a re-infected person can still spread the disease to others. And we don’t know what will happen if a person’s risk factors – such as age, smoking status, diabetes status, etc. – have increased in the time since their last infection.
7: “How is the shutdown causing harm?“
If you turn on Fox News, I imagine you’d hear people talking about the damage we’re doing to our economy. They might discuss stock market numbers.
Who gives a shit? In my opinion, you’d have to be pretty callous to think that maintaining the Nasdaq bubble is more important than saving lives.
In this report, they estimate that the shutdown we’ve had so far will cause hundreds of thousands of children to die, many from malnutrition and the other health impacts of poverty. The longer the shutdown continues, the more children will die.
That’s a worldwide number, and most of those children live outside the United States. But I’d like to think that their lives matter, too.
The report also discusses the lifelong harm that will be inflicted on children from five months (or more!) of school closure. Drop-outs, teen pregnancy, drug abuse, recruitment of child soldiers, and the myriad health consequences of low educational attainment.
I live in a wealthy college town, but even here there is a significant population of students who don’t have internet access. Students with special needs aren’t getting the services they deserve. Food insecurity is worse.
You’re lucky that privacy protections prevent me from sharing a story about what can happen to poor kids when all the dentists’ offices are closed. I felt ashamed that this was the best my country had to offer.
As the shutdown continues, domestic violence is rising. We can assume that child abuse is rising, also, but we won’t know until later, when we finally have a chance to save children from it. In the past, levels of child abuse have been correlated with the amount of time that children spend in the presence of their abusers (usually close family), and reporting tends to happen during tense in-person conversations at school.
The shutdown has probably made our drug epidemic worse (and this was already killing about 70,000 people per year in the U.S.). When people are in recovery, one of the best strategies to stay sober is to spend a lot of time working, out of the house, and meeting with a supportive group in communal space. Luckily, many of the people I know who are in recovery have been categorized as essential workers.
A neighbor recently sent me a cartoon suggesting that the biggest harm caused by the shutdown is boredom. (I’m going to include it, below, but don’t worry: I won’t spend too much time rattling sabers with a straw man.) And, for privileged families like mine, it is. We’re safe, we’re healthy, we get to eat. My kids are still learning – we live in a house full of computers and books.
But many of the 75 million children in the United States don’t live in homes like mine, with the privilege we have. Many of our 50 million primary and secondary school students are not still learning academically during the shutdown.
Whether the shutdown is preventing or merely delaying the deaths of people at risk of serious complications from Covid-19, we have to remember that the benefit comes at a cost. What we’ve done already will negatively impact children for the rest of their lives. And the longer this goes on, the more we’re hurting them.
8: “What about the rate at which people get sick? Isn’t the shutdown worthwhile, despite the risks described above, if it keeps our hospitals from being overwhelmed?“
In writing this, I struggled with how best to organize the various responses. I hope it doesn’t seem too ingenuous to address this near the end, because slowing the rate of infection so that our hospitals don’t get overwhelmed is the BEST motivation for the shutdown. More than the hope that a delay will yield a new vaccine, or new therapies to treat severe cases, or even new diagnostics to catch people before they develop severe symptoms, we don’t want to overwhelm our hospitals.
If our physicians have to triage care, more people will die.
And I care a lot about what this epidemic will be like for our physicians. My father is a 67-year-old infectious disease doctor who just finished another week of clinical service treating Covid-19 patients at the low-income hospital in Indianapolis. My brother-in-law is an ER surgeon in Minneapolis. These cities have not yet had anything like the influx of severe cases in New York City – for demographic and environmental reasons, it’s possible they never will. But they might.
Based on the case fatality rate measured elsewhere, I’d estimate that only 10% of the population in Minneapolis has already been infected with Covid-19, so the epidemic may have a long way yet to go.
If we ended the shutdown today for everyone, with no recommendation that at-risk groups continue to isolate and no new measures to protect them, we would see a spike in severe cases.
If we ended the shutdown for low-risk groups, and did a better job of monitoring people’s health to catch Covid-19 at early, more-easily-treatable stages (through either PCR testing or oxygen levels), we can avoid overwhelming hospitals.
And the shutdown itself is contributing toward chaos at hospitals. Despite being on the front lines of this epidemic, ER doctors in Minneapolis have received a 30% pay cut. I imagine my brother-in-law is not the only physician who could no longer afford day care for his children after the pay cut. (Because so many people are delaying care out of fear of Covid-19, hospitals are running out of money.) Precisely when we should be doing everything in our power to make physicians’ lives easier, we’re making things more stressful.
We could end the shutdown without even needing to evoke the horrible trolley-problem-esque calculations of triage. Arguments could be made that even if it led to triage it might be worthwhile to end the shutdown – the increase in mortality would be the percentage of triaged cases that could have survived if they’d been treated, and we as a nation might decide that this number was acceptable to prevent the harms described above – but with a careful plan, we need not come to that.
9: “Don’t the antibody tests have a lot of false positives?“
False positives are a big problem when a signal is small. I happen to like a lot of John Ioannidis’s work – I think his paper “Why Most Published Research Findings Are False” is an important contribution to the literature – but I agree that the Santa Clara study isn’t particularly convincing.
When I read the Santa Clara paper, I nodded and thought “That sounds about right,” but I knew my reaction was most likely confirmation bias at work.
Which is why, in the essay, I mostly discussed antibody studies that found high percentages of the population had been infected with Covid-19, like the study in Germany and the study in the Italian town of Robbio. In these studies, the signal was sufficiently high that false positives aren’t as worrisome.
In Santa Clara, when they reported a 2% infection rate, the real number might’ve been as low as zero. When researchers in Germany reported a 15% infection rate, the real number might’ve been anywhere in the range of 13% to 17% – or perhaps double that, if the particular chips they used had a false negative rate similar to the chips manufactured by Premier Biotech in Minneapolis.
I’m aware that German response to Covid-19 has been far superior to our bungled effort in the United States, but an antibody tests is just a basic ELISA. We’ve been doing these for years.
Luckily for us, we should soon have data from good antibody studies here in the United States. And I think it’s perfectly reasonable to want to see the results of those. I’m not a sociopath – I haven’t gone out and joined the gun-toting protesters.
But we’ll have this data in a matter of weeks, so that’s the time frame we should be talking about here. Not months. Not years. And I’ll be shocked if these antibody studies don’t show widespread past infection and recovery from Covid-19.
10: “What about the political ramifications of ending the shutdown?“
I am, by nature, an extremely cautious person. And I have a really dire fear.
I’m inclined to believe that ending the shutdown is the right thing to do. I’ve tried to explain why. I’ve tried to explain what I think would be the best way to do it.
But also, I’m a scientist. You’re not allowed to be a scientist unless you’re willing to be proven wrong.
So, yes. I might be wrong. New data might indicate that writing this essay was a horrible mistake.
Still, please bear with me for a moment. If ending the shutdown soon turns out to be the correct thing to do, and if only horrible right-wing fanatics have been saying that we should end the shutdown soon, won’t that help our current president get re-elected?
There is a very high probability that his re-election would cause even more deaths than Covid-19.
Failing to address climate change could kill billions. Immigration controls against migrants fleeing war zones could kill millions. Weakened EPA protections could kill hundreds of thousands. Reduced access to health care could kill tens of thousands.
And, yes, there are horrible developments that neither major political party in the United States has talked about, like the risk that our antibiotics stop working, but I think it’s difficult to argue that one political party isn’t more dangerous than the other, here.
I feel pretty confident about all the scientific data I’ve discussed above. Not as confident as I’d like, which would require more data, but pretty confident.
I feel extremely confident that we need to avoid a situation in which the far right takes ownership of an idea that turns out to have been correct. And it’ll be dumb luck, just a bad coincidence. The only “data” they’re looking at are stock market numbers, or maybe the revenue at Trump-owned hotels.
EDIT: I also wrote a more careful explanation of the takeaways of the Harvard study. That’s here if you would like to take a look!
First, some background: in case you haven’t noticed, most of the United States is operating under a half-assed lockdown. In theory, there are stay-at-home orders, but many people, such as grocery store clerks, janitors, health care workers, construction workers, restaurant chefs, delivery drivers, etc., are still going to work as normal. However, schools have been closed, and most people are trying to stand at least six feet away from strangers.
We’re doing this out of fear that Covid-19 is an extremely dangerous new viral disease. Our initial data suggested that as many as 10% of people infected with Covid-19 would die.
That’s terrifying! We would be looking at tens of millions of deaths in the United States alone! A virus like this will spread until a majority of people have immunity to it – a ballpark estimate is that 70% of the population needs immunity before the epidemic stops. And our early data suggested that one in ten would die.
My family was scared. We washed our hands compulsively. We changed into clean clothes as soon as we came into the house. The kids didn’t leave our home for a week. My spouse went to the grocery store and bought hundreds of dollars of canned beans and cleaning supplies.
And, to make matters worse, our president was on the news saying that Covid-19 was no big deal. His nonchalance made me freak out more. Our ass-hat-in-chief has been wrong about basically everything, in my opinion. His environmental policies are basically designed to make more people die. If he claimed we had nothing to worry about, then Covid-19 was probably more deadly than I expected.
Five weeks have passed, and we now have much more data. It seems that Covid-19 is much less dangerous than we initially feared. For someone my age (37), Covid-19 is less dangerous than seasonal influenza.
Last year, seasonal influenza killed several thousand people between the ages of 18 and 49 in the United States – most likely 2,500 people, but perhaps as many as 5,800. People in this age demographic account for about 10% of total flu deaths in the United States, year after year.
Seasonal influenza also killed several hundred children last year – perhaps over a thousand.
There’s a vaccine against influenza, but most people don’t bother.
Seasonal influenza is more dangerous than Covid-19 for people between the ages of 18 and 49, but only 35% of them chose to be vaccinated in the most recently reported year (2018). And because the vaccination rate is so low, our society doesn’t have herd immunity. By choosing not to get the influenza vaccine, these people are endangering themselves and others.
Some people hope that the Covid-19 epidemic will end once a vaccine is released. I am extremely skeptical. The biggest problem, to my mind, isn’t that years might pass before there’s a vaccine. I just can’t imagine that a sufficient percentage of our population would choose to get a Covid-19 vaccine when most people’s personal risk is lower than their risk from influenza.
When I teach classes in jail, dudes often tell me about which vaccines they think are too dangerous for their kids to get. I launch into a tirade about how safe most vaccines are, and how deadly the diseases they prevent.
Seriously, get your kids vaccinated. You don’t want to watch your child die of measles.
And, seriously, dear reader – get a flu vaccine each year. Even if you’re too selfish to worry about the other people whom your mild case of influenza might kill, do it for yourself.
We already know how dangerous seasonal influenza is. But what about Covid-19?
To answer that, we need data. And one set of data is unmistakable – many people have died. Hospitals around the world have experienced an influx of patients with a common set of symptoms. They struggle to breathe; their bodies weaken from oxygen deprivation; their lungs accumulate liquid; they die.
For each of these patients saved, three others are consigned to an agonizing death in the hospital, intubated among the flashing lights, the ceaseless blips and bleeps. At home, they’d die in a day; in the hospital, their deaths will take three weeks.
And the sheer quantity of deaths sounds scary – especially for people who don’t realize how many tens of thousands die from influenza in the United States each year.
Indeed, when people die of Covid-19, it’s often because their lungs fail. Smoking is obviously a major risk factor for dying of Covid-19 – a significant portion of reported Covid-19 deaths could be considered cigarette deaths instead. Or as air pollution deaths – and yet, our current president is using this crisis as an opportunity to weaken EPA airquality regulations.
Air pollution is a huge problem for a lot of Black communities in the United States. Our racist housing policies have placed a lot of minority neighborhoods near heavily polluting factories. Now Covid-19 is turning what is already a lifelong struggle for breath into a death sentence.
I would enthusiastically support a shutdown motivated by the battle for clean air.
But if we want to know how scary this virus is, we need to know how many people were infected. If that many people died after everyone in the country had it, then Covid-19 would be less dangerous than influenza. If that many people died after only a hundred thousand had been infected, then this would be terrifying, and far more dangerous than influenza.
Initially, our data came from PCR testing.
These are good tests. Polymerase chain reaction is highly specific. If you want to amplify a certain genetic sequence, you can design short DNA primers that will bind only to that sequence. Put the whole mess in a thermocycler and you get a bunch of your target, as long as the gene is present in the test tube in the first place. If the gene isn’t there, you’ll get nothing.
PCR works great. Even our lovely but amnesiac lab tech never once screwed it up.
So, do the PCR test and you’ll know whether a certain gene is present in your test tube. Target a viral gene and you’ll know whether the virus is present in your test tube. Scoop out some nose glop from somebody to put into the test tube and you’ll know whether the virus is present in that nose glop.
The PCR test is a great test that measures whether someone is actively shedding virus. It answers, is there virus present in the nose glop?
This is not the same question as, has this person ever been infected with Covid-19?
It’s a similar question – most people infected with a coronavirus will have at least a brief period of viral shedding – but it’s a much more specific question. When a healthy person is infected with a coronavirus, the period of viral shedding can be as short as a single day.
A person can get infected with a coronavirus, and if you do the PCR test either before or after that single day, the PCR test will give a negative result. Nope, no viral RNA is in this nose glop!
And so we know that the PCR test will undercount the true number of infections.
When we look at the age demographics for Covid-19 infections as measured by PCR test, the undercount becomes glaringly obvious.
Friends, it is exceedingly unlikely that such a low percentage of children were exposed to this virus. Children are disgusting. I believe this is common knowledge. Parents of small children are pretty much always sick because children are so disgusting.
Seriously, my family has been doing the whole “social distancing” thing for over a month, and yet my nose is dripping while I type this.
Children are always touching everything, and then they rub their eyeballs or chew on their fingers. If you take them someplace, they grubble around on the floor. They pick up discarded tissues and ask, “What’s this?”
“That’s somebody’s gross kleenex, is what it is! Just, just drop it. I know it’s trash, I know we’re not supposed to leave trash on the ground, but just, just drop it, okay? Somebody will come throw it away later.”
The next day: “Dad, you said somebody would throw that kleenex away, but it’s still there!”
Bloody hell. Children are little monsters.
It seems fairly obvious that at least as high a percentage of children would be infected as any other age demographic.
But they’re not showing up from the PCR data. On the Diamond Princess cruise ship, the lockdown began on February 5th, but PCR testing didn’t begin until February 11th. Anyone who was infected but quickly recovered will be invisible to that PCR test. And even people who are actively shedding viral particles can feel totally well. People can get infected and recover without noticing a thing.
We see the same thing when we look at the PCR data from Italy. If we mistakenly assumed that the PCR data was measuring the number of infections, and not measuring the number of people who were given a PCR test while shedding viral particles, we’d conclude that elderly people went out and socialized widely, getting each other sick, and only occasionally infected their great-grandchildren at home.
Here in the United States, children are disgusting little monsters. I bet kids are disgusting in Italy, too. They’re disgusting all over the world.
A much more likely scenario is that children spread this virus at school. Many probably felt totally fine; some might’ve had a bad fever or the sniffles for a few days. But then they recovered.
When they got their great-grandparents sick – which can happen easily since so many Italian families live in multigenerational homes – elderly people began to die.
So we know that the PCR test is undercounting the true number of infections. Unless you’re testing every person, every day, regardless of whether or not they have symptoms, you’re going to undercount the number of infections.
In a moment, we can work through a way to get a more accurate count. But perhaps it’s worth mentioning that, for someone my age, Covid-19 would seem to be about as dangerous as influenza even if we assumed that the PCR data matched the true number of infections.
If you’re a healthy middle-aged or young person, you should not feel personally afraid.
That alone would not be an excuse to go out and start dancing in the street, though. Your actions might cause other people to die.
(NOTE & CORRECTION: After this post went up, my father recommended that I add something more about personal risk. No one has collected enough data on this yet, but he suspects that the next most important risk factor, after smoking and age, will be type 2 diabetes. And he reminded me that many people in their 30s & 40s in this country are diabetic or prediabetic and don’t even realize it yet. Everyone in this category probably has elevated risk of complications from Covid-19.)
After you’ve been infected with a virus, your body will start making antibodies. These protect you from being infected again.
Have you read Shel Silverstein’s Missing Piece book? Antibodies work kind of like that. They have a particular shape, and so they’ll glom onto a virus only if that virus has outcroppings that match the antibody’s shape. Then your body sees the antibodies hanging out on a virus like a GPS tracker and proceeds to destroy the virus.
So to make an antibody test, you take some stuff that looks like the outcroppings on the virus and you put it on a chip. Wash somebody’s blood over it, and if that blood contains antibodies that have the right shape to glom onto the virus, they’ll stick to the chip. All your other antibodies, the ones that recognize different viruses, will float away.
An antibody test is going to be worse than a PCR test. It’s easier to get a false positive result – antibodies are made of proteins, and they can unfold if you treat them roughly, and then they’ll stick to anything. Then you’ll think that somebody has the right antibodies, but they don’t. That’s bad.
You have to be much more careful when you’re doing an antibody test. I wouldn’t have asked our lab tech to do them for me.
An antibody test is also going to have false negatives. A viral particle is a big honking thing, and there are lots of places on its surface where an antibody might bind. If your antibodies recognize some aspect of the virus that’s different from what the test manufacturers included on their chip, your antibodies will float away. Even though they’d protect you from the actual virus if you happened to be exposed to it.
If you’re a cautious person, though – and I consider myself to be pretty cautious – you’d much rather have an antibody test with a bunch of false negatives than false positives. If you’re actually immune to Covid-19 but keep being cautious, well, so what? You’re safe either way. But if you think you’re immune when you’re not, then you might get sick. That’s bad.
Because antibody tests are designed to give more false negatives than false positives, you should know that it’d be really foolish to use them to track an infection. Like, if you’re testing people to see who is safe to work as a delivery person today, use the PCR test! The antibody test has a bunch of false negatives, and there’s a time lag between the onset of infection and when your body will start making antibodies.
If you use the antibody test on a bunch of people, though, you can tell how many were infected. And that’s useful information, too.
In the town of Robbio in Italy (pop. 6,000), the PCR test showed that only 23 people had been infected with Covid-19. But then the mayor implored everyone to get an antibody test, and 10% of people had actually been infected with – and had recovered from – Covid-19. Most of them couldn’t even recall having been sick.
I don’t know who made the tests used in Robbio – maybe they were a little better, maybe they were a little worse. Based on my experience, I wouldn’t be so surprised if the true infection rate with Covid-19 in that town was really just 10% – nor would I be surprised to hear that the chips had a high false-negative rate and that the infection rate was 20% or more.
If you calculate the fatality rate of Covid-19 in Italy by assuming that the PCR tests caught every infection, you’d get a terrifying 10%.
If you instead assume that many other towns had a similar infection rate to Robbio, you’ll instead calculate that the fatality rate was well under one percent.
Italy has higher risk than the United States due to age demographics, smoking rates, and multigenerational households – and even in Italy, the fatality rate was probably well under one percent.
When researchers in Germany randomly chose people to take a Covid-19 PCR test (many of whom had no symptoms), they found that 2% of the population was actively shedding virus – a much higher number of cases than they would have found if they tested only sick people. And when they randomly chose people to take an antibody test, they found that 15% had already recovered from the infection (again, many of whom had never felt sick). According to these numbers – which are expected to be an undercount, due to false negatives and the time lag before antibody production – they calculated a case fatality rate of 0.37%.
That would be about three-fold more dangerous than seasonal influenza.
In the United States, our bungling president gutted the CDC, leaving us without the expertise needed to address Covid-19 (or myriad other problems that might arise). During the first few months of this epidemic, very few people managed to get a PCR test. That’s why our data from the PCR tests is likely to be a dramatic undercount – indeed, when we finally started producing accurate tests, the apparent growth in Covid-19 caseload superimposed with the growth in test availability.
In the absence of good PCR data, we have to rely on antibody data to track infections after the fact. Which is why a town in Colorado with zero reported infections, as measured by PCR, had sufficiently widespread exposure that 2% of the population had already recovered from Covid-19.
Yes, there were problems with the Stanford study’s data collection – they displayed advertisements to a random selection of people, but then a self-selected subset responded. The pool of respondents were enriched for white women, but Santa Clara’s outbreak probably began among Asian-Americans. And we all know that random sampling doesn’t always give you an accurate depiction of the population at large – after all, random polling predicted that a competent president would be elected in 2016.
Now look at us.
It’s also likely that people with a poor understanding of the biology could misinterpret the result of the Stanford study. They found that PCR tests had undercounted the infection rate in Santa Clara county, at the time of this study, by 85-fold.
It would be absurd to assume that you could simply multiply all PCR results by 85 to determine the true infection rate, but some people did. And then pointed out the absurdity of their own bad math.
In places where more people are being tested by PCR, and they’re being tested more often, the PCR results will be closer to the true infection rate. If you gave everyone in the United States a PCR test, and did it every day, then the PCR data would be exactly equal to the true infection rate.
If we had data like that from the beginning, we wouldn’t have been scared. We would’ve known the true case fatality rate early on, and, also, at-risk people could’ve been treated as soon as they got infected. We’d be able to save many more lives.
10% is roughly the proportion of young people who die of seasonal influenza. But only 1% of Covid-19 deaths are people younger than 35. The news reports don’t always make clear how much the risk of Covid-19 is clustered in a small segment of the population.
This has serious implications for what we should do next. If we were dealing with a virus that was about three-fold more dangerous than seasonal influenza for everyone, we might just return to life as normal. (Indeed, we carried on as normal during the bad years when seasonal influenza killed 90,000 people instead of last year’s 30,000.)
Because the risk from Covid-19 is so concentrated, though, we can come up with a plan that will save a lot of lives.
Healthy people under retirement age should resume most parts of their lives as normal. Schools should re-open: for students, Covid-19 is much less dangerous than seasonal influenza. I think that people should still try to work from home when possible, because it’s the right thing to do to fight climate change.
At-risk people should continue to isolate themselves as much as possible.
This sounds crummy, but at-risk people would just continue to do the thing that everyone is doing currently. And the plan would save many lives because the epidemic would end in about 3 months, after the virus had spread to saturation among our nation’s low-risk cohort.
Their data are easy enough to understand. In each of these graphs, they show a blue box for how long social distancing would last, and then four colored lines to represent how many infections we’d see if we did no social distancing (black), medium quality social distancing (red), good social distancing (blue), or excellent social distancing (green).
So, from top to bottom, you’re looking at the graphs of what happens if we do a month of social distancing … or two months … or three, or four … or forever.
And you can see the outcomes in the panels on the right-hand side. The black line shows what would happen if we did nothing. Infections rise fast, then level off after the virus has reached saturation. There are two important features of this graph – the final height that it reaches, which is the total number of severe cases (and so a good proxy for the number of deaths), and the slope of the line, which is how fast the severe cases appear. A steeper hill means many people getting sick at the same time, which means hospitals might be overwhelmed.
So, okay. Looking at their graphs, we see that social distancing saves lives … if we do it forever. If you never leave your house again, you won’t die of Covid-19.
But if social distancing ends, it doesn’t help. The slopes are nearly as steep as if we’d done nothing, and the final height – the total number of people who die – is higher.
(Often, one of their curves will have a gentler slope than the others — usually the good-but-not-excellent social distancing seems best. So you’d have to pray that you were doing a precisely mediocre job of not infecting strangers. Do it a little better or a little worse and you cause people to die. This isn’t an artifact — it’s based on the density of uninfected people when social distancing ends — but let’s just say “mathematical models are wonky” and leave it at that.)
In a subsequent figure, the Harvard team tried to model what might happen if we occasionally resumed our lives for a month or so at a time, but then had another shutdown. This is the only scenario in which their model predicts that social distancing would be helpful.
Even in the extreme case that we mostly stayed in our homes for the better part of two years, social distancing would case more deaths from Covid-19 than if we had done nothing.
That’s not even accounting for all the people who would die from a greater risk of domestic violence, hunger, drug addiction, suicide, and sedentary behavior during the shutdown.
When our data was limited, the shutdown seemed reasonable. We wouldn’t be able to undo the damage we’d done by waiting.
Except, whoops, we waited anyway. We didn’t quarantine travelers in January. The shutdown didn’t begin March, when the epidemic was well underway in many places.
Now that we have more data, we should re-open schools, though. For most people, Covid-19 is no more dangerous than seasonal influenza. We already have enough data from antibody testing to be pretty confident about this, and even if we want to be extremely cautious, we should continue the shutdown for a matter of weeks while we conduct a few more antibody studies. Not months, and certainly not years.
At the same time, we need to do a better job of protecting at-risk people. This means providing health care for everyone. This means cleaning our air, staunching the pollution that plagues low-income neighborhoods. This might mean daily medical checkups and PCR tests for people who work closely with at-risk populations.
Our country will have to be different in the future, but mostly because we, as a people, have done such a shitty job of creating justice and liberty for all. We need to focus on addressing the inequities that we’ve let fester for generations. That’ll help far more than using a bandanna to cover up your smile.
This is a riff on an essay from several years ago.
In 1974, evolutionary biologist Richard Alexander gave a lecture describing the conditions that might spawn eusocial vertebrates.
Alexander was a bug guy – “eusocial” refers to extremely cooperative animals like bees, ants, and termites. Individuals sacrifice themselves for others. Non-breeders help with childcare. The colony seems more intelligent than its members.
Alexander proposed that a eusocial mammal could evolve if the animals were small compared to their food sources, and if they lived in underground burrows that could be expanded easily and defended by a small percentage of the colony.
After the lecture, an audience member mentioned that this “hypothetical eusocial mammal” sounded a lot like the naked mole-rat. Alexander was introduced to Jennifer Jarvis, who had studied individual naked mole-rats but not their social lives. Alexander and Jarvis collaborated to write The Biology of the Naked Mole-Rat.
Eliot Weinberger condensed this 500-page textbook into his 3-page essay, “Naked Mole-Rats.”
Like us, naked mole-rats are both good and bad. They are cooperative. They are affectionate. They are always touching. When they meet strangers, they fight to the death. When a breeding female dies, many other females regain fertility and the colony erupts into civil war.
Weinberger wrote that naked mole-rats “are continually cruel in small ways.” But they are outdone by naked apes.
For a research paper published in 2008, Thomas Park and colleagues found that being pinched by tweezers causes naked mole-rats pain, but injection with caustic acid does not.
“We tested naked mole-rats in standard behavioral models of acute pain including tests for mechanical, thermal, and chemical pain. We found that after noxious pinch or heat, the mole-rats responded similarly to mice.”
“In contrast to the results using mechanical and thermal stimuli, there was a striking difference in responses to strong chemical irritants. Two chemicals were used – capsaicin from hot peppers and hydrochloric acid – which normally evoke very intense pain in humans and other animals. Injection of either rapidly evoked intense licking and guarding behaviors in mice.”
“In contrast, naked mole-rats showed virtually no response.”
Perhaps you worry that acid-resistant naked mole-rats could conquer the world. Fear not. A form of kryptonite exists. Injection of an 11-amino-acid signaling peptide allows acid to hurt naked mole-rats just as much as it hurts mice. Or us.
Half a dozen animals were subjected to each treatment.
Naked mole-rats don’t die from cancer.
They should. Their cells, like ours, are copied from copies of copies. Errors compound.
Some errors are particularly deadly. Our cells are supposed to stop growing when they touch. They are supposed to commit suicide when old. But the instructions telling a cell when and how to kill itself can be lost, just like any other information.
This is cancer.
In cancer, a single cell proliferates at the expense of others. A cancer cell claims more than its fair share of space. It commandeers nutrients. This cell, and its progeny, and its progeny’s progeny, will flourish.
Then the scaffolding creature dies. Then the cancer cells die, too.
But every cell that isn’t an egg or sperm is terminal anyway. In the colony of our body, most cells are non-breeding members. From a cancer cell’s perspective, it has nothing to lose.
We develop cancer often. With each passing day, we produce about 100 billion new cells. Each time we produce a new cell, all 3 billion letters of our genome must be copied.
The enzymes that copy our genome make one mistake every billion letters. Each cell division: three new mutations. Each day: three hundred billion new mutations.
Some mutants are trouble.
Our bodies kill cancer. Your immune system – the same mess of mucous, inflammation, and goo that goes haywire during the flu – seeks and destroys renegade cells. Your body is a fascist enterprise; white blood cells, its militarized police.
Chemotherapy does not kill cancer. Chemotherapy means flooding the body with poisons that stop all cells from reproducing. With luck, if the spread of cancer is slowed, your immune system can kill it before it kills you.
In naked mole-rats, cancers always grow as slowly as if the rodents were receiving chemo, allowing their immune systems to squelch cancers at a leisurely pace. Their cancers are slowed by a heavy sugar called “hyaluronan,” which is packed so tightly into the space between cells that there is no room to grow.
In 2013, biologist Xiao Tian and colleagues wrote that “naked mole-rats may have evolved a higher concentration of hyaluronan to provide the skin elasticity needed for life in underground tunnels. This trait may have then been co-opted to provide cancer resistance and longevity.”
They became impervious to cancer almost by mistake.
The record lifespan for a naked mole-rat in captivity is 28 years, 4 months. The record-holder was nicknamed James Bond. He was senior consort to his queen and continued rutting – and siring pups – up until the day he died.
Bond was dissected. His cells showed extensive oxidative damage in their lipids, proteins, and DNA. Bond should have been hobbled by age. But time did not slow him down.
Science writer David Stipp described him as “a little buck-toothed burrower who ages like a demigod.”
Humans typically cease breeding long before we die. From an evolutionary perspective, as soon as we stop having children, our fitness drops to zero.
And yet, we have long lifespans. The dominant theory is an offshoot of “the grandmother hypothesis” – because we often care for grandchildren, there may have been evolutionary pressure to maintain good health until our grandchildren also reach reproductive age.
With twenty-year generations, there’d be an incentive to survive until our sixties.
After that, perhaps our ancestors were no longer helpful. And so we’ve inherited a propensity to decay. Expensive medical interventions can preserve us longer, but once we pass our natural lifespans, brains and bodies weaken.
When scientists starve animals in the lab, it’s called “caloric restriction.” This protocol extends lifespan in a wide variety of species. Monkeys, mice, flies, and worms. Ten-fold increases in lifespan have been observed.
Caloric restriction should extend the lives of humans, too.
There are unpleasant side effects. Caloric-restricted mice spend their time staring at empty food bowls. They are listless: barely moving, barely sleeping. They live longer, but worse – and if they are fed slightly less, they die of malnutrition.
Frequent starvation in the wild may have caused naked mole-rats to evolve their prodigious longevity.
Naked mole-rats expand their colonies outward, searching for edible roots. When they find a good root, they gnaw it carefully, attempting to keep the plant alive as long as possible. But a colony of naked mole-rats eats faster than any plant can grow. When the plant dies, the colony plunges into famine.
Most eusocial animals carefully ventilate their homes. Termites build giant pylons in the desert. Although temperatures outside careen from 35 degrees at night to over 100 during the day, the interior of the mound remains a constant 87 degrees. And the termites do not asphyxiate. Their exhalations are swept away by circulating air.
Naked mole-rats burrow with less care. They sleep in piles, hundreds of bodies lumped together underground. Those near the center soon run out of oxygen.
We would die.
Most animals, deprived of oxygen, can’t fuel their brains. Thoughts are expensive. Even at rest, our brains demand a constant influx of energy or else the neurons “depolarize” – we fall apart.
Since the death penalty was reintroduced in the United States in 1976, we have killed eleven prisoners in gas chambers. During the 1983 execution of Jimmy Lee Gray in Mississippi, officials cleared the observation room after eight minutes. Gray was still alive, gasping for breath. His attorney said, “Jimmy Lee Gray died banging his head against a steel pole in the gas chamber while reporters counted his moans.”
Gas chambers are pumped full of cyanide gas, carbon monoxide, or carbon dioxide. Carbon dioxide is cheapest.
With each breath, we inhale oxygen, burn sugar, and exhale carbon dioxide. When we drive, our cars intake oxygen, burn gasoline, and exhaust carbon dioxide.
In small amounts, carbon dioxide is beneficial. Carbon dioxide allows plants to grow. But when you put too much inside a chamber, somebody dies. Put too much in the air worldwide and we all die.
The planet Venus was habitable, once. Humans could have lived there. Venus had a deep ocean and mild weather.
Through some fluke, Venus experienced a temporary bump in the amount of carbon dioxide in the air. Carbon dioxide traps heat, which caused water to evaporate. Clouds formed, which trapped more heat. The cycle continued.
Venus is now a fiery inferno. The ground is bare rock. Sulfuric acid rains from the sky.
Lab mice die in gas chambers. Sometimes one mouse is set inside the plexiglass box; sometimes several mice inside a Chinese-food takeout container are gassed together. A valve for carbon dioxide is opened; the mice lose consciousness; they shit; they die.
A naked mole-rat would live. Unless a very determined researcher left the gas flowing for half an hour. Or so found Thomas Park and colleagues – the same team that discovered that naked mole-rats dislike being pinched. As they reported in 2017:
Human brains drink sugar. We are like hummingbirds that way. And our brains are very fussy eaters. We are fueled exclusively by glucose.
Naked mole-rats are less particular. Their minds slurp fructose to keep from dying.
Naked mole-rats are the most cooperative of mammals. They are resistant to cancer. Unperturbed by acid. They age with the libidinous gracelessness of Hugh Hefner.
They are able to withstand the horrors of a gas chamber.
And yet, for all these talents, naked mole-rats are easily tormented by human scientists.