Responses to “On testing.”

Responses to “On testing.”

My spouse posted my previous essay on social media, and I’d like to address some of people’s comments.  There were some excellent points! 

My apologies if I failed to address everything that people said, but I tried my best.

Scroll to find my responses to:

  1. A shutdown could have prevented the Covid-19 epidemic.
  2. We know that the current shutdown is either delaying or preventing deaths due to Covid-19. 
  3. Ending this epidemic with a vaccine would be ideal. 
  4. Ending the shutdown while requesting that at-risk people continue to self-isolate would save lives.
  5. Why is it urgent to end the shutdown soon?
  6. Why might more people die of Covid-19 just because we are slowing the spread of the virus?
  7. How is the shutdown causing harm?
  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?
  9. Don’t the antibody tests have a lot of false positives?
  10. What about the political ramifications of ending the shutdown?


1: “A shutdown could have prevented the Covid-19 epidemic.”

If we’d acted early enough, we could have isolated all cases of Covid-19 and prevented this whole debacle.

But we didn’t.

Covid-19 is highly infectious, and we made no effort toward containment or quarantine until the virus was already widespread.  We took action in March, but we already had community transmission of Covid-19 by January.  Given where we are now, current models predict that the epidemic will continue until the level of immunity reaches somewhere near 70%.


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.

Yes, the influenza vaccine tends to be less effective than many others – some years it gives as little as ten percent protection, other years about sixty percent protection.  By way of comparison, the HPV vaccine has over 90% efficacy.

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.

Also, the efficacy of influenza vaccines is measured in terms of the likelihood that vaccination prevents infection.  The influenza vaccine is not great at keeping people from getting sick.  But vaccination also tends to reduce the severity of your illness, even if you do catch influenza.  Because you got sick, it seems as though the vaccine “failed,” but your case might have been far more severe if you hadn’t been vaccinated.

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 air pollution 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.

Stores will need to set aside morning hours for at-risk shoppers, and undertake rigorous cleaning at night.  We know that infectious viral particles can persist for days on a variety of surfaces.

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.

We’ve seen that immunity to other coronaviruses fades within a year.  If immunity to Covid-19 is similar, we really don’t want to prolong the epidemic past a year.

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.

At the same time, I think you’d have to be pretty callous to not feel extremely concerned by the United Nations’ policy brief, “The impact of Covid-19 on children.”

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.

We know that online sex work has increased during the shutdown.  There is an increased supply of sex workers who are experiencing increasing financial insecurity.  We don’t yet have data on this, but I’d be shocked if the shutdown hasn’t led many to feel pressured into riskier acts for lower amounts of money, including meeting clients in isolated (and therefore unsafe) spaces.

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.

But any slip can kill someone recovering from addiction.  One of my friends froze to death last year.

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!


Header image by Goran Paunovic.

On testing.

On testing.

UPDATE: Wow, this got a lot of readers! Honestly, though, I wrote a response to common questions and comments about this essay and it is probably a better read.


My spouse recently sent me a link to the article “Concerns with that Stanford study of coronavirus prevalence” by Andrew Gelman, a statistician at Columbia University.  From reading this article, I got the impression that Gelman is a good mathematician.  And he raises some legitimate concerns. 

But I’ve noticed that many of the people criticizing the work coming out of the Ioannidis group – such as the study of how many people in Santa Clara county might have antibodies to Covid-19 – don’t seem to understand the biology underlying the numbers.


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. 

That’s shocking. 

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.

Many people have been put on ventilators, but that’s often the beginning of the end.  Most people put on ventilators will die.  Among patients over 70 years old, three quarters who are put on ventilators will 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.

Or, consider: cigarette smoking causes 480,000 deaths per year in the United States, including 41,000 people who die from second-hand smoke exposure.  Those 41,000 aren’t even choosing to smoke!  But cigarettes kill them anyway.

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 air quality 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.


So, Covid-19.  We know how many people have died – already (CORRECTION AS OF APRIL 21) forty-two thousand in the United States

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.

Consider the PCR test data from the Diamond Princess cruise ship.  To date, this is our most complete set of PCR data – everyone on board was tested multiple times.  And from this data, it appears that very few children were exposed to the virus.

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.

It can be dangerous to use antibody tests to address the wrong questions.

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.

The PCR test measured 23 cases.  The antibody test suggested there’d been at least 600.  And antibody tests, by design, will generally have a bunch of false negatives.  When a team at Stanford assessed the antibody tests manufactured by Premier Biotech in Minneapolis, they found that for every 3 people who’d been infected with Covid-19, the tests registered only 2 positives.

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.

And it’s why the data from the Stanford Santa Clara county study is so unsurprising. 

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.

If access to health care were considered a basic right in the United States, we might’ve done something like this. 


In Italy, it seems like Covid-19 is three- or four-fold more dangerous than seasonal influenza.  My guess is that Italy might have had about 50,000 deaths if they hadn’t enacted the lockdown.

In the United States, on a population level, Covid-19 is probably also more dangerous than seasonal influenza.  But there’s a big difference in terms of the distribution of risk.

The New York Times is running a series with short biographies of people who’ve died of Covid-19.  As of noon on April 17, about 10% of the people profiled were younger than 35.

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. 

Indeed, when a team of researchers from Harvard’s School of Public Health modeled the Covid-19 epidemic, they found that social distancing was generally unhelpful.  That’s what their data show, at least – but in their abstract, they instead recommend that we continue social distancing for the better part of two years.

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.

But, unfortunately, there’s a problem.  Research done with other coronaviruses shows that immunity fades within a year.  Because the Harvard model would cause the epidemic to last longer than a year, people would have time to lose their immunity and get infected again.

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.



UPDATE: Wow, this got a lot of readers! Thanks if you made it this far. I’ve also written a response to common questions and comments about this essay.

On the study of naked mole-rats.

On the study of naked mole-rats.

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.




Featured image from Wikimedia Commons.

On happiness and mind control.

On happiness and mind control.

Many of us would like to feel happier.

In the United States, people are having sex less often.  And between alcohol, marijuana, recreational painkillers – not to mention anti-depressants and anti-anxiety medication – we take a lot of drugs. 

Many of us work long hours at jobs we dislike so that we can afford to buy things that promise to fill some of the emptiness inside.  The most lucrative businesses are advertising companies … one of which, Facebook, is designed to make you feel worse so that you’ll be more susceptible to its ads.

The suicide rate has been rising.

From Dan Diamond’s Forbes blog post
Stopping The Growing Risk Of Suicide: How You Can Help.”

It might seem as though we don’t know how to make people happier.  But, actually, we do.

Now, I know that I’ve written previously with bad medical advice, such as the suggestion that intentionally infecting yourself with the brain parasite Toxoplasma gondii could make you happier.  This parasite boosts dopamine levels in your brain (dopamine is a neurotransmitter that conveys feelings of pleasure and mirth) and makes you feel bolder (in controlled laboratory experiments, infected mice show less stress when making risky decisions, and observational data suggests the same to be true for infected humans).  You also might become more attractive (infected rodents have more sex, and portrait photographs of infected human men are perceived as more dominant and masculine).

There are drawbacks to Toxoplasma infection, of course.  Infected rodents are more likely to be killed by cats.  Infected humans may become slower as well, both physically and intellectuallyToxoplasma forms cysts in your brain.  It might increase the chance of developing schizophrenia.  It can kill you if you’re immunocompromised.  And the surest way to contract toxoplasmosis, if incidental exposure hasn’t already done it for you, is by eating cat excrement.

My advice today is different.  No feces required! 

And I’m not suggesting anything illegal.  I mentioned, above, that people in the United States take a lot of drugs.  Several of these boost dopamine levels in your brain.  Cocaine, for instance, is a “dopamine re-uptake inhibitor,” ensuring that any momentary sensation of pleasure will linger, allowing you to feel happy longer.

But cocaine has a nasty side effect of leading to incarceration, especially if the local law enforcement officers decide that your epidermal melanin concentration is too high.  And jail is not a happy place.

Instead, you could make yourself happier with a bit of at-home trepanation, followed by the insertion of an electrode into the nucleus accumbens of your brain.  Now, I know that sounds risky, what with the nucleus accumbens being way down near the base of your brain.  But your brain is rather squishy – although you’ll sheer some cells as you cram a length of conductive wire into your cranium, the hope is that many neurons will be pushed out of the way.

The nucleus accumbens tends to show high activity during pleasure.  For instance, cocaine stimulates activity in this part of your brain.  So does money — tell research subjects that they’ve won a prize and you’ll see this region light up.  If rats are implanted with an electrode that lets them jolt their own nucleus accumbens by pushing a lever, they’ll do it over and over.  Pressing that lever makes them happier than eating, or drinking water, or having sex.  They’ll blissfully self-stimulate until they collapse.  From James Olds’s Science paper, “Self-Stimulation of the Brain”:

If animals with electrodes in the hypothalamus were run for 24 hours or 48 hours consecutively, they continued to respond as long as physiological endurance permitted.

Setup for Olds’s experiment.

Perhaps I should have warned you – amateur brain modification would carry some risks.  Even if you have the tools needed to drill into your own skull without contracting a horrible infection, you don’t want to boost your mood just to die of dehydration.

After all, happiness might have some purpose.  There might be reasons why certain activities – like eating, drinking water, having sex … to say nothing of strolling outdoors, or volunteering to help others – make us feel happy.  After discussing several case studies in their research article “How Happy Is Too Happy,” Matthis Synofzik, Thomas Schlaepfer, and Joseph Fins write that using deep brain stimulation for the “induction of chronic euphoria could also impair the person’s cognitive capacity to respond to reasons about which volitions and preferences are in his or her best interests.

When an activity makes us feel happy, we’re likely to do it again.  That’s how people manage to dedicate their lives to service.  Or get addicted to drugs.

And it’s how brain stimulation could be used for mind control.

If you show me a syringe, I’ll feel nervous.  I don’t particularly like needles.  But if you display that same syringe to an intravenous drug user, you’ll trigger some of the rush of actually shooting up.  The men in my poetry classes have said that they feel all tingly if they even see the word “needle” written in a poem.

For months or years, needles presaged a sudden flush of pleasure.  That linkage was enough for their brains to develop a fondness for the needles themselves.

If you wanted to develop a taste for an unpalatable food, you could do the same thing.  Like bittermelon – I enjoy bittermelons, which have a flavor that’s totally different from anything else I’ve ever eaten, but lots of people loathe them.

Still, if you used deep brain stimulation to trigger pleasure every time a person ate bittermelon, that person would soon enjoy it.

Bittermelon. Image by [cipher] in Tokyo, Japan on Wikimedia.

Or you could make someone fall in love. 

Far more effective than any witch’s potion, that.  Each time your quarry encounters the future beloved, crank up the voltage.  The beloved’s presence will soon be associated with a sense of comfort and pleasure.  And that sensation – stretched out for long enough that the pair can build a set of shared memories – is much of what love is.

Of course, it probably sounds like I’m joking.  You wouldn’t really send jolts of electricity into the core of somebody’s brain so that he’d fall in love with somebody new … right?

Fifty years passed between the discovery of pleasure-inducing deep brain stimulation and its current use as a treatment for depression … precisely because one of the pioneering researchers decided that it was reasonable to use the electrodes as a love potion.

In 1972, Charles Moan and Robert Heath published a scientific paper titled “Septal stimulation for the initiation of heterosexual behavior in a homosexual male.”  Their study subject was a 24-year-old man who had been discharged from the military for homosexuality.  Moan and Heath postulated that the right regimen of electrode stimulation – jolted while watching pornography, or while straddled by a female prostitute whom Moan and Heath hired to visit their lab – might lead this young man to desire physical intimacy with women.

Moan and Heath’s paper is surprisingly salacious:

After about 20 min of such interaction she begun [sic] to mount him, and though he was somewhat reticent he did achieve penetration.  Active intercourse followed during which she had an orgasm that he was apparently able to sense.  He became very excited at this and suggested that they turn over in order that he might assume the initiative.  In this position he often paused to delay orgasm and to increase the duration of the pleasurable experience.  Then, despite the milieu [inside a lab, romping under the appraising eyes of multiple fully-clothed scientists] and the encumbrance of the electrode wires, he successfully ejaculated.  Subsequently, he expressed how much he had enjoyed her and how he hoped that he would have sex with her again in the near future.

The science writer Lone Frank recently published The Pleasure Shock, a meticulously researched book in which she concludes that Heath was unfairly maligned because most people in the 1970s were reticent to believe that consciousness arose from the interaction of perfectly ordinary matter inside our skulls.  Changing a person’s mood with electricity sounds creepy, especially if you think that a mind is an ethereal, inviolable thing.

But it isn’t.

The mind, that is. The mind isn’t an ethereal, inviolable thing.

Zapping new thoughts into somebody’s brain, though, is definitely still understood (by me, at least) to be creepy.

Discussing the contemporary resurgence of electrical brain modification, Frank writes that:

In 2013, economist Ernst Fehr of Zurich University experimented with transcranial direct current stimulation, which sends a weak current through the cranium and is able to influence activity in areas of the brain that lie closest to the skull. 

Fehr had sixty-three research subjects available.  They played a money game in which they each were given a sum and had to take a position on how much they wanted to give an anonymous partner.  In the first round, there were no sanctions from the partner, but in the second series of experiments, the person in question could protest and punish the subject. 

There were two opposing forces at play.  A cultural norm for sharing fairly – that is, equally – and a selfish interest in getting as much as possible for oneself.  Fehr and his people found that the tug of war could be influenced by the right lateral prefrontal cortex.  When the stimulation increased the brain activity, the subjects followed the fairness norm to a higher degree, while they were more inclined to act selfishly when the activity was diminished.

Perhaps the most thought-provoking thing was that the research subjects did not themselves feel any difference.  When they were asked about it, they said their idea of fairness had not changed, while the selfishness of their behavior had changed. 

Apparently, you can fiddle with subtle moral parameters in a person without the person who is manipulated being any the wiser.

The human brain evolved to create elaborate narratives that rationalize our own actions.  As far as our consciousness is concerned, there’s no difference between telling a just so story about a decision we made un-aided, versus explaining a “choice” that we were guided toward by external current.

Frank believes that Heath was a brilliant doctor who sincerely wanted to help patients. 

When bioethicist Carl Elliott reviewed The Pleasure Shock for the New York Review of Books, however, he pointed out that even – perhaps especially – brilliant doctors who sincerely want to help patients can stumble into rampantly unethical behavior.

The problem isn’t just that Heath pulsed electricity into the brain of a homosexual man so that he could ejaculate while fooling around with a woman.  Many of Heath’s patients – who, it’s worth acknowledging, had previously been confined to nightmarish asylums – developed infections from their electrode implantations and died.  Also, Heath knowingly promoted fraudulent research findings because he’d staked his reputation on a particular theory and was loathe to admit that he’d been wrong (not that Heath has been the only professor to perpetuate falsehoods this way).

Elliott concludes that:

Heath was a physician in love with his ideas. 

Psychiatry has seen many men like this.  Heath’s contemporaries include Ewen Cameron, the CIA-funded psychiatrist behind the infamous “psychic driving” studies at McGill University, in which patients were drugged into comas and subjected to repetitive messages or sounds for long periods, and Walter Freeman, the inventor of the icepick lobotomy and its most fervent evangelist.

These men may well have started with the best of intentions.  But in medical research, good intentions can lead to the embalming table.  All it takes is a powerful researcher with a surplus of self-confidence, a supportive institution, and a ready supply of vulnerable subjects.

Heath had them all.

It’s true that using an electrode to stimulate the nucleus accumbens inside your brain can probably make you feel happier.  By way of contrast, reading essays like this one make most people feel less happy.

Sometimes it’s good to feel bad, though.

As Elliott reminds us, a lot of vulnerable people were abused in this research.  A lot of vulnerable people are still treated with cavalier disregard, especially when folks with psychiatric issues are snared by our country’s criminal justice system.  And the torments that we dole upon non-human animals are even worse.

Consider this passage from Frans De Waal’s Mama’s Last Hug, discussing empathy:

[University of Chicago researcher Inbal Ben-Ami Bartal] placed one rat in an enclosure, where it encountered a small transparent container, a bit like a jelly jar.  Squeezed inside it was another rat, locked up, wriggling in distress. 

Not only did the free rat learn how to open a little door to liberate the other, but she was remarkably eager to do so.  Never trained on it, she did so spontaneously. 

Then Bartal challenged her motivation by giving her a choice between two containers, one with chocolate chips – a favorite food that they could easily smell – and another with a trapped companion.  The free rat often rescued her companion first, suggesting that reducing her distress counted more than delicious food.

Is it possible that these rats liberated their companions for companionship?  While one rat is locked up, the other has no chance to play, mate, or groom.  Do they just want to make contact?  While the original study failed to address this question, a different study created a situation where rats could rescue each other without any chance of further interaction.  That they still did so confirmed that the driving force is not a desire to be social. 

Bartal believes it is emotional contagion: rats become distressed when noticing the other’s distress, which spurs them into action. 

Conversely, when Bartal gave her rats an anxiety-reducing drug, turning them into happy hippies, they still knew how to open the little door to reach the chocolate chips, but in their tranquil state, they had no interest in the trapped rat.  They couldn’t care less, showing the sort of emotional blunting of people on Prozac or pain-killers. 

The rats became insensitive to the other’s agony and ceased helping. 

You could feel happier.  We know enough to be able to reach into your mind and change it.  A miniscule flow of electrons is enough to trigger bliss.

But should we do it?  Or use our unhappiness as fuel to change the world instead?

On two degrees and the worst year (yet) to be alive.

On two degrees and the worst year (yet) to be alive.

The United States is pumping more carbon dioxide into the atmosphere than we were last year.

The amount of heat-trapping gas in our atmosphere is already too high – ideally, our net emissions should be negative.  Which is entirely feasible.  When we cultivate forests, trees pull carbon from the air.  But each tree can do only so much.  We also need to reduce the amount of energy we consume.

We don’t need to be less happy, though.  As the economy improved, people began flying more … but many flights aren’t producing happiness.  Most people look harried and sullen in airports.  If we all switched to taking trains, the cultural expectations for the rhythm of our lives would shift – instead of short bursts of misery, our travels could be pleasant spells of intermediate time. 

And the giant server farms needed to run websites like Facebook gobble energy.  Facebook, just like any other advertising company, profits by making people less happy.  Many people would be happier in a world where these servers used less energy.

We have a compelling reason to change our behaviors.  If we don’t, the global climate will rise by two degrees Celsius or more.  (Of course, any individual location could become much warmer or colder – a nearby warm ocean current keeps Europe’s climate mild, but if melting polar ice redirects this current, countries like England could become quite frigid.)

How different might life be if global temperatures changed by two degrees?

In the year 536, global temperatures were about two degrees lower than they are today.  (Which does prove, obviously, that the global climate can change for reasons that are not humanity’s fault.  But the current changes are caused by us.)

Historian and archaeologist Michael McCormick believes that this two degree change in temperature made our planet an utterly miserable place to live. A volcanic eruption had darkened the sky, preventing incoming sunlight from warming Earth.  “It was the beginning of one of the worst periods to be alive, if not the worst year,” says McCormick. Snow fell in summertime; crops failed; people starved.

And now we, in all our wisdom, are about to tug the needle just as far (if not farther!) in the other direction.

The Dark Ages were literally dark.  Ashen clouds lurked overhead.  Beset by such nightmarish conditions, people feared that God had forsaken them.  Europeans abandoned science and literacy partly as penance, hoping to appease the source of wrath that was killing them and their children.

Plants have evolved on Earth for many millions of years.  Many plant species will find a way to endure even if we change our planet’s climate.  But human food crops are quite young, in evolutionary terms, and exist in precarious swaths of monoculture. A two degree increase in global temperatures will cause these plants to die.  Famine will ensue.  Global violence and warfare will increase as hungry people fight to survive. 

A two degree change in temperature is totally sufficient to usher in a new worst year to be alive.

Sadly, nobody will be eating any Doritos made from these drought-scorched corn plants.

If we change the global climate by two degrees, there’s also no assurance that our planet won’t keep warming.  Weather is dictated by complex feedback loops that we don’t yet understand.  Our oceans soak up heat, which is changing their chemistry; warmer water takes up more space, flooding the coasts, and will melt the polar ice caps from underneath, which further accelerates warming because ice reflects sunlight, but bare ground or water absorbs it.

Venus may have been habitable, once. But climate change spiraled out of control after the atmosphere filled with too much heat-trapping carbon dioxide.  The oceans evaporated.  Now, searing sulfuric acid falls as rain from the sky.

If we tip over the precipice, every living creature on earth will be doomed.  No one understands enough about the feedback loops that dictate a planet’s climate to know how close to the precipice we are.

Although, really, a two degree change would be awful enough.

Which is worth reiterating … especially because the cohort of humans that has contributed most to climate change, and currently holds the wealth and political power needed to prevent catastrophe, is of an age that perhaps they want the world to be a little warmer.  Wealthy Americans in their fifties to seventies have long migrated south in pursuit of warmer climate.

The current generation of 50- to 70-year-olds was given the most of the Earth’s plenitude.  The world of their youth was very different from the world in which my children were born. While that generation was alive, insect populations plummeted by 90% or more.  The fecundity of other wildlife diminished in turn.  Forests were clearcut, and the environment – including the very air we breathe – was devastated to produce the world’s current wealth.

Perhaps some of the people in power now do want a warmer planet.  But it is not theirs.  As phrased by Wendell Berry,

the world is not given by [our parents], but borrowed from [our] children.”

We should feel horrifically embarrassed to return this world in worse condition than when we were lent it.

Featured image: Night Landscape with Ruined Monastery by Lluís Rigalt (1814 – 1894).

On the dangers of reading.

On the dangers of reading.

During most of human evolution, children died regularly.  In some cultures, the risk was so high that children weren’t named until they’d survived their second birthday.

But the advent of modern medicine – vaccines, antibiotics, sterile technique – has dramatically reduced childhood mortality.  Wealthy parents in the U.S. expect their children to survive.  And yet, this expectation can increase anxiety.  Families are smaller; children are less replaceable.  Parents pour so much of themselves into children’s early years that we’d be devastated if something went wrong.

And so modern parents hover.  Rather than letting children roam free, comforted by the thought that out of six kids, surely one will be fine, wealthy parents in the U.S. strive to control the development of their one or two offspring.

In the book On Immunity, Eula Biss describes how difficult it can be to relinquish that control.

CaptureI already practiced some intuitive toxicology before my pregnancy, but I became thoroughly immersed in it after my son was born.  As long as a child takes only breast milk, I discovered, one can enjoy the illusion of a closed system, a body that is not yet in dialogue with the impurities of farm and factory.  Caught up in the romance of the untainted body, I remember feeling agony when my son drank water for the first time.  “Unclean!  Unclean!” my mind screamed.

Because I didn’t breastfeed my child, I glossed over this passage when I first read it.  Even early on, I sometimes used water to dilute the milk that my partner pumped at work – when my kid was thirsty, I needed to offer something.

But I found myself thinking about this passage recently, when our eldest learned to read.  Our family loves books – we’ve probably read to our children for an hour or more each day, and they spend more time flipping through the pages on their own.

When I read to my kids, I reflexively alter texts.  In our version of James Marshall’s Fox on the Job, Fox had a bicycle accident while showing off for “his friends,” not “the girls.”  In Fox is Famous, a character bemoans the challenges of baton twirling by saying “I’m just not good at this yet,” that (unprinted) final word used to convey a growth mindset.

Go_dog_go_hat.jpgAnd our kids would probably be puzzled by Raquel D’Apice’s essay about Go Dog Go because the voices I’ve used while reading led them to assume that the pink poodle was a fashionable male asking a female friend for advice (“Well, maybe he doesn’t have a mirror at home,” I explained when N was curious, “Why does he keep asking that?”).

I could control the stereotypes that my children were fed.

But books are dangerous!  At the beginning of summer, our eldest learned how to read.  A week later, I hid all the Calvin and Hobbes.  She loves these!  So do I.  But four is too young to really understand concepts like “irony” or “anti-hero” – her behavior promptly tanked in mimicry of Calvin.

About a week after that, I hid the Peanuts.  And Garfield (“He shouldn’t kick Odie off the table, right?  Just like you shouldn’t have hit your sibling”).

She loves comics, but the only books we kept out were good, wholesome Mutts by vegan artist Patrick McDonnell.


And I hid others, like James Howe’s Howliday Inn (too scary – she could hardly sleep that night).  We look over the front-page headlines of our local newspaper before deciding whether it can be left on the table.

Like Viet Thanh Nguyen, I’ve felt a little sad to see my child venture off into the intellectual world of books without me.  I still worry what she’s ready for.

For much of human history, the paternal impulse to restrict access to books was blatantly evil.  The medieval Christian church was reticent to use local languages because then poor people could interpret religious precepts for themselves.  And the written word was considered exceptionally dangerous in the U.S.  It was illegal to teach literacy to the people who were being tortured on sweltering plantations.

I’d like to think that my motivation for wanting to sculpt my child’s library is more benign.  More akin, perhaps, to the scientists dismayed when the untrained general public dabble with misleadingly curated excerpts from research journals.

On Immunity documents the efforts that Eula Biss made to learn about vaccination.  She writes that:

vaccinationUnvaccinated children, a 2004 analysis of CDC data reveals, are more likely to be white, to have an older married mother with a college education, and to live in a household with an income of $75,000 or more – like my child.

The mothers I knew began debating whether or not to vaccinate our children against the novel influenza virus long before any vaccine became available to us.

Another mother said that her child had screamed frighteningly all night following her first vaccination and she would not risk another vaccination of any kind.

Although many of these women have received extensive schooling in the humanities, and clearly care deeply for their offspring, they are putting lives at risk, including those of their own children.

It’s possible to remain ignorant even after extensive schooling.

Cattle_herdWhen my son was six months old, at the peak of the H1N1 flu pandemic, another mother told me that she did not believe in herd immunity.  It was only a theory, she said, and one that applied mainly to cows.  That herd immunity was subject to belief had not yet occurred to me, though there is clearly something of the occult in the idea of an invisible cloak of protection cast over the entire population.

In Biss’s social circle, people doubted demonstrable principles.  Herd immunity, like the theory of evolution, is not only correct, it is the mathematical implication of uncontroversial assumptions.  In the case of herd immunity, that viral diseases are communicable and that severe symptoms tend to make a virus more contagious.  In the case of evolution, that the DNA replication process producing gametes has a non-zero error rate, that heritable DNA gives rise to traits, and that individuals with different traits might have different numbers of offspring (perhaps because one critter was eaten as a child, whereas the other survived).

But the people making ignorant decisions in Biss’s social circle certainly don’t think of themselves as ignorant.  After all, they’re trying their best to stay informed.  They aren’t scientists, but they read.  They look up information, ingest it as best they can, and try to make good decisions.

When people read (and spin) articles in scientific journals without putting forth the effort to understand what the data really mean, they create an incentive for scientists to hide their findings.  Sometimes there are caveats to the truth.  For instance, each year’s flu vaccine is often much less effective than other vaccinations.  Some years, the flu vaccine is dramatically ineffective.

I read that report – then went and got my vaccination.

If people are using papers like this as propaganda, though – trying, for whatever reason, to convince people not to get vaccinated (you want an evil conspiracy theory?  Vaccines are cheap, and they prevent deadly, expensive illnesses.  Are wealthy imbeciles recommending you forgo vaccination simply so that you’ll need to pay for more medical care?) – it stifles scientific discourse.

Every scientist knows that vaccines are helpful.  They write papers about the rare failures in order to make vaccines even more helpful.  But nobody wants to provide fodder for the ignoramuses to distort.

Roald Dahl wrote an open letter urging parents to have their children vaccinated.  He describes his own family’s tragedy – before a vaccine was developed, his seven-year-old daughter died of measles.  He thought she was getting better; he was wrong.

Are you feeling all right?” I asked her.

I feel all sleepy,” she said.

In an hour, she was unconscious.  In twelve hours, she was dead.

Incidentally, I dedicated two of my books to Olivia, the first was James and the Giant Peach.  That was when she was still alive.  The second was The BFG, dedicated to her memory after she had died from measles.  You will see her name at the beginning of each of these books.  And I know how happy she would be if only she could know that her death had helped to save a good deal of illness and death among other children.



On loneliness.

On loneliness.

Most laboratory animals live in bleak environs.  With mice, each cage typically contains a single animal.  There is bedding, food, and water.  There is very little space.

A lab mouse will be illuminated for many hours each day – sometimes twenty-four, sometimes slightly fewer – by fluorescent lights.  It will hear the constant thrum of ventilation fans and refrigerator compressors.  At least once a week, an apex predator – wafting stress-inducing smells, especially if it’s male – will reach into its home and grab it.

Chances are, it will see other mice.  A rotating cadre will fill adjacent cages during its tenure in the lab.  They will never touch.

Our cruelty makes for bad science, too.

When social animals are stored in isolation, their bodies and brains decay.  Neuron growth slows, which impedes learning.  Lifespan is curtailed.  Obesity rates increase.

Lab_animal_careIf we stop mistreating laboratory animals, though, new research might be inconsistent with past results.  When describing mice, scientists don’t say that deprivation stunts brain development.  Instead we write things like, “If a lab is studying the impact of stress on the growth of new neurons, for example, and then it lets mice exercise on a running wheel – which has been shown to spark neuron growth – the study could be jeopardized” (from David Grimm’s recent news article for Science magazine).

4117496025_8024f879d6_zWe give ourselves a very skewed view of neurology if we let ourselves think that a creature’s normal habits are stimulating neuron growth, rather than admitting that deprivation stops it.  For decades, most researchers thought that neuron growth ceased in adults.  Even in the 2005 paper demonstrating structural plasticity, the authors wrote that “such changes are only seen in response to external perturbation,” because brain development is sluggish in lab mice housed in normal conditions, i.e. those little cages.

Of course, some scientists do care about the well-being of their furry test tubes.  For instance, biologist Daniel Weary, who told Grimm “Our dream is that our animals live a better life with us than if they had never been born.”  Animals in Weary’s lab get to touch actual dirt.

Maybe not the highest bar, but the lives of most animals on our planet are worse than if they’d never been born.

Vivek_Murthy_nomination_hearing_February_4,_2014Most social animals – like mice, rabbits, and humans – aren’t going to be very happy when they’re housed in isolation.  Former U.S. Surgeon General Vivek Murthy considers loneliness to be a public health crisis, leading to health risks as bad as smoking or obesity.

Unfortunately, most biomedical research is done with research animals amongst whom pervasive loneliness is standard.  And our political system gives outsize influence to wealthy corporations that earn more money when people feel lonely.

We shunt humans into jail when we feel that their behaviors are unacceptable for the world at large.  Incarceration sends a message: don’t beat your family; don’t steal; don’t sell drugs; don’t take drugs; don’t be late for an appointment with your parole officer; don’t be too poor to pay your court fees.  To my mind, some of these offenses are worse than others.

The hope is that either the threat of incarceration deters people from these things, or that the experience of being incarceration cures them of the inclination.  (Or a third rationale – that seeing offenders punished will pacify others’ sense of fairness – which seems to encourage the evolution of cooperation, but, like many other evolved behaviors, seems unnecessarily vicious for the modern world.)

We’ve known for years that punishment doesn’t work well as a criminal deterrent.  And the experience of incarceration seems to make most people worse, not better.

Instead, we’re imposing loneliness on people who most need the help of friends and neighbors to turn their lives around.  Somebody screws up?  We store that person like a lab mouse.

10490113913_e3a697bdca_zI was recently chatting with somebody who’s done nine months so far for a parole violation – and is still waiting for his court date, which keeps being rescheduled.  (He’s already told the judge that he’ll plead guilty, and the prosecutor wanted to send him to rehab, but his PO nixed the deal.)

“It’s a lot better now, in J block.  Everybody said, you don’t wanna move from A block, you’ll get no bingo, you’ll get no … I don’t care about any of that.  We can look out the window, see people walking on the street.

“I spent almost an hour, the other day, watching this leaf blowing back and forth in the wind.  I was staring, thinking I’d say to the judge, ‘you can pile on whatever other charges you want, I’ll still plead guilty, I’ll plead guilty to all of it if you just let me out there to look at that leaf blowing around up close.  Just five minutes, just lemme see something!

“In D block, that was the worst.  All we could see was the parking garage.  On weekends, we’d see nothing, not even cars.  So I was starting fights every day.  I’d be like, hey, turn the TV to, I don’t know, some channel I don’t even like, just so I can start something with somebody.  Cause a fight would at least be something to do.”

John-Michael Bloomquist’s poem “The Prodigal’s Return,” about teaching poetry in jail, ends:

                                      Each day that I visit

the jail full of men, who hug me the way

their families cannot, write poems about childhoods

I couldn’t imagine, I feel the love of my father.

After nine months inside – un-touched, un-hugged, un-loved, under-slept – perhaps our man will finally be released.  Surely his time there will have cured him of his addiction!

On Sci-Hub, the Napster of science.

On Sci-Hub, the Napster of science.

Here’s a story you’ve probably heard: the music industry was great until Napster came along and complete strangers could “share” their collections online and profits tanked.  Metallica went berserk suing their fans.  It was too late.  The industry has never been the same.napster

Sci-Hub has been called a Napster equivalent for scientific research papers, and the major publishing companies are suing to shut it down.  The neuroscience grad student who created it faces financial ruin.  The original website was quickly shuttered by a legal injunction, but the internet is a slippery place.  Now the same service is hosted outside U.S. jurisdiction.

[Note: between writing and posting this essay, Sci-Hub has lost another lawsuit requesting all such sites to be blocked by internet service providers.]

The outcomes of these lawsuits are a big deal.  Not just for the idealistic Kazakhstani grad student charged with millions in damages.  Academic publishers will do all they can to accentuate the parallels between Sci-Hub and Napster – and, look, nearly a quarter of my living relatives are professional musicians, so I realize how much damage was wrought by Napster’s culture of theft – but comparing research papers to pop songs is a rotten analogy.  Even if you’ve never wanted to read original research yet … even if you think – reasonably – that content producers should be paid, you should care about the open access movement.  Of which Sci-Hub is the most dramatic foray.

My own perspective changed after I did some ghostwriting for a pop medicine book.  Maybe you know the type: “Do you have SCARY DISEASE X?  It’ll get better if you take these nutritional supplements and do this type of yoga and buy these experimental home-use medical devices!”  Total hokum.  And yet, people buy these books.  So there I was, unhelpfully – quite possibly unethically – collaborating with a friend who’d been hired to ghostwrite a new one.

Central_core_disease_NADH_stainI read huge numbers of research papers and wrote chapters about treating this particular SCARY DISEASE with different foods, nutritional supplements, and off-label pharmaceuticals.  My sentences were riddled with un-truths.  The foods and drugs I described are exceedingly unlikely to benefit patients in any way.

Still, I found research papers purporting to have found benefits.  I dutifully described the results.  I focused on the sort of semi-farcical study that concludes, for instance, that cancer patients who drink sufficient quantities of green tea have reduced tumor growth, at which point newspapers announce that green tea is a “superfood” that cures cancer, at which point spurious claims get slathered all over the packaging.

Maybe nobody has written a paper (yet!) claiming that green tea ameliorates your particular SCARY DISEASE.  But there’s also turmeric, kale, fish oil, bittermelon, cranberries… I’m not sure any ingredient is so mundane that it won’t eventually be declared a superfood.  Toxoplasma gondii has been linked to schizophrenia, but low-level schizophrenia has been linked to creativity: will it be long before cat excrement is marketed as a superfood for budding artists?

cat-shit-2-flat-1.jpgAs it happens, enough people suffer from our book’s SCARY DISEASE that many low-quality studies exist.  I was able to write those chapters.  And then felt grim.  The things I’d written about food weren’t so bad, because although turmeric, coconut oil, and carpaccio won’t cure anybody, they won’t cause much harm either.  But the drugs?  They won’t help, and most have nasty side effects.

My words might mislead people into wasting money on unnecessary dietary supplements or, worse, causing serious damage with self-prescribed pharmaceuticals.  Patients might follow the book’s rotten advice instead of consulting with a trained medical professional.  I’d like to think that nobody would be foolish enough to trust that book – the ostensible author is probably even less qualified to have written that book than I am, because at least I have a Ph.D. in biochemistry from Stanford – but, based on the money being thrown around, somebody thinks it’ll sell.

And I helped.

Whoops.  Mea culpa, and all of that.

But I didn’t perpetrate my sins alone.  And I’m not just blaming the book’s publishers here.  After all, the spurious results I described came from real research papers, often written by professors at major universities, often published in legitimate scientific journals.

It’s crummy to concentrate all that slop in a slim pop medicine book, I agree, but isn’t it also crummy for all those spurious research papers to exist at all?

Maybe you’ve heard that various scientific fields suffer from a “replication crisis.”  There’s been coverage on John Oliver’s Last Week Tonight and in the New York Times about major failures in psychology and medicine.  Scientists write a paper claiming something happens, but that thing doesn’t happen in anyone else’s hands.  That’s if anyone even bothers to check.  Most of the time, nobody does.  Verifying someone else’s results won’t help researchers win grants, so it’s generally seen as a waste of time and money.

Still, the news coverage I’ve seen hasn’t stated the problem sufficiently bluntly.  Modern academic science is designed to be false.

This is tragic.  It’s part of why I chose not to stop working in the field.  I became a writer.  Of course, this led to my stint of ghostwriting, which… well, whoops.

Here’s how modern science works: most research is publishable only if it is “statistically significant.”  This means comparing any result to a “null hypothesis” – if you’re investigating the effect of green tea on cancer, the null hypothesis is simply “green tea does nothing” – then throwing out your results if you had more than a one in twenty chance to see what you did if the null hypothesis were true.

If you have a hundred patients, some of their tumors will shrink no matter what you do.  If you give everybody buckets of green tea and see the usual number of people improve, you shouldn’t claim that green tea saved them.

Here’s a graphic from Wikipedia to help:


Logical enough.  But bad.  Why?  Because cancer is a SCARY DISEASE.  Far more than twenty people are studying it.  If twenty scientists each decide to test whether green tea reduces tumors, the “one in twenty” statistical test means that somebody from that set of scientists will probably see an above-average number of patients improve.  When you’re dealing with random chance, there are always flukes.  If twenty researchers all decided to flip four coins in a row, somebody would probably see all four come up heads – doesn’t mean that researcher did anything special.

Or, did you hear the news that high folate might be correlated with autism?  This study probably sounds legitimate – the lead scientist is a professor at Johns Hopkins, after all – but the result is quite unlikely to be real.  That scientist hasn’t written about folate previously, so my best guess (this new study is currently unpublished) is that pregnant women were tested for many different biomarkers, things like folate, iron, testosterone, and more, and then tracked to see whose children would develop autism.  If the researchers tested the concentrations of twenty different nutrients and hormones, of course they’d see one that appeared to correlate with autism.

[Edit: these findings were recently published.  Indeed, the data appear rather unconvincing, and the measurements for folate were made after the fact, using blood samples – it’s quite possible that other data was gathered but excluded from the published version of the study.]

This is not science.  But if you neglect to mention how many biomarkers you studied, and you retroactively concoct a conspiracy theory-esque narrative explaining why you were concerned about folate, it can do a fine job of masquerading as science.  At least long enough to win the next grant.

Which means that, even though the results of many of these studies are false, they get published.  When somebody checks twenty nutrients, one might appear to cause autism.  When twenty scientists study green tea and cancer, somebody might get results suggesting green tea does work.  Even if it doesn’t do a thing.

In our current system, though, only the mistaken researcher’s results get published.  Nobody knows that there were twenty tests.  The nineteen other biomarkers that were measured get left out of the final paper.  The nineteen researchers who found that green tea does nothing don’t publish anything.  Showing that a food doesn’t cure cancer?  How mundane.  Nobody wants to read that; publishers don’t want it in their journals.  But the single spurious result showing that green tea is a tumor-busting superfood?  That is exciting.  That study lands in a fancy journal and gets described in even briefer, more flattering language in the popular press.  Soon big-name computer CEOs are guzzling green tea instead of risking surgery or chemo.

I generally assume that the conclusions of research studies using this type of statistical testing are false.  And there’s more.  Data are often presented misleadingly.  Plenty of scientists are willing to test a pet theory many ways and report only the approach that “works,” not necessarily because they want to lie to people, but because it’s so easy to rationalize why the test you tried first (and second, and third…) was not quite right.  I worked in many laboratories over a decade and there were often results that everybody in the lab knew weren’t true.  Both professors I worked under at Stanford published studies that I know weren’t done correctly.  Sadly, they know it too.

This subterfuge can be hard for outsiders to notice.  But sometimes the flaws are things that anybody could be taught to identify.  With just a little bit of guidance, anybody foolish enough to purchase the pop medicine book I worked on would be able to look up the original research papers and read them and realize that they’re garbage.

There’s a catch: most of those papers cost between twenty and thirty dollars a pop.  The chapters I wrote cite nearly a hundred articles.  I’d describe a few studies about the off-label use of this drug, a few about that one, on and on, “so that our readers feel empowered to make their own decisions instead of being held at the paternalistic mercy of their healthcare professionals.”  A noble goal.  But I’m not sure that recommending patients dabble with ineffectual, oft-risky alternative medicines is the best way to pursue it.  Especially when the book publisher was discussing revenue sharing agreements with sellers of some of the weird stuff we shilled.

So, those hundred citations?  You could spend three thousand dollars figuring out that the chapters I wrote are crap.  The situation is slowly getting better – the National Institute of Health has mandated that taxpayer-funded studies be made available after a year, but this doesn’t apply to anything published before 2008, and I’m not sure how keen sick patients will be to twiddle their thumbs for a year before learning the latest information about their diseases.  Plus, there are many granting organizations out there.  Researchers who get their money elsewhere aren’t bound by this requirement.  If somebody asks you, “Would you like to donate money to fight childhood cancer?” and you chip in a buck, you’re actually contributing to the problem.

Photo by diylibrarian on Flickr.

I was only able to write my chapters of that book because I live next to a big university.  I could stroll to the library and use their permissions to access the papers I’d need.  Sometimes, though, that wasn’t enough.  Each obscure journal, of which there are legion, can cost a university several thousand dollars a year for a subscription.  A few studies I cited were published in specialty journals too narrowly focused for Indiana University to subscribe, so I’d send an email to a buddy still working at Stanford and ask him to send me a copy.

If you get sick and worry yourself into looking for the truth, you’ll probably be out of luck.  Even doing your research at a big state university library might not be enough.

That’s if you keep your research legal.

Or you could search for the papers you need on Sci-Hub.  Then you’d just type the title, complete a CAPTCHA on a page with instructions in Cyrillic (on what was until recently, at least), and, bam!  You have it!  You can spend your thirty dollars on something else.  Food, maybe, or rent.

Of course, this means you are a thief.  The publisher didn’t get the thirty dollars they charge for access to a paper.  And those academic publishers would like for you to feel the same ethical qualms that we’re retraining people to feel when they pirate music or movies.  If you steal, content producers won’t be paid, they’ll starve, and we’ll staunch the flow of beautiful art to which we’ve become accustomed.

The comparison between Napster and Sci-Hub is a false analogy.  Slate correspondent Justin Peters described the perverse economics of academic publishing, in particular the inelastic demand – nobody reads research journals for fun.

With music and movies, purchasing legitimate access funds creators.  Not so in academia.  My laboratory had to pay a journal to publish my thesis work; this is standard practice.  It costs the authors a lot of money to publish a research article, and “content producers” only do it, as opposed to slapping their work up on a personal website for everyone to read free, because they need publication credits on their CVs to keep winning grants.

With music and movies, stealing electronic copies makes content producers sad.  With research articles, it makes them happy.

In fact, almost everyone believes research articles should be free.  At the European Union’s recent Competitiveness Council, the member states agreed that all scientific papers should be freely available by 2020 – these  are the governments whose enforcement is necessary to maintain the current copyright system!  The only people making statements in favor of the status quo are employed by the academic publishers themselves.  Their ideological positions may be swayed somewhat by the $2 billion plus profit margins major publishers are able to extract from their current racket.

Academic publishers would argue that they serve an important role as curators of the myriad discoveries made daily.  This doesn’t persuade me.  The “referees” they rely on to assess whether each study is sound are all unpaid volunteers.  Plus, if the journals were curating well, wouldn’t it have been harder for me to fill that pop medicine book with so much legitimate-looking crap?

Most importantly, by availing yourself of Sci-Hub’s pirated material, you the thief no longer live in ignorance.  With our current healthcare model, ignorance is deadly.  The United States is moving toward an a la carte method of delivering treatment, where sick people are expected to be knowledgeable, price-sensitive consumers rather than patients who place their trust in a physician.  Most sick people no longer have a primary care physician who knows much about their personal lives – instead, doctors are forced for financial reasons to join large corporate conglomerates.  Doctors try their best moment by moment, but they might never see someone a second time.  It’s more important than ever for patients to stay well-informed.

Unless Sci-Hub wins its lawsuit, you probably can’t afford to.

On animals that speak, including humans.

On animals that speak, including humans.

Prairie-DogsWhen prairie dogs speak, they seem to use nouns – hawk, human, wooden cut-out – adjectives – red, blue – and adverbs – moving quickly, slowly.  They might use other parts of speech as well.  Prairie dogs chitter at each other constantly, making many sounds that no humans have yet decoded.

Ever wonder about the evolutionary origin of human intelligence?  The leading theory is that, over many generations, our ancestors became brilliant … in order to gossip better.  It takes a lot of working memory to keep track of the plot of a good soap opera, and our ancestors’ lives were soap operas.  But Carl knows that Shelly doesn’t know that Terrance and Uma are sleeping together, so …

Tool use is pretty cool.  So’s a symbolic understanding of the world – who doesn’t love cave art?  But gossip probably made us who we are.  All those juicy stories begged for a language to be shared.

Many types of birds, such as parrots and crows, spend their lives gossiping.  These busybodies also happen to be some of the smartest species (according to human metrics).  Each seems to have a unique name – through speech, the birds can reference particular individuals.  They clearly remember and can probably describe past events.  Crows can learn about dangerous humans from their fellows.

When I walk around town, squirrels sometimes tsk angrily at me.  But I’ve definitively observed only a single species using its capacity for speech to denounce all other animals.  From Tom Wolfe’s The Kingdom of Speech:

9780316404624_custom-3522b1f2a1f684ab94261905a4d4c9ddf86ca882-s400-c85There is a cardinal distinction between man and animal, a sheerly dividing line as abrupt and immovable as a cliff: namely, speech.

Without speech the human beast couldn’t have created any other artifacts, not the crudest club or the simplest hoe, not the wheel or the Atlas rocket, not dance, not music, not even hummed tunes, in fact not tunes at all, not even drumbeats, not rhythm of any kind, not even keeping time with his hands.

This claim is obviously false.  Several different species do create artifacts – either speech is unnecessary for this task, or else other species of animals can speak.  Or both.  In any case, this claim is so easily rebutted – all you’d need is an example of chimpanzees drumming, let along cooking – that it seems a strange conclusion for Wolfe to make.

Don’t get me wrong: humans are pretty great at thinking.  I’m more impressed by mathematical than emotional intelligence, which makes it easy for me to think that the average human is way brighter than the average elephant.

In all likelihood, though, humans have been pretty great at thinking for hundreds of thousands of years.  The cultural evolution that produced the Atlas rocket and skyscrapers was a very sudden development.  For most of the time that humans have been on the planet, our behavior probably didn’t look so different from the behavior of orcas, chimps, or parrots.

Throughout The Kingdom of Speech, Wolfe mocks the various theories about human language presented by Noam Chomsky.  (I’m ignoring Wolfe’s claims about evolution, which he says can’t be tested, replicated, or used to elucidate otherwise inexplicable phenomena – in his words, “sincere, but sheer, literature.”  Here and here are two of many recent experiments tracking evolution in progress.)

tom-wolfe-400I often found myself nodding in agreement with Wolfe.  For instance, I’d hope that a linguist making broad claims about human language would learn as many languages as possible.  I think that contradictory evidence from the real world holds more weight than pretty theories.  From Wolfe’s Kingdom of Speech:

In the heading of the [2007 New Yorker] article [“The Interpreter: Has a Remote Amazonian Tribe Upended Our Understanding of Language?”] was a photograph, reprinted many times since, of [Dan] Everett submerged up to his neck in the Maici River.  Only his smiling face is visible.  Right near him but above him is a thirty-five-or-so-year-old Piraha sitting in a canoe in his gym shorts.  It became the image that distinguished Everett from Chomsky.  Immersed! – up to his very neck, Everett is … immersed in the lives of a tribe of hitherto unknown na – er – indigenous peoples in the Amazon’s uncivilized northwest.  No linguist could help but contrast that with everybody’s mental picture of Chomsky sitting up high, very high, in an armchair in an air-conditioned office at MIT, spic-and-span … he never looks down, only inward.  He never leaves the building except to go to the airport to fly to other campuses to receive honorary degrees … more than forty at last count … and remain unmuddied by the Maici or any of the other muck of life down below.

But Chomsky being wrong doesn’t make Wolfe right.

9780262533492In Why Only Us, authors Robert Berwick and Noam Chomsky make some suspicious claims.  They argue that human language stems from an innate neurological process that they’ve dubbed “merge,” akin to the combination of two sets to produce a single, indivisible result.  {A} merged to {B} yields {C}, where {C} contains all the elements of {A} and {B}.

This sounds pretty abstract, so an example might help.  Berwick & Chomsky think that a verb and a direct object would be combined into a single “verb phrase” that is treated as a single unit by our brain.  Or, even more complexly, the word “that” leading into a subordinate clause would produce a whole slew of words that is treated as a single unit by our brain.  (In the preceding sentence, the phrase “that is treated as a single unit by our brain” would be one object.)

Robert C. Berwick and Noam ChomskyBerwick & Chomsky’s idea is that complex sentences can be built either by listing the final units in a row or using that hierarchical “merge” operation again, i.e. putting a verb phrase inside a subordinate clause, or one subordinate clause inside another.  Leading eventually to the tangled, twisty syntax of Marcel Proust.

But as far as I could tell (their book has a lot of jargon, and I read it while walking laps of the YMCA track with a sleeping baby strapped to my chest, so it’s possible I missed something), they don’t discuss the difference between two ideas being placed at the same level of interpretation, such as two independent clauses joined by an “and” or “or,” versus a dependent clause adjoined to an independent clause with “but,” “which,” “that,” or what have you.  I couldn’t identify a feature of their argument that suggested why some adjacent words would be processed by a human brain is this special way but others would not.  I could certainly address the way this happens in English, but an evolutionary argument ought to apply to all human language, and I know so little about most others that my opinions seem unhelpful here.

Some of Berwick & Chomsky’s ideas don’t seem to hold even in English, though.  For instance, they claim that:

there is no room in this picture for any precursors to language – say a language-like system with only short sentences.  There is no rationale for positing such a system: to go from seven-word sentences to the discrete infinity of human language requires emergence of the same recursive procedure as to go from zero to infinity, and there is of course no direct evidence for such “protolanguages.”  Similar observations hold for language acquisition, despite appearances, a matter that we put to the side here.

But we’re very confidant that spoken language arose long before written language, and the process they describe isn’t how many humans interact with spoken language.  There are definite limits to how many clauses most people can keep in mind at any one time – indeed, much of Why Only Us would sound incomprehensible if read aloud.

Is it reasonable to compare human written language with the spoken language of other animals?  The former is decidedly more complex.  Sure.  But the language actually used by most humans, most of the time, seems much simpler.

When I write, I can strangle syntax as well as any other pedant.  But when I actually talk with people, most of what I say is pretty straightforward.  I get confused if somebody says something to me with too many embedded clauses, or if words intended to operate together on a “structural” level aren’t in close proximity – Berwick & Chomsky spend a while writing about the phrase “instinctively birds that fly swim,” which sounds like gibberish to me.  Just say either “birds that fly instinctively can swim” or “birds that fly can swim instinctively” and you won’t get as many funny looks.  Except for the fact that I don’t think this is true, in either phrasing.  Syntactically, though, you’d be all set!

Colorful_Parrots_CoupleIn any case, all you’d need to show to demonstrate a linguistically equivalent behavior in other animals would be two parrots discussing the beliefs of a third.  This would be the same recursion that Berwick & Chomsky claim produces the “infinity of human language.”

Given that other social animals understand the (false) beliefs of their compatriots, I’d be shocked if they didn’t talk about it.  We just haven’t learned how to listen.

Humans are great.  We’ve accomplished a lot, especially in these last few thousand years (which is incredibly fast compared to evolutionary timescales).  The world has changed even in the short time that I’ve been alive.  But the unfounded claims in both The Kingdom of Speech and Why Only Us made me feel sad: with so much to be proud of, why should we humans also strive to distinguish ourselves with supremacist arrogance?

On ethics and Luke Dittrich’s “Patient H.M.”

On ethics and Luke Dittrich’s “Patient H.M.”

The scientific method is the best way to investigate the world.

Do you want to know how something works?  Start by making a guess, consider the implications of your guess, and then take action.  Muck something up and see if it responds the way you expect it to.  If not, make a new guess and repeat the whole process.

Image by Derek K. Miller on Flickr.

This is slow and arduous, however.  If your goal is not to understand the world, but rather to convince other people that you do, the scientific method is a bad bet.  Instead you should muck something up, see how it responds, and then make your guess.  When you know the outcome in advance, you can appear to be much more clever.

A large proportion of biomedical science publications are inaccurate because researchers follow the second strategy.  Given our incentives, this is reasonable.  Yes, it’s nice to be right.  It’d be cool to understand all the nuances of how cells work, for instance.  But it’s more urgent to build a career.

Both labs I worked in at Stanford cheerfully published bad science.  Unfortunately, it would be nearly impossible for an outsider to notice the flaws because primary data aren’t published.

A colleague of mine obtained data by varying several parameters simultaneously, but then graphed his findings against only one of these.  As it happens, his observations were caused by the variable he left out of his charts.  Whoops!

(Nobel laureate Arieh Warshel quickly responded that my colleague’s conclusions probably weren’t correct.  Unfortunately, Warshel’s argument was based on unrealistic simulations – in his model, a key molecule spins in unnatural ways.  This next sentence is pretty wonky, so feel free to skip it, but … to show the error in my colleague’s paper, Warshel should have modeled multiple molecules entering the enzyme active site, not molecules entering backward.  Whoops!)

Another colleague of mine published his findings about unusual behavior from a human protein.  But then his collaborator realized that they’d accidentally purified and studied a similarly-sized bacterial protein, and were attempting to map its location in cells with an antibody that didn’t work.  Whoops!

No apologies or corrections were ever given.  They rarely are, especially not from researchers at our nation’s fanciest universities.  When somebody with impressive credentials claims a thing is true, people often feel ready to believe.

antibodies.JPGIndeed, for my own thesis work, we wanted to test whether two proteins are in the same place inside cells.  You can do this by staining with light-up antibodies for each.  If one antibody is green and the other is red, you’ll know how often the proteins are in the same place based on how much yellow light you see.

Before conducting the experiment, I wrote a computer program that would assess the data.  My program could identify various cellular structures and check the fraction that were each color.

As it happened, I didn’t get the results we wanted.  My data suggested that our guess was wrong.

But we couldn’t publish that.  And so my advisor told me to count again, by hand, claiming that I should be counting things of a different size.  And then she continued to revise her instructions until we could plausibly claim that we’d seen what we expected.  We made a graph and published the paper.

This is crummy.  It’s falsehood with the veneer of truth.  But it’s also tragically routine.


41B1pZkOwmL._SX329_BO1,204,203,200_Luke Dittrich intertwines two horror stories about scientific ethics in Patient H.M.: A Story of Memory, Madness, and Family Secrets.

One of these nightmares is driven by the perverse incentives facing early neurosurgeons.  Perhaps you noticed, above, that an essential step of the scientific method involves mucking things up.  You can’t tell whether your guesses are correct until you perform an experiment.  Dittrich provides a lovely summary of this idea:

The broken illuminate the unbroken.

An underdeveloped dwarf with misfiring adrenal glands might shine a light on the functional purpose of these glands.  An impulsive man with rod-obliterated frontal lobes [Phineas Gage] might provide clues to what intact frontal lobes do.

This history of modern brain science has been particularly reliant on broken brains, and almost every significant step forward in our understanding of cerebral localization – that is, discovering what functions rely on which parts of the brain – has relied on breakthroughs provided by the study of individuals who lacked some portion of their gray matter.

. . .

While the therapeutic value of the lobotomy remained murky, its scientific potential was clear: Human beings were no longer off-limits as test subjects in brain-lesioning experiments.  This was a fundamental shift.  Broken men like Phineas Gage and Monsieur Tan may have always illuminated the unbroken, but in the past they had always become broken by accident.  No longer.  By the middle of the twentieth century, the breaking of human brains was intentional, premeditated, clinical.

Dittrich was dismayed to learn that his own grandfather had participated in this sort of research, intentionally wrecking at least one human brain in order to study the effects of his meddling.

Lacking a specific target in a specific hemisphere of Henry’s medial temporal lobes, my grandfather had decided to destroy both.

This decision was the riskiest possible one for Henry.  Whatever the functions of the medial temporal lobe structures were – and, again, nobody at the time had any idea what they were – my grandfather would be eliminating them.  The risks to Henry were as inarguable as they were unimaginable.

The risks to my grandfather, on the other hand, were not.

At that moment, the riskiest possible option for his patient was the one with the most potential rewards for him.


By destroying part of a brain, Dittrich’s grandfather could create a valuable research subject.  Yes, there was a chance of curing the patient – Henry agreed to surgery because he was suffering from epileptic seizures.  But Henry didn’t understand what the proposed “cure” would be.  This cure was very likely to be devastating.

At other times, devastation was the intent.  During an interview with one of his grandfather’s former colleagues, Dittrich is told that his grandmother was strapped to the operating table as well.

It was a different era,” he said.  “And he did what at the time he thought was okay: He lobotomized his wife.  And she became much more tractable.  And so he succeeded in getting what he wanted: a tractable wife.”


Compared to slicing up a brain so that its bearer might better conform to our society’s misogynistic expectations of female behavior, a bit of scientific fraud probably doesn’t sound so bad.  Which is a shame.  I love science.  I’ve written previously about the manifold virtues of the scientific method.  And we need truth to save the world.

Which is precisely why those who purport to search for truth need to live clean.  In the cut-throat world of modern academia, they often don’t.

Dittrich investigated the rest of Henry’s life: after part of his brain was destroyed, Henry became a famous study subject.  He unwittingly enabled the career of a striving scientist, Suzanne Corkin.

Dittrich writes that

Unlike Teuber’s patients, most of the research subjects Corkin had worked with were not “accidents of nature” [a bullet to the brain, for instance] but instead the willful products of surgery, and one of them, Patient H.M., was already clearly among the most important lesion patients in history.  There was a word that scientists had begun using to describe him.  They called him pure.  The purity in question didn’t have anything to do with morals or hygiene.  It was entirely anatomical.  My grandfather’s resection had produced a living, breathing test subject whose lesioned brain provided an opportunity to probe the neurological underpinnings of memory in unprecedented ways.  The unlikelihood that a patient like Henry could ever have come to be without an act of surgery was important.

. . .

By hiring Corkin, Teuber was acquiring not only a first-rate scientist practiced in his beloved lesion method but also by extension the world’s premier lesion patient.

. . .

According to [Howard] Eichenbaum, [a colleague at MIT,] Corkin’s fierceness as a gatekeeper was understandable.  After all, he said, “her career is based on having that exclusive access.”

Because Corkin had (coercively) gained exclusive access to this patient, most of her claims about the workings of memory would be difficult to contradict.  No one could conduct the experiments needed to rebut her.

Which makes me very skeptical of her claims.

Like most scientists, Corkin stumbled across occasional data that seemed to contradict the models she’d built her career around.  And so she reacted in the same was as the professors I’ve worked with: she hid the data.

Dittrich: Right.  And what’s going to happen to the files themselves?

She paused for several seconds.

Corkin: Shredded

Dittrich: Shredded?  Why would they be shredded?

Corkin: Nobody’s gonna look at them.

Dittrich: Really?  I can’t imagine shredding the files of the most important research subject in history.  Why would you do that?

. . .

Corkin: Well, the things that aren’t published are, you know, experiments that just didn’t … [another long pause] go right.