Over the years, I’ve taught various sciences to various people of a wide range of ages. And I’ve spent a lot of time thinking about why (and whether) children should learn science in elementary school. Because I ultimately believe they should, I’m spending part of my time this year teaching science at Fulcrum School. In the past, I’ve argued that children should learn science because it teaches them to observe the world accurately, to see reality as a source of true information and the senses as their means of obtaining that information. I’ve also argued that science is the best opportunity to introduce etymology, learning the Greek and Latin roots of the disciplines themselves (botany, geology, anatomy, etc) and the specialized terms within them. Science is also the place where we learn what it means to know. A child can memorize that limestone is made from the remains of long-dead sea animals, or she can encounter Nicolaus Steno dissecting a shark’s head and trying to understand how once-living creatures can wind up inside solid stone.

Not surprisingly for anyone who reads my blog, I also believe that science is a powerful source of inspiration. Scientists who challenged conventional authority, like Andreas Vesalius, or dared professional opposition, like William Harvey, or faced religious persecution, like Galileo, are heroes who inspire us to do the same. The history of science is also the way in which a child learns that the ordinary conditions of their own lives are hard-won. The luxuries we enjoy today were earned by learning about the world, and using that knowledge to transform it.

All of these are reasons to teach science.

Now, if I had agreed to teach biology this year, or any of its sub-domains–zoology, botany, anatomy, genetics, evolution–I would have confidently created a curriculum in a week and taught it with relatively little prep. Instead, I agreed to teach earth science.¹ Starting with rocks. Unfortunately for me, Ms. Frizzle never explored rocks. (Full disclosure: apparently she did. I must have missed that day, or we never watched it in class) So this is how, at 42, I became a “rock kid.” Two months ago, I would have been hard pressed (pun intended) to tell you the difference between igneous and metamorphic, and I did not know what the rock cycle was. I could not tell obsidian from basalt, or limestone from sandstone. Today, I am on a first-name basis with the incredible people who work at Nature’s Treasures, my local rock shop, and if you live in Austin you should definitely go see them. I spend my weekends rock hounding in 100+ degree Texas weather, and even on neighborhood walks with my dog, I return with pockets bulging with interesting rocks. Apologies to any of my neighbors from whom I have inadvertently stolen landscaping materials. And I have come to a new conclusion about why we teach science.

All the old reasons hold: we should teach science because observation skills matter, and the vocabulary is hugely beneficial, and the history of science is a treasure trove of progress stories and heroes. But then I see my youngest students run in from recess, arms straining to hold the biggest piece of limestone they can find, breathlessly eager to scratch it with copper and make it fizz with vinegar. Parents tell me they have been convinced to go to creeks on Saturday mornings to find evidence of shells inside rocks. And suddenly, it is clear to me why elementary students need science. Why it is as essential, as foundational, as reading or writing or math. We teach science so that our students fall in love with the world.

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Austin is built on limestone, and my students have walked on, walked past, tripped on, and ignored limestone their entire lives. Now they love it. They know its story, its secrets, its identity. They ooh and ahh when they first see a geode bursting with sparkling quartz, but that visual impression is nothing compared to the sheer joy in discovering that amethyst is a type of quartz, and so is citrine, and even chalcedony. They are walking through the world more deeply connected to it, more interested in it, than they were before.

Falling in love with the world also means understanding how it supports and enables human life. Last week, we mixed hydrated lime with sand and water to create prehistoric lime plaster that is currently hardening in molds on the classroom shelves. This week, my students are noticing that the bricks in their homes are held together with mortar. How many times have they walked past walls without ever thinking, “What is this made of? How do these bricks stay together, how is this wall so smooth?” How many sidewalks have failed to captivate them, that now serve as a source of interest and excitement?

Imagine looking at the ceiling of the Sistine Chapel. And seeing not just the beauty of the images, but appreciating the material world they represent. Knowing that Michelangelo smoothed the surface of the ceiling with a mix of lime, sand, and volcanic ash. That his paints were made by grinding ochre, charcoal, lime, even lapis lazuli. Imagine walking through a park and thinking, “In these hills, and these rocks, are the kinds of materials that painted the Sistine Chapel.” Imagine seeing the world as a wonderland of beauty and understanding, every rock, every tree, every animal holding its story and its mysteries, and knowing that you can unlock those mysteries if you try. And that by unlocking those mysteries, you can transform the world more effectively than any magician.

We teach science because we love the world. We teach science to pass on that love.

¹Thank you to for convincing me we needed to focus on earth science despite my arguments in favor of biology!

It is probably worth stating directly: these views are false, and they are provably false. The percent of the population living in extreme poverty has dropped significantly since 2000. Through the 19th century, about 50% of children died before reaching maturity. Today, the average is less than 4% and the country with the highest child mortality, Niger, sits at around 11%. A tragic number, but this negative outlier is still dramatically better than the best positive outlier a hundred years ago. And the positive outliers today show what is possible: in the European Union, child mortality is less than 0.5%.

The world today has major problems. 4% of children dying before they can grow up is far too many. But the real numbers, the real trends, tell a story of passionate optimism for anyone brave enough to join the fight. We have succeeded in making dramatic positive change, and the need for more change should drive motivation, not despair. Especially for a young person just starting out in the world! Imagine a young warrior, inheriting generations of heroic victories, now handed the opportunity to gain glory in the current fight. But overwhelmingly, these past victories are either unknown or forgotten. We don’t sing songs to the battles we’ve won, and too many people believe the war has already been lost.

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This summer, I teamed up with and at Institute to see if we could do something about that. Teens today are not just pessimistic. They’re misinformed about the actual state of the world. So we wanted to know: what would happen if they learned the history? Not just a statistical review, but a deep dive into how the world has changed over time. We brought together 30 high school students for Progress in Medicine, a pilot summer program created with the goal of inspiring young people towards builder careers. The students were ambitious, intelligent, and high-achieving. And still, in their initial applications, interviews, and surveys, they shared a feeling of pessimism about the future and a lack of confidence in their own ability to influence it.

I built a curriculum that focused on some of the biggest problems in medicine and health throughout history: from infectious diseases, to obesity, cancer, and longevity. In each topic, we started with stories of the past. How could a physician operating in an era before germ theory even approach the challenge of childbed fever? What was it like for Lady Mary Wortley Montagu, ravaged by smallpox, to consider trying the inoculation procedures she saw in Constantinople on her own child? We met the major innovators and discoverers who moved the world forward, and learned how their discoveries changed everyday life. We interpreted data, but we also focused on the tangible and visceral. Students reviewed their own family trees, and looked at life expectancy across generations. We compared the outcomes of George Washington’s sore throat to their own childhood experiences with taking penicillin. And we ended each case study with a review of the current challenges and cutting-edge work. This included the mantra that progress breeds problems. Antibiotics lead to antibiotic resistance; a world without starvation is a world with an obesity epidemic; a world of increasing lifespans is a world with more cancer. And for each of these problems, the students met directly with some of the people fighting them today.

We found mentors for the program by putting out a call for “people who love their work in medicine, health, and biotechnology, and want to share that passion with students.” If there is a better cure for pessimism, I haven’t found it. We were inundated with incredible volunteers, all of them doing ambitious, meaningful work in the world, all of them excited and willing to share generously of their time, energy, and expertise. They were doctors, nurses, founders, policymakers, researchers, engineers, and more. All of them problem solvers. Not ignoring the challenges, but with the audacious confidence to say, “I can make it better.” A confidence rooted in the knowledge that throughout history, people have made things better.

I had a lot of fun this summer. I got to build coursework around my favorite topics and work with 30 of the brightest, most engaged students I’ve ever taught. And as I review the end-of-course surveys, I think we also answered our question. Admittedly, we took a cohort of students already predisposed to action, who were motivated and ambitious. But it was still a cohort that had grown up in the cynicism, despair, and doomerism that permeates our culture today. These are the young people who should be poised to change the world, and might instead inherit a hopelessness about the future that makes a builder career seem pointless.

While I don’t know what will happen for these students next, and I look forward to finding out, I do not think they will fall into hopelessness. I do think they will change the world. I’ll offer you some of their own words, in the end-of-course survey, as my best evidence for that belief:

It isn’t just that students didn’t know the numbers. The graphs of declining poverty rates or rising life expectancies are helpful. But if the mechanism of change is a mystery, numbers alone are not helpful enough to defeat despair. This summer, a group of teenagers learned that the world they live in was built by people who faced seemingly insurmountable problems and made them better. And I learned that at least one answer to the question, “why aren’t young people more optimistic about the future?” is surely: they don’t know the past.

And that is a problem we can solve.

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As a medical student, I saw a woman come into the emergency room with chest pain. She spoke no English, and in my bashful attempt to preserve her dignity and not impose or offend, I completed her exam without removing her shirt. I presented her case to my resident, who asked for the results of my breast exam, which I had to admit I had not performed. We ultimately found a phone interpreter who spoke a dialect similar to, but not the same as, our patient’s native tongue. With a fair bit of discomfort all around, we finally had her don a hospital gown. At which point we discovered the fungating mass almost entirely replacing her left breast.

I had never seen cancer like this. I had, by that point, seen cancer. I had removed a melanoma, from incision through sutures, from a woman’s leg. I had watched a colonoscopy uncover a cauliflower-like mass in the right colon of an elderly gentleman. I had even seen breast cancer, presenting as firm, fixed nodules lurking under the skin. But this? A healthy, 23-year-old woman who didn’t smoke, didn’t drink, and had no family history? Cancer, I was learning, lurked everywhere, and always in a different form.

I was not the first to have this realization. An ancient Egyptian physician writing in 1600 BCE described the diversity of breast tumors, which could be hot or cold, oily or solid, painful or insensate. Hippocrates described cancer appearing in the colon, on the skin, in the uterus. Even the monsters of the Mesozoic were not immune: there are dinosaur fossils with tumors. And cancer is not only diverse in its appearance. It is also maddeningly varied in its targets. As early as 1713, Italian physicians noticed that nuns have high rates of breast cancer but virtually no cervical cancer. In 1775, a British surgeon noticed that chimney sweeps were predisposed to scrotal cancer. Some things cause cancer; other things seem bizarrely to protect against it.

How, with such diversity of appearance and population, could the physicians of antiquity identify the common vein of cancer? The Egyptians, the Greeks, up to and including the physicians of the 20^th century, became increasingly adept at identifying—if not treating—the disease. Because cancer has a signature, a hallmark, that sets it apart from other thing. An abscess caused by infection resolves; an abscess from cancer never does. A wound from trauma heals; a wound from cancer grows. What begins as one crab-like invading mass becomes hard, enlarged lumps in the groin, the armpits, the neck. And cancer takes, wherever the original lesion sits. Someone dying of cancer wastes away, exhausted, emaciated, sallow, as if the tumor growing within them steals their strength and vitality. A disease of a thousand faces, but one soul.

The breakthrough bird

The mystery of the common pathway carried into the late 19^th century. All of the strange things that seemed either to promote or protect against cancer—a nun’s celibacy, a chimney sweep’s exposure—led to a disease seemingly infinite in its variety. The answer, or at least a first part of the answer, came from an unexpected source. Dr. Peyton Rous was a young man, just four years out of medical school, when he was placed in charge of the cancer research laboratory at the Rockefeller Institute in New York. A naturalist at heart, Rous had as a teenager published a column called “Wildflowers of the Month” in the Baltimore Sun. He liked to classify things.

Just months after he started at Rockefeller, a poultry farmer from Long Island brought Dr. Rous a barred Plymouth Rock hen with a large mass growing from its breast. As the chicken strutted on the table, alternately pecking at and defecating on the lab material, the farmer shared his worry that such growths would spread to the rest of his flock. Under the microscope, Dr. Rous initially reassured the man: the animal was riddled with cancer, not bacteria. The cells from the tumor, and indeed from other parts of the hen’s body, showed classic findings of a connective tissue cancer called sarcoma.

Rous then performed what was at the time a common test, taken from the playbook of microbiology. Tumors, like infectious diseases, can be transferred between animals—but only if live tumor cells are transferred, and the animals involved are highly inbred. So when Rous took his chicken tumor and implanted it in the breast of another member of the inbred flock, it was not surprising to find the new animal developed similar tumors. What was surprising was that the tumors became more aggressive with each successive transplant. Usually, as fewer and fewer cells survive transplant, the recipient has a lower disease burden. But this sarcoma behaved unusually. So Rous tried something unusual: a process then being popularized as a means of identifying infectious agents too small to be seen by the microscope. These hypothesized-but-invisible particles were being called “viruses,” and to find them, scientists strained blood or tissue through a series of ever finer filters. Rous ground up the chicken tumor and passed it through a filter fine enough to remove the chicken’s own cells—those cells that should have been essential to create a new tumor. Using progressively smaller and finer filters, he made the resulting fluid as clean as possible. Under a microscope, it was empty. He injected the empty fluid into a new, healthy chicken. It should have done nothing.

The chicken got cancer.

This “tumor-inducing agent” (as Rous called it) would eventually be renamed the “Rous sarcoma virus.” He won the Nobel Prize for his discovery in 1966, and cancer biology officially entered a new era. At least one type of cancer had a demonstrable, repeatable, and—once electron microscopes allowed visualization of viruses in the 1960s—observable cause.

The cancer genes

One type of cancer was revealed: exposure to a virus caused sarcomas in Plymouth Rock fowls (and, in fact, other viruses cause other tumors in other chickens). But most cancers can’t be transmitted through filtered, cell-less fluid. And how did the discovery explain the chimney sweeps or the nuns, or tumors that showed up in different places? The story of cancer is like a Russian nesting doll: within each discovery, another question is waiting.

There’s a reason that Rous discovered his virus in 1909, and didn’t win the Nobel Prize until more than 50 years later. One virus that caused one type of cancer in birds did not unlock the mystery of cancer. It was closer in spirit to the epidemiological studies that linked chimney soot, snuff, or dye exposure to cancer prevalence. A risk factor more than an explanation. That changed as scientists continued to study the Rous Sarcoma Virus, or RSV. Rous himself had noticed that his transplant-recipient chickens developed tumors incredibly quickly. In the 1950s and 60s, researchers studying multiple cancer-causing viruses found that RSV was unique in its speed. Most tumor viruses took months to cause cancer, in a pathway that was—at the time—unknown. RSV transformed cultured cells into cancer within days.

Researchers began to look at different RSV strands. While most RSV caused cancer, there were mutant versions that infected cells, replicated to produce new virus, but never resulted in sarcomas. The scientists theorized that the RSV strain capable of causing cancer must possess a specific gene, something that wasn’t required for the virus to reproduce itself, something that specifically caused the uncontrolled host cell growth and reproduction. They named the gene src, for “sarcoma.”

This was a major step forward. Not only does a virus cause cancer, but a specific gene within the virus is the cause of cancer. The virus, without the gene, does not generate tumors. This realization went beyond correlation: the pathway by which a virus causes cancer was understood. But the mystery of non-viral cancers remained as opaque as ever. Until J. Michael Bishop and Harold Varmus at the University of California in San Francisco started making things glow in the dark. The assumption, for most scientists, was that src, the “cancer gene,” was something foreign, brought to the cell by the virus. Bishop and Varmus created a radioactive DNA probe that would attach to the gene, and mixed it with tumor tissue. Sure enough, the gene glowed in every sarcoma-infested chicken. But then they mixed the probe with the blood of normal, healthy chickens with no tumors. And the DNA probe glowed radiant in those cells, too. The probe that should only attach to the cancer gene, assumed to be a viral implant, glowed in every normal, healthy, non-cancerous chicken cell. The src gene didn’t come from the virus. It was already present in the chickens.

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So what causes cancer? Inside the realization that cancer can be caused by a virus, is the discovery that the virus has a specific gene that triggers host cells to reproduce without stopping. And then the bombshell: those “cancer-causing genes” are not viral implants. They are the normal, everyday genes in our cells that control growth and reproduction. Viruses are one means of turning those genes permanently “on,” if they promote cellular reproduction, or “off,” if they shut down reproduction. And finally, the common pathway to cancer became clear. The reason that nuns, and chimney sweeps, and chickens, and cigarette smokers get cancer, and the reason that cancer occurs in a specific cell type. In each case, there’s some causative factor—a virus or a toxin—that directly damages the DNA responsible for cellular growth and division. When that damage, those mutations, lead to altered growth signals, the result is cancer. The likelihood of a mutation altering the gene in just the right way is a lightning bolt chance, but you have tens of trillions of cells, and there are a lot of things that damage DNA. Your odds get worse over time.

Why does cancer come back, when a tumor is removed? Because it’s living in our cells, and even one minuscule, tiny cell—broken off from the tumor and floating free in the blood stream—can reproduce and cause a relapse. Why does every species, from dogs to dinosaurs, get cancer? Because every species has genes that tell cells to divide, and when those genes are turned permanently on, the cells divide and reproduce without stopping.*

At the heart of the Russian nesting dolls, the smallest doll is us. Cancer is our own cells, just a little bit broken.

A needle in a pile of needles

A disease made of our own cells, just a little bit broken, is a hard disease to treat. Our own immune system can’t recognize it—cancer cells look too much like us. So a lot of treatments for cancer don’t try for precision. They kill everything, and hope the host is hardier than the disease. One of the very first truly effective medical treatments for cancer came from a chemical so deadly that its use as a weapon was banned by the Geneva Protocol. In 1942, two Yale pharmacologists were studying derivations of mustard gas. They were intrigued by the observations of World War 1 physicians, who found that men dying from mustard gas exposure had almost no white blood cells. As a weapon, a chemical that wipes out your white blood cells is pretty terrible. But there is one situation where a doctor and patient might welcome a drug that selectively targets and kills one type of cell.

“JD,” a 47-year-old factory worker from Connecticut, was dying in the Yale cancer ward from lymphosarcoma. The aggressive blood cancer caused his lymph nodes to grow so large that he couldn’t swallow. JD had very little time left, and no medical or surgical options. So he and his doctors were willing to try an extreme option. Since the research was classified as part of the war effort, the nitrogen mustard treatments were recorded in JD’s chart only as “Substance X.” And remarkably—it worked. JD’s tumors shrank dramatically, and for the first time in weeks he rested comfortably, even ate and got out of bed. JD’s cancer came back, and he died of his disease only a few months later. But the idea was launched.

Even today, many therapies still target either all cells of one type (like Substance X did), or all cells in one area (like radiation or surgery), or even all cells that divide and reproduce (like many chemotherapies, which explains why you also lose your hair, for example). None of these treatments truly differentiate between cancer and host: they just try and minimize the collateral damage.

That started to change in the 1990s, when drugs appeared that could do the previously impossible: distinguish between tumor and tissue, self and non-self. Our cells have hundreds of genes that control growth and division, all of which can potentially break. But there are repeatable signatures of gene, type of break, and resulting disease. Like the src gene whose “always on” mutation leads to sarcoma. And for Chronic Myeloid Leukemia (CML), the BCR-ABL gene is almost always broken in a predictable way. The combined work of many minds brought together a new kind of drug. The mutated gene codes for an abnormal protein that tells the cell to reproduce without stopping. Imatinib, or Gleevec (trade name), binds to that protein and blocks its action. With the approval of Gleevec in 2001, CML transformed from a fatal disease to a manageable chronic illness, treatable with a single daily pill. And cancer treatment entered an era of magic bullets.

Cancer and Longevity: Opposite sides of the same coin

A longevity researcher and a cancer researcher walk into a bar. The longevity researcher says, “I’ll have that new health drink, the one that reactivates telomerase, boosts stem cell renewal, and keeps cells young and dividing forever!” The bartender turns to the cancer researcher. “And for you?” She replies, “Same thing. I’ll just wait.”

If we didn’t die of trauma, or infectious disease, or even cancer, we still wouldn’t live forever. The mutations that cause cancer are only one form of the damage of daily life; other mutations alter protein folding, change lipid oxidation, and in a thousand ways, reduce functioning and lower the threshold for disease. And even if you avoid the direct damage, the cells in our body can’t replicate and reproduce forever. There’s a baked-in limit to the number of times our cells can divide, and when we hit that limit, time’s up for those cells.

Longevity researchers are looking for ways to slow, reverse, or stop the process. They look for ways to extend the telomeres, for example, those end caps on chromosomes that shorten with each cellular division. Or to prevent the pathways that tell an injured cell to go to sleep, or to die. Keep cells dividing forever, even when the environmental or internal signals tell them it’s time to stop. If our cells can live forever, so can we. But the longevity folks are newcomers to an old party. Because of course, there’s already a place where telomeres stay long, injured cells never die, and cells keep dividing regardless of the environmental signals. The dreams of longevity are also the hallmarks of cancer. And many of the mechanisms of aging are also our built-in protection against cancer.

On the one hand, that’s a sobering thought for the longevity field. Telomerase is a classic example. Telomerase is the enzyme that regrows telomeres, allowing cells to keep dividing much longer than normal. In the late 1990s, scientists were able to use a virus to insert an extra telomerase-coding gene into human cells in culture. The result? Cells that used to divide 50 times and then die now divided hundreds, thousands of times. Immortal cells! There was genuine speculation that aging could be solved by simply turning on telomerase. But we were not the first ones to the fountain of youth: about 80% of human cancers also have a reactivated telomerase gene somewhere in their pathway. Shortened telomeres do cause aging. They also prevent cancer.

Cancer and aging are opposite sides of the same coin, but that also means cancer has been able to jailbreak many of our mechanisms of aging. If we can combine the immortality-granting mutations from cancer, with better genetic fail-safes against mutations? Perhaps the most exciting and unexpected outcome from the fight against cancer may be their application to the pursuit of life itself.

Because after all: where there’s life, there’s cancer.

^{*For a long time, the interesting exception to “every species gets cancer” was the naked mole rat. In 2016, naked mole rats in a zoo did get cancer, making them the exception that proves the rule. But they are still fascinatingly resistant, and the mechanisms of that resistance are yielding potential results for human treatments.}

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There have always been people who are, statistically speaking, larger than average. The “Venus” figurines of prehistoric cultures imply a reverence for this body type, and the closer a tribe was to the glacial fronts the more they depicted abundant adipose in their art. But abundance in a world of scarcity sends a different signal than in a world of plenty, and obesity today is both more common and more complex than it was for our Paleolithic ancestors. Is obesity a purely physical description, whose social consequences depend on cultural conditioning? Or is it, as Hippocrates argued, a disease in itself? Or a risk factor for disease, as the statistics surely support—everything from heart disease and stroke to diabetes, sleep apnea, and cancer?

While the Paleolithic Venus may have implied a survival advantage, other historical examples argue the opposite. Sancho the Fat, King of Leon in the 10th century, earned his sobriquet by taking seven meals a day and weighing more than 500 lbs. His nobles argued that his weight prevented two essential roles of kingship: first, that the consummation of his marriage could not be observed by onlookers, and second, that he was too heavy to ride a horse. They revolted and drove Sancho out of Leon in 958.

Sancho’s grandmother, Queen Toda, was determined to regain the throne and took her grandson to the renowned physician Hasdai ibn Shaprut who locked the once-and-future monarch in a small room, sewed his lips shut, and fed him on a liquid diet of herbs, salt, and opium. Sancho lost half his body weight—and at a slim and trim 250 lbs, he was able to mount his horse and ride back into Leon to recover his throne.

In Sancho’s day, extreme obesity was a rare and unusual problem. Today, we have never been farther away from famine. Food insecurity still exists, but it exists in fewer places and at lower levels than ever before. The average calories per day per person have been steadily increasing, the cost of food (as measured by the number of hours the average person needs to work in order to get those calories) has never been lower. And in consequence, average weight, waist circumference, and body mass index have all been increasing for fifty years. And so have rates of heart disease, diabetes, arthritis, sleep apnea, and infertility. Obesity is no longer the problem of individual outliers, but an acknowledged public health crisis. And not surprisingly given the complexity of the problem, the search for a solution has been meandering.

The Puppy Surgeries

If we discount Sancho’s sewn lips, the first true bariatric surgery came to us from puppies. In 1954, Owen Wangensteen was running the surgical department at the University of Minnesota. And he noticed something: many of his patients who had a portion of small intestine removed for cancer or trauma struggled with malnutrition. That makes sense, since nutrition is controlled by the digestive tract. The interesting part was: some patients didn’t struggle. What made the difference? He assigned the question to Arnold Kremen, a young staff surgeon, who decided to approach the mystery by removing different segments of small intestine from a group of beagle puppies and recording the outcomes. He also gave the world of medical literature one of its great opening lines:

And it was true, and the puppies could testify to it. We have about 22 feet of small intestine. That’s more than the height of two regulation basketball hoops laid end-to-end, and taller than the average adult giraffe. And that intestine is—as surgeons like to say—not just pipes. Different parts have different functions, and Kremen tested those differences in his puppies. He found that losing even 70% of the intestine had a fairly small impact on weight and nutrition if it was the middle 70%. But removing the very beginning or very end was problematic, and led to severe nutrient deficiencies.

The paper was designed to guide operations for injury, trauma, or tumor. But it concluded with a suggestion that created a whole new field of surgery:

The logic: if there were puppies with moderate weight loss but without major side effects, then perhaps the surgery could be performed intentionally for this outcome.

It’s not just pipes

The beagle puppies told us: the different parts of those 22 feet of small intestine do different things. But the nascent field of bariatric surgery still treated obesity as a plumbing problem. Operations were classified into two groups:

1. Malabsorptive: intestines absorb nutrients. If you take out some of the absorptive surface, you get fewer nutrients from your food and therefore fewer calories. Even today, procedures like the Roux-en-Y gastric bypass are commonly described as “malabsorptive.”

2. Restrictive: like Sancho the Fat and his physician, the other side of the bariatric equation has sought to restrict the amount of food that can get in. If the lumen of the intestine is physically narrowed, you can’t force in a cheeseburger. These surgeries were incredibly popular in the 1970s and 80s, but fell out of favor as it became clear that—with hunger unaffected and absorption of nutrients maintained—patients almost always regained their weight.

Both of these mechanisms treat the intestines as pipes. Different types of pipes, perhaps, with different abilities to absorb nutrients, but pipes nonetheless. Shrink the lumen, less gets in. Take out a section, less absorption can happen. Simple as plumbing.

Except. Except that some people with type 2 diabetes, a chronic disease where the body either resists the effects of insulin or doesn’t produce enough of it, left the hospital off insulin after a bypass. It’s well known that diabetes is a common consequence of obesity, and weight loss is the most effective cure. But post-operatively, within 24-48 hours of surgery? These patients haven’t lost a pound. If it’s all just plumbing, how on earth do they leave the hospital off insulin and with normal blood sugar?

Except. Except that some surgeons started doing a particularly complex bypass in two parts: first, a partial resection of the stomach, and then bringing patients back for the bypass of a long segment of intestine. The stomach resection was supposed to be the restrictive part of the procedure, limiting the amount of food that got in. It wasn’t supposed to be effective long-term. Surgeons split the operation in two because long anesthesia times are dangerous, and bariatric patients are high risk. Except the patients lost weight, and stopped coming back for the second part of the operation. They lost more weight than a restrictive procedure should have caused. Restrictive procedures don’t curtail appetite. Except these patients had a lower food drive. If it’s all just plumbing, how did removal of a portion of the stomach rewire hunger?

The OG Hunger Hormones

Today, one in eight American adults is taking a GLP-1 drug. Hormonal mechanisms for obesity are well accepted, increasingly understood, and even manipulatable with a widening suite of medications. But back in the far-away days of the 1990s, surgeons believed that surgery—a physical solution—was fixing a physical problem.

Of course, the endocrinologists knew that obesity was a bit more complicated than plumbing. At least in mice. Researchers had an animal model of obesity as far back as the 1960s. A mouse with a mutation in the ob gene eats without stopping, and gains weight accordingly. While the mechanism wasn’t fully understood, scientists assumed there was some hormone that signaled satiety. And in 1994, a Nature paper with the unprepossessing title, “Positional cloning of the mouse obese gene and its human homologue,” found the hormone and (briefly) rocked the world. The ob gene, the authors determined, functions as part of a signaling pathway from adipose tissue, from fat. And in both humans and mice, a hormone they christened ‘leptin’ (from the Greek leptos, for ‘thin’) is the product of that gene. That means that our fat functions like an endocrine organ, releasing a hormone to tell the brain to stop eating. The more fat, the lower the appetite, because the body doesn’t need more reserves. Unless, like the ob/ob mice, you have a mutation in the gene that produces leptin, and you never get the signal to stop eating.

Very few people will choose major abdominal surgery if a pill is possible, and leptin was hailed as a potential miracle. Unfortunately, the promise wasn’t realized. Obese humans generally have very high leptin, not low; their problem, unlike the ob/ob mice, is not a deficiency in leptin secretion but a resistance to its effects. Leptin was a cure for rare congenital deficiencies. It wasn’t an answer to the obesity epidemic.

Leptin wasn’t the answer, and it also couldn’t explain the inexplicable observations after bariatric surgery. But it opened the door to a hormonal explanation for obesity, and a few years later in 1999, another Nature paper changed the game again. The original paper didn’t mention appetite: it identified ghrelin (“ghre” from the Proto-Indo-European for “grow”) as a growth hormone. Two years later, another group found an interesting side effect to ghrelin injections in humans: it made them eat. And in 2002, in the New England Journal of Medicine, a paper was published entitled, “Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery.”

When you diet and you lose weight, ghrelin increases. You get hungrier. Your body thinks you are in a food-restricted environment and sends out alarm bells. After gastric bypass, the bariatric surgery that supposedly caused weight loss through malabsorption? But which also had that mysterious, inexplicable result of an overnight cure for diabetes? And whose recipients, unlike the purely restrictive surgery patients, sometimes said they weren’t hungry anymore? After gastric bypass, ghrelin levels in the blood drop. The hormone signal for hunger gets turned down.

Today, we know that bariatric surgery’s most significant impact is not restrictive—which doesn’t work in the long term, and which people can eat through. And it’s not malabsorptive, which causes weight loss at the expense of potential malnutrition and other side effects. The most significant and promising mechanism of weight loss after bariatric surgery is hormonal. Ghrelin, it turns out, is produced by cells in the upper part of the stomach—the very portion removed in the sleeve gastrectomy. The operation that worked so much better than a restrictive operation should have worked, because it turns out it wasn’t working primarily by restricting food intake.

It’s not just pipes. The intestines, just like your fat cells, are endocrine organs: they’re releasing hormones to tell your brain what to eat, your pancreas what to secrete, and your tissues what to store. Your body is trying hard not to die of starvation. It’s just not great at adapting to a world of plenty.

Obesity Hormones Today

Today, the hormonal milieu that impacts hunger, weight, and growth is increasingly complex. Ghrelin impacts appetite, but so does somatostatin, and Peptide YY, and of course, GLP-1. Today, for the first time in 50 years, obesity rates are dropping in the United States and elsewhere. Rates of bariatric surgery are declining significantly as well, as a problem that is increasingly viewed as hormonal is being treated with hormones. Surgery still has its role: weight loss following bariatric surgery is still greater than medication alone, and surgery remains the most reliable cure for co-morbidities like diabetes.

The story of obesity is an evolution in our understanding. From Sancho’s sewn lips to the puppy operations, surgery originally managed the problem mechanistically. Today, we have a better understanding of the complexity of the body, and the modern solutions reflect that. The rise of GLP-1 drugs and the decline in obesity rates are the beginning of a new chapter whose conclusion is as yet unknown.

Part One: A Brief History of Smallpox

While the last several years have been incredibly polarizing, they have also made real to a new generation the cost of infectious disease. Because for most of my life, the scourge of infection has not been something many people experience personally. A drastic departure from the rest of human history, where diseases like smallpox killed millions every year.

But to compare COVID to smallpox is like comparing a young Mongol warrior who just burned his first yurt to Genghis Khan. And against smallpox, 17^th century Europe was nearly defenseless. Men had traversed the oceans, proved the Earth revolves around the sun, and mapped the circulation of blood through the body. But European medicine was still largely operating on a miasma theory of disease. The result was that treatments for smallpox (and other diseases) more often hastened death than prevented it. Bleeding, purgatives, laxatives, and blistering famously led Oliver Wendell Holmes, as late as 1860, to declare:

“I firmly believe that if the whole materia medica, as now used, could be sunk to the bottom of the sea, it would be better for mankind—and all the worse for the fishes.”

Even before germ theory, vaccination would emerge as the first definitive counterargument. In 1717, Lady Mary Wortley Montagu traveled with her husband from London to Constantinople. She left behind a city ravaged by smallpox, and carried with her a face ravaged by scars. Smallpox did not kill universally, but with a rash that characteristically erupted on face and hands, it left its survivors marked. As she prepared to leave London, Lady Mary wrote a poem about surviving the disease that took her beauty:

Upon arriving in Constantinople, Lady Mary was astonished to find that the women here had skin utterly unmarked. The aftermath of smallpox was omnipresent in London, but in Constantinople? The women told her: here, we have a way to prevent the disease. Each year, an old woman will go around to the house of some person who has the disease. She scrapes the lesions into a nutshell, and the neighbors host a party where each person endures a small cut on their arm and the introduction of a small amount of “smallpox material.” Those treated usually develop a mild reaction, maybe a few spots, and thereafter never get smallpox. Lady Mary was so convinced by what she saw that she had her own son undergo the procedure. While she was not entirely successful at convincing the Royal Society in London, she convinced other mothers. Upon returning home to England, she began to have her own secret smallpox parties, quietly protecting women and children with the procedure.

The next stage of the story hops across the Atlantic. In 1721, a particularly virulent strain of smallpox came to Boston—and here, too, there were rumors of a way to prevent infection. Onesimus, an enslaved African man, described the process of inoculation he had undergone as a child. As evidence, he pointed to the fact that the Africans in the community were largely spared from the current epidemic while a full half of the white townsfolk were sick. Dr. Zabdiel Boylston of Boston was convinced and, like Lady Mary, performed his first inoculation on his own son. He also kept better records. In Boston in 1721, 14% of people who became infected with smallpox died from the disease. Inoculation was not harmless, and it did involve an intentional exposure. 2% of those inoculated died from smallpox.

Although a major step forward, inoculation was far from perfect. The inoculated still needed a period of quarantine; they still risked spreading the full disease to others; and some people developed full-blown smallpox. The strategy also required the disease to always be present: inoculation requires disease matter.

In 1768, the tides would change again when a farmer presented to his local surgeon for inoculation, and had no reaction. The premise of inoculation is grounded in the observation that if you get smallpox once, you can’t get it again. Inoculation seemed to work in the same way: a smaller, safer version of the disease still prevents repeat infection. So the procedure only works if you do, in fact, get the “little” version of the disease. Luckily, there was a reliable marker: a raised pustule at the skin site that indicated the appropriate response. If the skin lesion didn’t occur, patients were asked to return for a second dose. But this farmer had no reaction to a second, or even a third dose. And he swore he had never had smallpox, and he had no scars. He had, however, recently overcome a bout of cowpox.

It was Dr. John Fewster who first recorded the story of a farmer who couldn’t get smallpox, and both he and others were interested in the correlation. But it was Edward Jenner, a surgeon’s apprentice, who pursued the idea systematically: the possibility that cowpox could act like a small dose of smallpox, providing immunity against the more deadly disease.

Cowpox had a number of advantages. It is passed almost entirely cow-to-person, so quarantine is unnecessary. Even a full-blown case is inconvenient, rather than deadly. And it does not require a reservoir of smallpox in the community! Jenner’s new type of inoculation used the virus variolae vaccinae, or “smallpox of the cow.” He therefore called his new method ‘vaccination,’ after ‘vacca,’ the Latin word for cow. The first vaccine. Reliable, safe protection against smallpox, a plague which had for so many thousands of years killed so indiscriminately. Now tamed, but not conquered.

Part Two: A History of Needles

Technical Challenges, Phase 1: The Lancet

If the goal is full eradication of a disease—zero infections worldwide—any number of challenges present themselves. From the potential for animal or environmental reservoirs (luckily not the case for smallpox) to the challenge of international cooperation and funding. But one unique challenge for smallpox eradication was technical, and related both to the primitive surgical tools of the era and the unique nature of the virus.

When Edward Jenner performed his first vaccination (a true ‘vacca’ vaccination, with cowpox) in 1796, the modern hypodermic needle did not exist. The procedure he employed was adopted from the Eastern practice of inoculation. In this method, the doctor would use a thumb lancet—essentially a pocket knife—to make an incision or a cross-hatch scrape pattern in the patient’s arm until it bled. They then took a bone spatula, dipped it into the effluent from a cowpox patient (often an actual cow), and smeared the fluid directly into the bleeding wound.

It worked. It worked, in fact, better than anything in history had ever worked to prevent smallpox. It was also painful, it left a large scar, and it required a trained professional to accomplish. In the early days when germ theory was in development and sterilization still a twinkle in Lister’s eye, it was also common to transfer fluid directly from one person’s oozing wound to another’s open cut—leading to incidental transmission of secondary diseases. Troops during the Civil War found this out the hard way, when they tried to inoculate themselves in the midst of a battlefield smallpox epidemic and caused a syphilis epidemic instead.

The areas of the world that had inoculation long before Europe were also early to explore less risky inoculation strategies. Written accounts in the 1500s in China describe a process called insufflation, where smallpox scabs were dried, ground, and blown into the nostril using a pipe. No cut, less risk, but lower efficacy and, without the classic pustule at the site of inoculation or vaccination, less confidence that the dose was effective. Early smallpox vaccination was limited by the available tools.

Technical Challenges, Phase 2: The Hollow-Bore Needle

The hollow-bore needle is one of those items so ubiquitous today that we forget it needed to be invented. But it plays a contradictory role in the history of smallpox vaccination.

As early as Ancient Greece, hollow reeds were used in simple medical processes; and Galen of Pergamon described early piston syringes for applying ointments. But these were for inserting things either on top of the skin or into a natural orifice. The idea of intentionally injecting a substance into the body, below the surface of the skin, was still fairly novel.

The landscape changed with the invention of a hollow metal needle capable of both puncturing the skin (and if necessary, a vein) and holding medicine. Francis Rynd, an Irish physician, was treating a woman who—despite taking morphine pills for years—had no relief for extreme pain localized on her face. He hypothesized that the pain was coming directly from a nerve, and created both a narrow tube to hold medicine and a trocar to cut the skin. He used the tool to create a puncture-hole and drip the medicine directly onto the nerve. There was no plunger, and the medicine travelled under the skin by gravity. Dr. Alexander Wood, from Scotland, would add a plunger to the design in 1853, and New York inventor Letitia Mumford Geer submitted a patent for a one-handed design in 1899.

By the time Louis Pasteur developed vaccines for rabies, the hypodermic syringe was a well-established method for delivering dissolved substances into tissue with far less trauma, pain, and incidental infection than the lancet method. Pasteur used the hypodermic needle to deliver his miracles into the subcutaneous space—the tissue just underneath the skin.

The hollow bore needle is a massive step forward for drug delivery, and it is a big part of the overall story of vaccines. It is not part of the story of smallpox. The smallpox vaccine was created from live cowpox virus. It was essential that the virus be live to achieve the effect. In fact, the difficulty with storing vaccine led to one of the stranger stories in the history of medicine. In 1803, King Charles IV of Spain wanted to send a philanthropic vaccination expedition to the Americas. He faced the dilemma of sending the cowpox virus, which usually resolves in a few days, across the Atlantic on a trip that took months. His solution was to send along 22 orphan boys as human carriers. One boy was vaccinated before leaving, and when his characteristic pustule formed, it was used to vaccinate the next boy, and so on arm-to-arm across the ocean, ensuring that there would be live virus ready for use in America.

Although they didn’t yet know why, physicians in the early 19th century observed that a hypodermic injection— so clean, neat, and nearly painless—did not reliably cause the pustule that indicated successful vaccination against smallpox. Decades later, research would reveal that the more superficial epidermal layer of skin is uniquely rich in certain cell types that, when disrupted, create the cascade that leads to immunity. And head-to-head comparison trials would show that intramuscular, intradermal, subcutaneous, or even intraperitoneal (into the abdominal cavity) injections all failed to provide the reliable immunity seen with the scrape-and-smear method.

In short: although the hypodermic needle was transformative, it could not transform smallpox vaccination.

Technical Challenges, Phase 3: The Jet Injector

Amazingly, the vaccination technique went largely unchanged into the mid-20^th century. Although sterilization improved, the general process did not. Vaccination against smallpox still required a cut or scratch, the scraping of the vaccine into the bleeding wound, and observation to see the pustule emerge.

By that time, though, there was widespread commitment to an eradication campaign. The world was tired of smallpox. An effective vaccine existed. The medical discovery was made; the challenge now was implementation and engineering. And in the 1960s, the first tentative technical step forward occurred. The jet injector, a gun-like device, forced liquid through the skin under pressure without a needle. Its benefits were significant, especially in outbreak situations. It was easy to use for untrained volunteers and incredibly fast—up to a thousand patients could receive a vaccine in an hour. The WHO called it a “peace gun,” and advertising campaigns claimed it could be used on a sleeping baby.

But the peace gun had its challenges too. While its needle-less administration meant less pain and scarring, it also meant less reliable delivery into the right layer of skin. The logistical problems quickly compounded, too; the machines were expensive and required regular maintenance. And while it seemed like an administration process without skin puncture would eliminate cross-contamination, the truth was more complicated. The jet of liquid hitting the skin at roughly 100 meters per second would punch a small hole in the epidermis, and some of the blood-contaminated fluid would splash back into the machine. While vaccinators did swab the nozzle between patients, they later realized the blood was being drawn inside the device, deeper than surface disinfection could treat.

The jet injector was not going to work for worldwide smallpox eradication.

Technical Challenges, Phase 4: The Bifurcated Needle

The cowpox vaccine was first administered by Jenner in 1796. It was 1965, about 170 years later, when Benjamin Rubin and a sewing needle actualized its full potential.

Dr. Rubin, a microbiologist, approached the problem not as a “device design” challenge but as a “drug delivery” challenge. The standard method, the most reliable method, essentially scraped the skin to allow a little bit of vaccine into a superficial wound. How could he create a device that held a little bit of vaccine, that could create just a little wound—a scrape more than a cut? And, ideally, how could he create something ubiquitous, easy to manufacture, and cheap?

The answer came from collaborating with Gust Chaknos, not a doctor but a textile engineer—perhaps because the textile industry had long ago solved the problem of mass-producing needles. Together, they ground down the end of a sewing needle, essentially opening the thread hole and resulting in a needle that divides into two branches like a fork.

The new needle was cheap and easy to produce, and possible to sterilize completely. The fork could be designed to hold exactly the right amount of vaccine, eliminating the need for measuring. The design required an engineer and a microbiologist; the implementation required a physician, epidemiologist, and administrator. Dr. D.A. Henderson was already leading the World Health Organization’s campaign to eradicate smallpox when Rubin developed the bifurcated needle. It was Henderson who completed the studies to identify the right angle at which to enter the skin; the number of punctures (15!) to create sufficient skin trauma; and the protocol for documenting skin pustule response.

The bifurcated needle solved the challenges of mass smallpox vaccination. They are cheap: $5 per thousand, rather than a dedicated jet injector. They are much more efficient at vaccine utilization, and less wasteful. Where the jet injector could get 25 vaccines per vial, the bifurcated needle gets 100. And they’re easy to use, enabling an untrained volunteer to learn the technique within minutes and be vaccinating immediately. And crucially: they are designed for the unique biology of the smallpox vaccine. They direct the live virus into the superficial tissue, where the immune cells can see it and respond.

The Result

More than 200 years after Jenner first scraped pus from a cow, the last documented smallpox case in the world came and went. The smallpox story is remarkable simply because of its impact: one of our oldest enemies, that plague which killed so many, so indiscriminately, around the world for so many centuries—not just tamed but eliminated. Smallpox eradication redefines what is possible.

It’s a remarkable story, too, because it showcases so many truths about the nature of medical progress. As usually happens, the need arose long before understanding. The original innovation came from centuries-old observational wisdom, that people who survived smallpox never got the disease again. Somewhere hidden in the mists of time, someone intentionally exposed themselves or their child to the disease, and inoculation was born. People like Mary Wortley Montagu, Onesimus, Zabdiel Boylston, and others brought inoculation to a new world that looked upon it with analytical eyes. And then an anecdote—a data point that didn’t fit—was noticed and explored when Edward Jenner became obsessed with the farmer who never got smallpox. The result was a truly transformative medical innovation: the first vaccine.

That medical innovation immediately saved lives, but the scope and scale of the victory required so much more than a medical breakthrough. Some of the fights were against early anti-vaccine sentiment, whether from those that thought the pox was given by God and therefore should be welcomed, or those simply suspicious of the new and seemingly bizarre. New medical innovations, after all, are often bizarre when introduced, and frequently contradict what is considered common sense. Those fights are still alive and well today.

The engineering challenge described above was one of, but not the only, major hurdles to overcome. Other innovators figured out how to preserve the vaccine, so you didn’t need a chain of infected orphans to get it across continents. Still others built the infrastructure to deploy the people and equipment needed. Even the infrastructure to document and track cases and outbreaks was a major part of the process.

Smallpox, today, lives only in highly secured laboratories—one at the CDC in Atlanta, and one in Russia. The CDC still has on its YouTube page instructional videos for the administration of the vaccine should the unthinkable happen, and that vaccine is still delivered through a bifurcated needle.

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What’s next?

We have eradicated only one other disease through an intentional campaign: Rinderpest, known as ‘cattle plague,’ a devastating livestock disease. Like smallpox, rinderpest went under thanks to a highly stable vaccine and a decades-long international campaign.

Today’s eradication targets face new challenges. The World Health Organization (WHO) and partners are currently targeting two diseases for eradication. Human cases of dracunculiasis, or guinea worm disease, dropped 99% from 1986-2023, but the eradication efforts stalled when new animal reservoirs were found. Poliovirus has been tantalizingly close to eradication for decades, but the live oral vaccine can revert to a transmissible form in undervaccinated populations, and the last endemic areas face both vaccine hesitancy and political instability.

Disease eradication is monumental, landing-on-the-moon type stuff, and it takes the combined work of scientists, physicians, engineers, policy makers, and populations. And none of this is accidental. Today, vaccines are once again under fire. Measles, declared eliminated in the US in 2000, is back, with outbreaks in multiple states. Tamed is not conquered. “Regional elimination” is a far cry from eradication. The smallpox story is a testament to what is possible, and other such victories are likely in the near future. But it should also stand as a reminder that the natural state is pandemic, not panacea, and the trajectory of progress is not guaranteed.

Story 1

In 1936, a 28-year-old woman was admitted to a psychiatric hospital with debilitating obsessions, including a phobia of shoes. She was a graduate student in mathematics at Columbia University, but a new onset of hallucinations, obsessions, and compulsive behavior found her incapable of either work or social interaction. In despair, she turned to the most extreme—but also the only—treatment available to her. She agreed to have Dr. Walter Freeman and Dr. James Watts perform a prefrontal lobotomy.

A procedure at once brutal, blind, and bizarre.

But for an otherwise rational and high-functioning woman paralyzed by a terror of shoes and facing lifelong incarceration, any chance was worth the risk. When Dr. Freeman followed up with her five years after the operation, she had finished her PhD and was teaching mathematics at the university level.

Story 2

Howard Dully was 12 years old when he met Walter Freeman in 1960. He was bright, particularly with solving puzzles and learning math. He was also big for his age, energetic, and struggled to focus. He questions whether he would, today, be diagnosed with ADHD.

Howard’s childhood was marked by grief for his mother, who had died when he was young, and physical and emotional abuse from his stepmother. She, in turn, decided that his behavioral problems warranted medical intervention and consulted renowned neurologist Walter Freeman. Freeman was at the end of his career, already infamous in his own lifetime. The medical establishment that had once embraced him and his methods now shunned the technique. But Freeman never wavered in his belief in surgical solutions for psychiatric problems, and when Howard’s stepmother shared her concerns, he told her about the 10-minute office procedure that could transform her problematic stepson into a docile, loving child.

Howard became one of Freeman’s youngest patients (although not the youngest—his biographer reports patients as young as four)¹, and he spent the two decades following the operation in and out of institutions, psychiatric and criminal. Although he would eventually rebuild his life successfully, even telling his own story in a PBS documentary and an autobiography, his life was in many ways defined by the operation perpetrated on him, and the unknown of who he might have been without it.

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You’re asking the wrong question

Did the lobotomy work? After all, the distinction between snake oil and medicine largely lies in efficacy. The history of medicine is full of treatments that worked before we understood why. For a 12-year-old with disciplinary problems, brain surgery is surely and unquestionably inhumane. Not merely because the operation hurt him, but because he could not consent, and the adults entrusted with his care failed to protect his interests. For the math professor who shed her phobia of shoes, however, the question becomes more difficult. Was her lobotomy an indicated and ethical procedure?

The operation is often remembered today for its barbarism and its brutality, but it is not usually a surgeon or surgical historian who describes it in those terms. Because every operation is brutal. Open heart surgeons crack the breastbone with a saw, splintering it into two pieces before inserting a vise to wrench apart the rib cage in order to save a life. Surgery is always brutal. It is always, when first attempted, bizarre. Surgery takes by force what cannot be gained by strategy.

It’s hard to read descriptions of the procedure, and harder still to see images or video, without shuddering. And so, it’s no wonder that modern writers have condemned the lobotomy simply on its brutality, and that many readers need no further evidence of its barbarism. But in the 1930s and 40s, it was hailed by doctors and the popular press alike as the “10-minute miracle” for the “obsessive,” the “insane,” and the “soul-sick,” promising to resolve everything from schizophrenia, to depression, to chronic pain and “unmanageable loved ones.” A mere decade later, popular acclaim had already turned to cultural reckoning. By the time One Flew Over the Cuckoo’s Nest was published in 1962, the cultural portrait of lobotomy was solidified as a cruel tool of oppression perpetrated on the social outcast and disenfranchised. All of it within the professional career of the man behind the leucotome: Walter Freeman, lobotomist and true believer.

The question to ask the story of lobotomy is not whether it is brutal, because it is; and not whether it worked, although sometimes it did. The question lies in the obligation of innovators who must by necessity test their hypotheses on human beings. Who must stake someone else’s life on the conclusions of their mind.

António Egas Moniz

Surgical treatment for psychiatric illness is probably as old as surgery itself, with evidence of trepanation—drilling a hole into the skull, possibly to release “evil spirits”—dating back 10,000 years. But the frontal lobotomy in its most well-known form emerged in the 1930s. In 1935, Yale researchers John Fulton and Carlyle Jacobsen presented their chimp research at the Second International Neurological Congress in London. Two chimps, Lucy and Becky, underwent surgical removal of the entire frontal lobe on each side of their brain. Lucy, who had been a calm animal uninterested in the researchers, became prone to emotional outbursts after the surgery. Becky, who had been clingy and anxious with frequent temper tantrums, turned calm. While her performance on cognitive tasks was slower, she no longer reacted with frustration when she failed to solve a puzzle.

António Egas Moniz, a Portuguese neurologist famous for inventing cerebral angiography (a method for visualizing the brain’s blood vessels still used today), was in the audience. Fulton and Jacobsen later claimed that their presentation was Moniz’s inspiration for trying the procedure on people; Moniz himself denied the connection. But the relevance was clear: a near-human primate could survive the removal of up to 30% of the cerebral cortex, with personality changes and minor cognitive impairment, but without devastation. Surgery to change the nature of the personality appeared possible.

Moniz, as head of the newly created Department of Neurology at the University of Lisbon, was intensely familiar with the challenges of caring for psychiatric patients. He would have seen how hallucinations, paranoid delusions, depression, or anxiety transformed previously functional and productive minds into inmates of state-funded asylums. With no antipsychotics, mood stabilizers, or antidepressants available, the standard of care was often more torture than treatment: cold water baths, colonics, strait jackets and other physical restraints.

Neurology was in its infancy; psychiatry, not yet a board-certified medical specialty. These diseases were not even catalogued by symptom, let alone connected to a cause or offered a cure. But Moniz, like many of his era, had a hypothesis: the possibility that psychiatric illness had a physical cause. And physical causes are amenable to physical cures. Moniz theorized that an “abnormal adhesion” between nerve cells would result in the same signals being sent over and over, resulting in the “predominant, obsessive ideas” that so tortured his patients.² Perhaps, he theorized, he could literally divide the cells, break the adhesion, and block the hyperactive pathway.

It’s not an unreasonable hypothesis. The challenge comes in testing it. If zebrafish or white mice experience auditory hallucinations, they have yet to describe them to researchers. The evidence of Lucy and Becky, sparse and even contradictory as it was, represented better animal data than was present in most of experimental psychiatry. Faced with an asylum full of patients, Egas Moniz began to experiment. He could practice the technical steps on cadavers, but to see if it was safe, and if it worked, he went to the patients under his care. He drilled small holes in the top of the skull on each side, above the frontal lobe that he believed contained the overactive and obsessive neural pathways. He invented a small trocar that contained a wire loop, which he called a leucotome. When inserted into the brain, he could extend the wire, rotate it, and cut 1-centimeter cores of brain tissue.

Moniz published his first results in 1936, describing 20 patients who underwent the surgery. He summarized his findings:

In other words, he might not know why it worked, but it worked, so nothing else mattered.

But experimental psychology faces challenges beyond the lack of an animal model. Moniz experimented on people, and confidently reported success. In no other field of medicine is the presence or absence of disease, the degree of disability, or the cause of recovery, so unclear. Until the 1970s, psychiatric diagnoses were largely impressionistic, and two psychiatrists examining the same patient routinely reached different conclusions.⁴ Even the dramatically improved math professor who lost her phobia of shoes, who Walter Freeman considered a stand-out success, attributed her own recovery to post-operative psychoanalysis rather than surgery.¹

Moniz reported that seven of his twenty patients were healed, and seven improved. He noted in passing that some of them developed new symptoms, like bladder or bowel incontinence, visual changes, apathy, or abnormal hunger. They were changed, he acknowledged, but in his accounting, not for the worse. In his paper, Moniz concluded,

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Walter Freeman

Although they did not meet at the time, there was another neurologist and lobotomy pioneer-in-the-making in the audience when the personality changes of Lucy and Becky were revealed for international scrutiny. Walter Freeman, a third-generation American physician, had fallen in love with neurology as a medical student. He was a tireless worker, spending nights and weekends in the lab exploring the mysteries of the brain. He was not a preternaturally gifted student, but he was bright, ambitious, and willing to work twice as hard. And there was also a tinge of desperation in Walter Freeman; a need to be known, seen, remembered. A need to document and prove that the events of his life really happened. In one famous anecdote, Freeman treated a young man who presented to the emergency room with a gold ring stuck around his erect penis. After clipping and removing the ring, he refused the patient’s request to return it, claiming it was a surgical specimen. Instead, Freeman had it welded onto a watch chain which he wore—and displayed at parties—for years afterwards.

When Freeman finished his training, his grandfather (the famous William Keen, who had performed America’s first brain tumor resection) secured him a position as Director of Laboratories at St. Elizabeths Hospital in Washington, DC. He was one of the only neurologists in DC at the time, with little to no professional mentorship or guidance, and suddenly responsible for running a laboratory and an asylum. He quickly began to treat the latter as a natural extension of the former. The laboratory was the place to prove his belief in an organic origin for psychiatric illness, and he spent countless hours in the dissecting room looking for physical proof. The asylum was the motivation that kept him going, the frustration and dismay he felt at the human tragedy that was his new field. For any clinician overseeing the asylums of the 1930s, it must have been a feeling of almost unbearable helplessness to serve as guardian to that mass of human misery and have no balm, no solace, no anodyne to offer.

Freeman was fascinated by the primate research he heard described in London, but unlike Moniz, he did not immediately rush home to attempt it on people. It was not exactly an unwillingness to risk patients. Freeman had become somewhat known in the hospital for performing what he called a “jiffy spinal tap,” a version of the common diagnostic procedure that involved accessing the spinal fluid through the neck rather than the lower back. It was faster, more efficient, and required no assistant. It also carried a much higher risk of fatal injury. Freeman valued efficiency over safety, but he was not a surgeon, and thus far in his career he had never ventured into the territory of brain surgery. This changed when he read Moniz’s first published work. He later wrote:

Freeman was eager to emulate Moniz’s experiments, but being untrained and uncredentialed as a surgeon, he needed a partner. James Watts, a neurosurgeon at George Washington University, agreed to work with him on the procedure. The pair began practicing Moniz’s technique on cadaver heads while searching for the right patient to serve as their first trial. In 1936, they found Alice Hammatt: 63 years old, recently admitted to the psychiatric ward, and with a life-long history of depression and “nervous breakdowns.” She was, when admitted, “unable to sleep, laughed and wept hysterically.”¹ As she and her husband contemplated long-term incarceration, Freeman offered them an alternative. A surgical procedure that he promised would cure her permanently. Her husband and relatives encouraged her to consent, and she became the first American patient to be treated surgically for a psychiatric illness. The age of lobotomy was launched.

What was the outcome of Alice Hammatt’s surgery? Was it successful? Freeman’s first lobotomy is representative of all of his work, in that he cared deeply about long-term follow-up, documented obsessively, and still leaves modern readers utterly unsure of the outcome. He published the results in a case report in the Southern Medical Journal in 1937, along with five other patients. Hammatt was discharged home 18 days after her surgery. She apparently reported to Dr. Freeman that her “anxiety and apprehension were no longer present…that she was content to grow old gracefully.” He goes on to report that “her husband said that she was more normal than she had ever been.”⁵ She died five years later, with her husband adamant that the five post-lobotomy years were the happiest of her life. Freeman recalled this first case throughout his career, adamant that “the result was spectacular.”¹ If success equated to independent living outside of an institution, Alice Hammatt was a success story. Freeman certainly treated it as one.

But in the early days of his lobotomy career, Freeman was relatively restrained. He was aware of the limitations and risks of the new operation. As late as 1942, more than a hundred lobotomies into his career, Freeman was still cautioning:

He would spend the next thirty years progressively abandoning that caution in ever more egregious circumstances. Perhaps the biggest transition point from cautious innovator to self-blinded zealot was the development of the ice pick method. For several years, Freeman and Watts performed frontal lobotomies modeled on the Moniz technique. These patients were selected carefully, with extensive preoperative documentation, and the operations were performed by a licensed neurosurgeon in a sterile operating room. But Freeman became increasingly convinced that the procedure’s benefits resulted not from destruction of the frontal lobes, but from the atrophy of the thalamus—a different region of the brain. If the thalamus was the real target, Freeman reasoned, the eye socket offered a more efficient route than the top of the skull.

His search for a sharp, thin, and strong object that could slide through the tear duct and puncture the bony wall was solved with the discovery of his kitchen ice pick. He found that he could, with the slight tap of a hammer, neatly puncture the orbital wall, slide through the frontal lobe, and land exactly where he wanted in the thalamus. The procedure required almost no technical skill, and because it was essentially a blind insertion along a straight line, almost no knowledge of neuroanatomy. It was terrifyingly easy to perform.

The first transorbital, or “ice pick” lobotomy, occurred in 1946 in Freeman’s clinic office. He used an electroconvulsive shock machine to render his patient unconscious, thereby eliminating the need for anesthesia. Within a few hours, the patient was in a taxi and on her way home. The patient herself, Sallie Ellen Ionesco, maintained that the procedure had saved her life, curing her of an overwhelming suicidal urge. But while Freeman saw a potentially transformative democratization of a previously limited resource, his surgical partner James Watts saw an unbelievably cavalier disregard for surgical caution. The disagreement led to the dissolution of their partnership, and Freeman began to operate alone without the need for hospital credentials, anesthesia, or surgeon back-up. From 1936 until 1942, Freeman and Watts collaborated on around 200 lobotomies, or approximately 33 a year. After 1946, Freeman alone performed more than 2,000. Where he once spent weeks evaluating a potential patient, he began now to expand his indications almost indiscriminately. He drove across the country (in an old camper van the press would, after his death, refer to as the “lobotomobile”) visiting state mental hospitals to offer both training for the staff and marathon procedures for the patients. Where he had once urged caution, he now modeled speed. Where he had once emphasized that not all patients would respond well to the procedure, he now began to dramatically widen his operative criteria. A TIME magazine article in 1952 reported that:

The benefits of the lobotomy were no longer, for Walter Freeman, open to question or additional evidence. And for a time, the world agreed with him. Because imagine that you’re running an asylum in 1940. You have in your care the full range of patients then incarcerated: the disabled; the delusional; the violent; the depressed, chronic or acute; the woman or child whose husband or father found her ‘unmanageable.’ And increasingly, the alcoholic, the neurosyphilitic, the demented. You have no antipsychotics or antidepressants. The in-vogue method of ‘psychoanalysis,’ so popular and attractive to private practice physicians seeing middle class patients in the afternoon in a comfortable office, is laughably inadequate for the conditions you see. You are underfunded, understaffed, and overwhelmed, with more patients every year.

In this setting, Walter Freeman comes to you and says: I have an operation that will cure up to 30% of these patients in less than an hour. Another 30% will improve enough to be discharged. Even if you learn the death rate was 3%, even if you learn that the remaining third will have significant side effects, even if you believe that this operation strips your patients of some essential spark or humanity, would you still take the chance? For an asylum director in 1940, the question was not moral, philosophic, or spiritual. It was intensely practical. And Walter Freeman—whatever controversy followed him in the journals and conferences—was viewed in the public institutions as a beacon of hope.

But in the 1950s, the landscape dramatically changed. For one thing, new nursing homes began removing older patients with dementia from the asylums, reducing the overcrowding. Penicillin was discovered in 1928, but it was not until 1943 that the drug was mass-produced, and not until the early 1950s that the impact was felt on numbers of advanced syphilis cases. The mass-scaling of Alcoholics Anonymous, the development of community mental health systems, and improved therapies like thiamine supplementation to prevent alcohol-induced dementia, all had their own impact on reducing asylum admissions. But the most transformative factor was the 1954 FDA approval of Thorazine (chlorpromazine), the first-ever antipsychotic medication. For the first time in history, doctors had an effective therapy to offer psychotic patients. Thorazine is by no means a panacea. It is a treatment, not a cure, and the side effects are significant. But it was a massive leap forward, and it was the death knell for the lobotomy.

The neurologic and psychiatric community recognized the sea change almost immediately. In fact, it seemed there was only one man oblivious to the impact of the discovery: Walter Freeman, ice pick lobotomy inventor and psychosurgery’s strongest advocate. The man who had once argued for lobotomy precisely as a means to cure the problem of widespread institutionalization found himself unable to confront an alternative, and drastically more successful, solution. Unable to pivot to the new reality, he found himself facing the erasure of his career. He began to be denied promotions, denied operating privileges, and not-so-subtly shown the door. Fleeing a world that no longer valued him, Freeman and his family moved to California where he set up a private practice in Sunnyvale. Instead of arriving in state as a major figure in American neurology, he found himself almost unable to get privileges at the local hospitals. He continued to perform lobotomies, but focused increasingly on his obsession with patient follow-up. His cross-country road trips now focused on finding former patients, interviewing their families, photographing them, seemingly desperate to prove the enduring impact of his life’s work.

Freeman performed his final lobotomy in 1967, on a long-term patient at Herrick Memorial Hospital in Berkeley named Helen Mortensen. She had received two prior lobotomies from Freeman and, finding her still incarcerated, he opted to perform a third. She died of a cerebral hemorrhage, leading the hospital to revoke his privileges. He spent his remaining few years traveling, writing obsessively to former patients, and visiting those he could find, before dying of cancer in 1972 at the age of 76.

Psychosurgery today

Neurosurgery is a robust field today, with increasingly sophisticated technical means of removing tumors, identifying and destroying the foci of epileptic seizures, and treating strokes or hemorrhage. “Psychosurgery” is an outdated term, now, but surgery for psychiatric illness still occurs. Where neurosurgery targets visible, physical abnormalities on MRI or x-ray, psychosurgery treats the invisible. Just as in Freeman’s day, these operations involve the destruction of brain tissue that looks normal.

For patients with severe obsessive compulsive disorder (OCD) where medication and therapy have failed, the removal of a small amount of tissue in the anterior cingulate cortex can provide relief. Other areas of the brain are targeted for severe depression or anxiety. But today, the alternatives to surgery are much broader. To be referred for these procedures implies the likely failure of dozens of pharmaceutical and therapeutic regimens. Informed consent also looks far different than in Freeman’s era, with ethics boards and codes of practice to protect a still vulnerable group of patients. The precision of the surgery has improved dramatically, too, and includes deep brain stimulation and gamma knife approaches. Even so, side effects still exist, from seizures and headaches to personality or behavior changes.

One aspect of psychosurgery from the 1930s remains equally true today. Surgery takes by force what cannot be gained by strategy. What has changed is the non-surgical landscape. With an ever-broader range of medical and therapeutic options, the population of people willing to risk brain surgery for relief is thankfully much smaller.

The world moved on

The history of psychiatry is messy. It asks the most difficult of questions: what does it mean to be human? To be healthy? To be healed? For a woman paralyzed by an irrational phobia of shoes, the answer can feel obvious. She is better off with the phobia removed, even if she is changed in some fundamental and difficult to define way. But for a boy who struggles with impulse control? A woman with postpartum depression? Or any of the thousands of other patients who were treated by lobotomy during Walter Freeman’s career?

The lobotomy was called a “surgery of the soul” by the New York Times in 1937. An acknowledgement of the surgery’s power to change, more than cure; to alter, more than fix. But the truth is that the procedure’s appeal to practitioners was not so spiritual. It was too often a practical decision for physicians and caregivers who saw their patients as a burden, and saw discharge from an asylum or reduction in care needs as the best achievable outcome. In a world with little to offer not only for cure but even for palliation of psychiatric symptoms, what risks are acceptable? What outcomes are acceptable? And who gets to decide?

By the 1950s, the world had become less desperate. Not desperate enough, anymore, to consider an ice pick through the eye. And medical science was becoming more discriminating. Freeman’s narrative descriptions of outcomes—patients who became “much happier, according to her husband,” were no longer viewed as a paradigm of success. Diagnostic criteria were created and debated for different psychiatric illnesses. An evolving understanding of neurotransmitters made real the promise of a physical (if not exactly anatomical) etiology of mental illness. Patients and physicians asked for, and had access to, better options than the lobotomy. The world moved on.

The lobotomy is not alone in the annals of psychiatric history as a harm-to-help approach. Patients were subjected to near-toxic doses of everything from carbon dioxide to malaria, and some of those things actually worked. Freeman is certainly not alone in advocating for a treatment that would later be proven wrong, and would seem barbaric to modern eyes. He was sloppy in his methods and accounting, but he largely matched the tenor of his time. While he sometimes showed a deep and passionate care for his patients, he also sometimes failed to see them as fully human. But perhaps most deadly for a surgical innovator: he failed to recognize when the world changed. And so, tragically, his errors of knowledge became crimes of morality.

1. Jack El-Hai, The Lobotomist: A Maverick Medical Genius and His Tragic Quest to Rid the World of Mental Illness (Wiley, 2005).

2. Gross and Schäfer, "Egas Moniz (1874–1955) and the 'Invention' of Modern Psychosurgery," Neurosurgical Focus 30:2 (2011), E8. Link to article

3. Moniz, Tentatives opératoires (1936), as quoted in Gross and Schäfer, “Egas Moniz (1874–1955) and the ‘Invention’ of Modern Psychosurgery,” Neurosurgical Focus 30:2 (2011): E8.

4. Aaron T. Beck, C. H. Ward, M. Mendelson, J. E. Mock, and J. K. Erbaugh, “Reliability of Psychiatric Diagnoses: 2. A Study of Consistency of Clinical Judgments and Ratings,” American Journal of Psychiatry 119, no. 4 (1962): 351–357.

5. Walter J. Freeman and James W. Watts, “Prefrontal Lobotomy in the Treatment of Mental Disorders,” Southern Medical Journal 30 (1937): 23–31.

6. Walter Freeman and James W. Watts, Psychosurgery: Intelligence, Emotion and Social Behavior Following Prefrontal Lobotomy for Mental Disorders (Springfield, IL: Charles C. Thomas, 1942).

7. "Medicine: Mass Lobotomies," TIME, November 24, 1952, https://time.com/archive/6619316/medicine-mass-lobotomies/.

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Perhaps love represents the highest and noblest of emotions, the confluence of all our values reflected in another human spirit. Then there are those that argue for a hormonally mediated process driven by a primal urge to pass on our genetic code. And- in a blog about anatomy- what’s love got to do with it, anyway?

Throughout history, people have asked not just the what but the where of love. In an acknowledgement of the inextricability of our physicality with our emotionality, we have throughout history put the seat of love firmly in the body. And today, as we exchange flowers and chocolates (and maybe, if you’re a traditionalist, some honeycomb), it seems like a good opportunity to explore the anatomy of love throughout the ages.

Arguments for the Heart

Close your eyes with me for a moment, and imagine your first kiss. Mine was in a train station in Philadelphia. If you’ve ever ridden SEPTA, you know that means it was dirty, dark, and it smelled bad. I know that. But in my memory? The light was rose colored, and the only smell was of our combined skin. I remember the anxious anticipation of inching closer, the tingle in my hands and feet, and the thud of my heart beating so loud I was sure it was audible.

Keep your eyes closed, and imagine your child laughing and playing on the swing set, and you suddenly see him—balanced precariously on the top of the monkey bars—begin to waver and fall. It’s your heart that responds, an immediate staccato beat that threatens to break out of your ribcage. Or maybe, imagine stepping out on a summer’s morning to see your soon-to-be wife in her wedding dress for the first time. As you turn around for that first look, the sudden rush of love can feel like a physical ache—and that pain is in your chest, not your head. And it’s not just you. The anchoring of emotions in the body shows consistency across age, gender, and culture.

So perhaps it is only natural that the earliest civilizations anchored the seat of love firmly in the heart.

In Ancient Egypt, the heart held the soul: the home of thought, memory, will, and emotion. Egyptians believed that bodily integrity after death was essential for the soul’s survival in the afterlife, a belief that continued over the eons. In Ancient Greece, Antigone risks (and accepts) death in order to bury her brother rather than see his desecrated corpse prevent his spiritual continuation. In the Middle Ages, Christians condemned the worst criminals not only to death but to dismemberment. The physical torture was compounded by punishment beyond the grave, as mutilation prevented access to heaven.

So it is all the more interesting that the Egyptian version of bodily integrity applied to one, and only one, organ. The process of mummification removed but respected the liver, intestines, and lungs, which were placed into ritual jars. The brain, on the other hand, was considered less of an organ than an internal heat sink. The embalmer pulled the brain out of the nose with a hook, and the gray stuff was discarded as useless waste. The heart, and only the heart, was left intact and in place to ensure a successful transition to the afterlife. The dead person’s fate could then be decided when Anubis weighed their heart against the feather of truth.

The Egyptians were not the only ones to place the seat of love in the heart. Both Plato and Aristotle argued for a cardio-centric model of emotion and consciousness. Plato (427-347 BCE) described a three-part soul: anchoring rationality in the head, appetite in the abdomen, and emotion in the chest. Aristotle (384-322 BCE) was more definitive. He observed fertilized chicken eggs, and saw that the heart developed before the brain (in fact, it was the spinal cord, but without a microscope he couldn’t tell). Because it developed first, he argued, the heart must be the essential part. Aristotle also observed that the brain lacks pain sensation, an observation he believed argued against its role in any higher sensations.

The heart-centric model of human emotion has never fully gone away. While the heart symbol itself is a topic of heated debate, its association with love is unquestionable. We love with all our heart; we give our heart away; when we lose someone, we are heartbroken; when we express emotions, we wear our heart on our sleeve. Home is where the heart is, not where the brain lives; and it is the heart that melts, or grows cold, as relationships change. If you’re giving someone a Valentine today, chances are you’re contributing to the age-old cardio-centric model of emotions. You can decide to break tradition and draw a brain instead, or you can appreciate the connection to a human tradition that has its origins in antiquity.

Arguments for… the Liver?

But not all of antiquity! While it’s hard to argue with the heart for emotional symbolism, earlier civilizations had other ideas. The Mesopotamians viewed the liver as the seat of the soul, and the home of the emotions, happiness in particular—even going so far as to create clay models of sheep livers for divination. The liver is slightly less obvious, from an introspection standpoint, as a candidate for seat-of-soul. Even the researchers who translated the cuneiform seem a bit unsure of the organ’s claim to greatness:

“The liver is prominent when you open up the body. As a big organ, people might have assumed that the soul lives in the liver.”

– Juha Lahnakoski, cognitive neuroscientist and lead author of “Embodied emotions in ancient Neo-Assyrian texts revealed by bodily mapping of emotional semantics”

And not to be outdone, one of my absolute favorite books, the Hugo award-winning graphic novel Digger offers an equally compelling case for the hepato-centric model.

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And indeed, the Greeks saw spiritual significance in the liver as well. Plato’s three-part soul, for example, was a theory he couldn’t demonstrate without the partnership of an anatomist. Galen of Pergamon provided observational evidence of a physical home for each of the soul’s pieces. Rationality lived in an arterial plexus at the base of the skull; emotions originated in a set of invisible pores in the heart; and appetite, or desire, was rooted in the liver. (note: all of these observations would later be disproven) So depending on if you experience love as an extension of your rational mind, as an emotion, or as a base desire, you can, like Galen, place the seat of love in the brain, heart, or liver.

Arguments for the Brain

While the heart reigned supreme for millennia, there were early inklings that the brain had some essential role to play in the feeling of love. Alcmaeon of Croton (c. 5^th century BCE) might be considered the great-grandfather of neuroscience, as he was the earliest writer to argue for the brain as the seat of intelligence, emotion, and thought. He discovered passages or channels connecting sensory organs (eyes, ears, nose) to the brain. Unlike Aristotle, who argued that the brain’s proximity to the sense organs was a mere coincidence, Alcmaeon argued that the organ was the seat of perception, and through perception, higher level thinking and feeling.

Hippocrates, perhaps influenced by Alcmaeon, had a surprisingly modern view of the role of the brain:

“Men ought to know that from the brain, and from the brain only, arise our pleasures, joys, laughter and jests, as well as our sorrows, pains, grief and tears. Through it, in particular, we think, see, hear, and distinguish the ugly from the beautiful, the bad from the good, the pleasant from the unpleasant.”

Today, functional MRI studies have mapped the brain activity of people in love when shown the photo of their partner, as compared with viewing photos of friends or strangers. While we may all perceive love in our heart, or feel fear in the tingling of our hands, imaging studies show that brain activity is equally consistent across age, gender, and culture. So much so, that different types of love—romantic, parental, friendship, pet—present differently on the scans.

It was not until the 17^th century that the heart’s function was understood, when William Harvey demonstrated that blood recirculates. The brain’s true function, theorized by Hippocrates, was not fully demonstrated experimentally until much later. Today, when scientists have made such great leaps in understanding the brain with detailed imaging, mapping of neural networks, and deciphering of chemical pathways, we might say confidently and even arrogantly that we understand the location of love, if not its full nature.

But perhaps an insistence on the brain as the seat of love is as flawed an organ-centric theory as our ancestors who advocated for the heart, the liver, or the knees. After all, it is the heart that races when our loved one approaches. Takotsubo cardiomyopathy, or broken-heart syndrome, is a well-known condition where extreme emotional distress causes the signs and symptoms of a heart attack. And the heart does influence emotion. While the brain can tell the heart to start racing in the face of arousal (or fear), the heart can talk back to the brain, too. When people are given drugs that speed up heart rate, they interpret the sensation as emotion.

So if you find yourself today, on Valentine’s Day, wondering if you should tell your partner you love them with your whole heart or your whole brain, consider instead: you love them with your whole being. Heart, brain, liver, and knees.

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Our children learn these facts like a catechism from parents and teachers. They repeat them like a truism, and believe them before experiencing any first-hand observational evidence. As I stared into his earnest eyes I couldn’t help but think: Ignaz Semmelweis would be delighted.

In a world where we know, know, from near-infancy that microscopic creatures exist and that they can cause disease, it is almost impossible to truly understand the mindset of a pre-germ theory human. Our world is premised on an understanding of infectious disease that dates back only to the late 1800s. Even our basic preference for cleanliness over dirt, in its modern iteration, is learned rather than innate. A modern person, transported to the world of 200 years ago, would be overwhelmed by the filth more than any other deprivation.

And for those of us who grew up in classrooms that wash their hands, the modern value of cleanliness makes the story of Ignaz Semmelweis easy to misrepresent. Today, Semmelweis enjoys a posthumous fame that would have shocked him in life. He is revered as the “Savior of Mothers,” a tragic figure whose brave fight to save young women from the hubris and ignorance of their physicians was met with scorn and derision by his peers.

He has all the hallmarks of a folk hero. He was an underdog with the wrong accent, the wrong background, and an unpopular theory that time proved to be true. He fought to protect poor young women, and—the story goes—paid with his life, driven literally mad by a world that didn’t recognize his wisdom until he died a lonely death in a sanatorium. The narrative is all the stronger because it doesn’t require complex scientific understanding. Semmelweis argued for something that today feels obvious to the point of being self-evident. In an era before personal protective equipment, when physicians simply rubbed their hands on a towel between cadaver dissections and clinic bed examinations, Ignaz Semmelweis asked his peers to wash their hands.

It’s the wrong story. But to appreciate the right one, you have to come with me to a time before germ theory. A time when chamber pots were emptied into the streets, and a surgeon’s prowess in the operating room was demonstrated by the thickness of the blood stains on his frock coat. The idea of a surgeon passing from autopsy to birth without a stop-over at the sink is appalling, until you learn, for example, that a single sponge was often used for repeated vaginal examinations of different women in labor. The sponge was rinsed with water: no visible contaminant remained. Would you be the one to suggest to serious men of science that some invisible and magical force remained thereon, to do mischief in a means unknown and unobservable?

So come with me, pre-germ theory scientists. But wash your hands first.

A tale of two wards

It’s 1846. In Europe, the feeling is one of modernity, progress, and scientific thought. Steam engines power giant ocean liners and support huge railroads, telegraph networks connect continents, and new factories are bringing industry, jobs, and political change to cities. Large public hospitals provide free care to people who previously went without. Microscopists are cataloguing the fascinating tiny world first glimpsed by Leeuwenhoek in the 1600s, and anatomists are performing autopsies on nearly every hospital death. Medical students gather in the dissecting rooms for hours, learning on real bodies what was once taught with models or pictures. Illness, in this very modern world, has real and physical causes; things that can be observed, quantified, explained, and remedied.

But it’s still 1846. Life expectancy hovers around 40. Anesthesia, using ether, was just tried for the first time this year. This is the year Robert Liston reportedly performed his infamous “most deadly operation in history,” and surgery of any kind is often fatal. The first antibiotic won’t be widely available for another century. Half of all children die before the age of five, and many women die in childbirth.

In Vienna, a young woman expecting her first child—if she was not wealthy enough to have a private physician make a house call—would have access to free care at the University Hospital. Vienna’s poor took advantage of the care, but they arrived at the hospital doors pre-warned. In whispers, friends and relatives would tell them: When you get there, ask to be admitted to the midwives’ ward.

The University of Vienna Hospital had two wards for pregnant women: one run by midwives, and one run by physicians and medical students. Both wards knew the terrifying specter of childbed fever. A woman would have a normal, healthy pregnancy, followed by uncomplicated labor and a seemingly healthy birth. Within hours, she would begin to grow weak, with a high fever, delirium, and eventual death. Often, but not always, her baby suffered the same fate. Childbed fever was the terror of the lying-in ward, and though its horror had accompanied births since antiquity, its cause and treatment remained unknown. It struck with curious intensity in certain places and times, and left others untouched. But most concerning for the scientific minds of the 1840s, its prevalence in public hospitals was skyrocketing.

In Vienna, as in most major cities, both maternity wards were busy, delivering thousands of babies a year. Unlike most major cities, the hospital in Vienna kept meticulous records.

In the maternity ward run by midwives, approximately one in 50 women would die of childbed fever. In the second ward, equally busy and staffed by physicians and medical students, the death toll could rise as high as one in four. A woman arriving to the hospital to give birth would have been warned. Please, she would beg the clerk. Please, send me to the midwives.

The Discovery

Ignaz Semmelweis grew up in Budapest, the fifth of ten children in a prosperous merchant family. As a German immigrant to Hungary, Ignaz grew up speaking German rather than Hungarian. The result was an accent that followed him into his professional life and, in his mind, marked him as an outsider everywhere he went.

When Semmelweis finished his schooling, obstetrics and gynecology did not yet hold a respected position in academic medicine. It was a field historically dominated by female midwives; with the establishment of new lying-in wards many early physicians found their way to obstetrics accidentally. Semmelweis was no exception, having been rejected in his original applications for posts in internal medicine. When an obstetrics post became available, he obtained a master’s in midwifery in order to apply. He was appointed assistant to Professor Johann Klein in the First Obstetrical Clinic of the Vienna General Hospital on July 1, 1846.

Semmelweis was struck immediately by the high mortality rate for laboring mothers, as well as the stark discrepancy between the midwives’ and doctors’ wards. Childbed fever was known throughout Europe, and everyone knew that it struck in some places more than others, and at some times more than others. One month, there might be almost no cases; at another time, hardly a bed would be left untouched. In the community, an obstetrician would suddenly find his patients falling victim one after another in rapid succession while a colleague’s patients were left untouched.

The obstetrics world had proposed any number of theories to explain the disease, and any number of attempts to treat or prevent it. With no concept of a germ theory of disease and a new reverence for anatomy, many physicians wanted to attribute the problem to some internal female structure. This was supported by long-held descriptions of breast milk as a transformation from menstrual blood, a physiologic theory handed down from Aristotle and Galen. Leonardo da Vinci proposed an anatomic explanation for this belief in his famous “coitus drawing,” which shows a duct connecting the woman’s uterus to her nipple—a duct necessary to explain the Galenic theory of milk production, but not a structure that exists in a woman’s body.

Physicians noticed that milk production slowed when a woman developed childbed fever. On autopsy, they found the abdomen full of thick, white fluid. Today, we know this fluid to be pus—the liquefied remains of dead white blood cells attempting to fight off an intra-abdominal strep infection. But at the time, it was seen as more evidence of a blockage in the feminine fluid flowing from uterus to breast.

Semmelweis initially ignored theories of physiology and focused on the observed difference in death rates. Regardless of the mechanism of disease, some difference in treatment or behavior must explain the different results seen in the two wards. Midwives, he found, had women lie on their sides during delivery. He had the doctors do the same, without effect. He saw that the priests who attended dying women would walk through the doctors’ wards ringing their bells to signal the death. Semmelweis asked them to avoid patient areas, which they did; it’s a good bet that patient morale improved as a result, but the mortality from childbed fever remained unchanged.

Semmelweis became obsessed with the problem, driven to distraction by the persistent and overwhelming death he saw around him. He spent more time than ever in the cadaver labs, personally inspecting the body of every woman who succumbed. His breakthrough moment came in 1847, when his close friend and fellow physician Jakob Kolletschka received a small cut on his finger while completing an autopsy of a woman who had died from childbed fever. Such an injury was not uncommon, and the result was also predictable: Jakob died of a fever himself only a few days later. As with most deaths in the hospital, Jakob received an autopsy—and the grieving Semmelweis pored over the description of his friend’s remains. In shock, he realized that “the disease from which Kolletschka died was identical to that from which so many hundred maternity patients had also died.”

Now armed with observations, Semmelweis dared to propose a new theory: there was some sort of “cadaver particle,” invisible to the eye, which could cause childbed fever. This theory finally explained the difference in the death rates between the wards, because unlike physicians, midwives did not have dissecting privileges. Without cadaver particles, they could not carry the disease from corpse to patient. It was a theory that gave Semmelweis a path towards prevention. If the cadaver particles could be eliminated, the disease transmission could be stopped. Since there was no visible contaminant that could be removed, Semmelweis focused on the one observable feature that clung to a physician after a dissection: the smell. Doctors had long used chlorine as a reliable way of removing the smell of cadavers from their hands. Reasoning that whatever caused the smell might cause the disease, Semmelweis mandated chlorine handwashing in the doctor’s ward in Vienna. In 1847, he saw the maternal mortality rate fall from almost 20%, to less than 2%, within months.

The Aftermath

In the light of history, it’s easy to imagine that only the willfully ignorant could dismiss Semmelweis’s results. Biographers and popular historians (including a 2023 movie) usually argue that:

“many [doctors] were outraged at the suggestion that they themselves were the cause of their patient’s miserable deaths. Consequently, Semmelweis met with enormous resistance and criticism.”

What alternative explanation is plausible? Semmelweis’s results were beyond question, as he himself would argue throughout his life. But to the modern reader, the narrative is compelling not because of the data but because of how deeply we have internalized the germ theory. We have learned practically from our cradles that germs cause disease, and handwashing prevents it. Semmelweis’s solution, simplified from “chlorine to eliminate cadaver particles” into “handwashing,” is self-evidently true to the modern mind.

Semmelweis found his conclusions self-evident, too. But he was speaking to scientists for whom invisible agents of transmission, without observational proof, were unconvincing. He was not the first person to suggest that doctors could transmit disease. For hundreds of years, “contagionists,” who believed that disease could be transmitted on infected material, debated with “anti-contagionists,” who argued for environmental factors like polluted air. While the germ theory would eventually prove the contagionists right, in the 1840s, both theories had strong observational evidence.

Semmelweis’s major contribution was a truly effective method of prevention, based in a contagionist framework. His chlorine solution, although he did not know it, was bactericidal. It killed the streptococcus bacteria that caused childbed fever. His own theory of transmission was incomplete (at best), but his observations were real and valid. Medical historian Sherwin Nuland notes that, having discovered what he believed to be the cause of the disease and a successful way to prevent it, Semmelweis should naturally have been drawn to publish his results, and conduct controlled laboratory experiments to prove them. He did neither.

In fact, he did the opposite. Anti-contagionist colleagues pointed out that at the time of his original reduction in death rates, the air filtration system of the doctors’ ward was replaced. Was his chlorine solution truly the cause, or was it the reduction in bad air? There were physicians in his own university working on animal studies, infecting rabbits with childbed fever to test the efficacy of various proposed treatments. Semmelweis could have done the same. He did not. There were microscopists examining bodily fluids under microscopes, including Filippo Pacini who first identified the cholera bacterium more than 30 years before Robert Koch. Had Semmelweis reached out to one of them, he might have advanced the cause of germ theory half a century early. He did not. He also did not publish his results, relying on word-of-mouth and the incomplete description of others to carry his method beyond his own ward, and becoming incensed when these partial accounts resulted in misunderstanding.

Once he became convinced of his theories, he became simultaneously unwilling to broker any criticism or questioning thereof.

Ignaz Semmelweis: Savior but not Saint

Semmelweis, when his story is told in science class today, is painted as a folk hero with broad, simplistic brush strokes. And there are stories in his life that fit this picture. While working in Budapest, Semmelweis saw the death rates rising in his obstetrics ward despite mandating the chlorine hand-washing. He traced the cause to a cut-rate laundry service, returning the linens so dirty they still reeked of the prior patient’s fluids. When his request for a new, and more expensive, laundry service was refused, he marched to the administrator’s office and buried his desk in a stinking pile of soiled sheets. A lone crusader for truth, in an arrogant and unscientific world.

But then there are the other stories.

His refusal to publish, despite the urging of friends and colleagues. His refusal to provide any confirmatory data, or to consider any alternative theories. And, as he aged, his increasingly violent outbursts towards supporters and detractors alike. He spent no time considering the need to change minds, convince others, or build systems. He seemed unable to fathom any legitimate or valid reason for doubt, and expressed as much to those around him. 13 years after his first public presentation of his method, Semmelweis finally published a written report of his theories. His 500-page epic entitled The Etiology, the Concept, and the Prophylaxis of Childbed Fever was, in the words of historian Sherwin Nuland:

“logorrheic, repetitious, hectoring, accusatory, self-glorifying, sometimes confused, tedious, detailed to the point of aridity—in sum, virtually unreadable.”

In between detailed clinical observations, it included ad hominem attacks on prominent obstetricians of the day and paranoid explanations of Semmelweis’s own professional history.

After the book’s publication, Semmelweis’s declining health, and his increasing irrationality, became impossible to ignore. He had always been a man of puritan morals, but he began to openly consort with a prostitute and make inappropriate remarks, often of a sexual nature, in hospital meetings. In 1865, his wife committed him to a public insane asylum, where he died 2 weeks later. His autopsy showed evidence of the same type of infection he had spent his life fighting—most likely transferred to him at the hands of the asylum’s staff, who were known to beat their charges. The cause of his neurological deterioration is unknown, with some favoring early onset Alzheimer’s and others arguing tertiary syphilis. How much of his lifelong erratic behavior could be attributed to a disease, and how much to personality, will likely never be known.

The myth of Semmelweis is the story of a misunderstood hero, whose Cassandreic adherence to his beliefs in the face of societal pressure drove him to insanity. The truth is more complicated. It is compelling to imagine him as a prophet, bringing to society the dramatic deduction of a brilliant mind. But it is the men and women who came after him, the ones who interrogated his conclusions, proved them right, communicated them widely, and built systems to implement them, who truly changed the world.

^{If you’re interested in learning more about Semmelweis, The Doctor’s Plague by Sherwin Nuland is one of the best written and most engaging medical history books I’ve ever read.}

I usually find conferences pretty soul-sucking: hotel conference rooms, fluorescent lighting, bad food. Trying to snatch a few moments of conversation with friends or colleagues while organizers remind you to clear the hallway and join the official sessions. Sitting in the back of a large ballroom, laptop out, sneaking in a little work while people disguise their own mini-talks as questions for the speaker.

Apparently, I’ve been going to the wrong sort of conferences.

Progress Conference 2025 was held at Lighthaven, a quirky and very Berkeley space filled with overgrown gardens, conversation nooks, and oddly shaped rooms that felt more like part of an eccentric mansion than a traditional conference center.

But the biggest difference? The people.

The conference was packed with talks, possibly too much so — compelling sessions sometimes ran concurrently. But the organizers encouraged what they called “the garden track,” blocking out time in the day to mingle in the garden and talk.

It was hard to define the “type” of person who attended the conference. I connected with third-generation farmers trying to bring progress to agriculture, physicians rethinking health policy, old friends in the urbanism space, and more. There was even a professional conference organizer who wants to advance the way we convene.

The plenary sessions were as diverse as the attendees. The first main stage event was an interview with Michael Kratsios, Trump’s science advisor and director of the Office of Science and Technology Policy (OSTP). The choice was controversial and emphasized the diversity of the crowd.

I found myself in frequent discussions about the “big tent” feel of the conference and the progress movement in general. Was it too diverse? Too open? Not clear enough on its aims or purpose? It did include a mixed group — and a very mixed bag of topics and viewpoints — but there was a vibe at the conference, a sense of life, a connection that made disagreements feel like opportunities.

In a plenary session on the second day, Blake Scholl, founder of Boom Supersonic, began to imagine what a better, more comfortable, more convenient airport could look like. Why don’t our airports look like that already? “We live in a world,” he explained, “full of things that are radically improvable, and yet we’ve learned to live with most of the problems.” To this sentiment, the crowd seems uniformly aligned: the big tent, the differing opinions, the differing fields, coming together in the belief that life is radically improvable and that each of us can be a part of that improvement. That each of us can bring about progress.

It is an inspiring ethos to live in, even just for a long weekend.

The pursuit of longevity

In the sections of the conference dedicated to health and longevity, the speakers and perspectives were as diverse as the plenaries. Many of the speakers did ostensibly fall under the umbrella of longevity science, and I took the opportunity to explore the topic as an area I’m less familiar with.

Science fiction, of course, includes many examples of extended lifespans, from Heinlein’s Lazarus Long to the reincarnating Time Lords of Doctor Who. But novelists usually focus on the extremes: the eons-old travelers who are functionally immortal compared to our own mere span of decades. Longevity researchers, by and large, chase a more proximal goal. What would an extra year mean to you, if it were a functional and healthy year? What if you could have five more years, or 10? What would it mean for society if people worked an average of 1, 5, or 10 more productive years?

But that’s still an incredibly broad target. Eradicating a specific childhood disease might have the same, or greater, impact on overall lifespan curves as finding a miracle drug to grant an extra year or two at the end of life to everyone who doesn’t succumb in childhood. The longevity crowd at Progress Conference 2025 played in both arenas: exploring the impact of specific technologies or treatments on longevity, and focusing on aging qua aging as its own disease.

Aging as a disease

Almost every speaker in the longevity group began their talk by sharing how underrepresented aging is in the science funding landscape, with only a small fraction of all science dollars going toward research in the field.

One challenge with breaking off aging as its own area of inquiry, especially with longevity as an outcome, is that most people don’t die of old age. Most people die of diseases, and many diseases become increasingly common as we age. So the first hurdle for the longevity field is defining its terms. Some speakers imagined how better preventive measures against cardiovascular disease could lead to increased longevity. Is that disease-targeted research or aging-focused?

Although still muddled, the emergence of longevity science as a standalone discipline is an exciting moment in the history of medicine. Throughout most of human history, most people died from a specific injury or disease. Childhood mortality rates were 10% in Europe as recently as 1950. They’re now below 1%, and in the past 75 years, life expectancy has nearly doubled across the world.

But these trends were not caused by eradicating “aging” — they came from curing or preventing diseases that cut life unnaturally short. The longevity talks, even those beginning with a plea for more focus on the field, oscillated between the potential impact of curing a specific disease and the potential impact of addressing the biological hallmarks of aging itself. Genomic instability, telomere shortening, mitochondrial dysfunction, cellular senescence — the new frontier is a challenge to find targeted interventions that impact these biological hallmarks. Not a cure for an illness, not a repair for an injury. Not the eradication of disease, but the pursuit of life. As the poet Alfred Tennyson wrote so many years ago, it is “…life, not death, for which we pant; More life, and fuller, that I want.”

Longevity economics

Interspersed with discussions of longevity science were talks on the economics of longevity. How would society change if people, on average, lived even one additional year? Of course, this depends on the quality of that year. Experts estimate that up to 25% of all Medicare spending goes toward treating and supporting beneficiaries during their final year of life. But if we could extend the average number of productive years, with each person working one additional year, the resulting benefit to the global economy would be in the trillions.

Discussing the economics of longevity is a challenge in part because the biggest thieves of productive years of life are specific diseases or injuries. An economic model of all-cause mortality does, by its nature, include all causes of mortality. John Burn-Murdoch, a data analyst and reporter for the Financial Times, hosted a Progress Conference 2025 session focused on the impact of suicide and drug use on longevity in the 20^th century. He argued that the historical trend for longer lifespans is threatened today by social mechanisms that particularly impact young people.

If longevity science includes funding toward addressing all threats to lifespan in its calculations, it is the most funded field in the world today. If it considers only funding that goes toward addressing biological markers of aging, it is a much smaller tent. But overall, the economists at the conference promoted one conclusion: More life, and fuller, is better for the economy. While the utilitarian argument is not the one that wins me over, it’s good to know that all of our interests are aligned in pursuit of longer, healthier lives.

Putting death on ice

Alongside the more general discussion of longevity science were fascinating deep dives into specific research areas. One of my favorites came from Laura Deming. Unlike most of us, who are only bothered by the idea of growing older when we start to experience the impacts of aging for ourselves, Deming became interested in the problem of aging when she was eight years old. She then began studying biogerontology at 12. Although she has a wide range of longevity interests and research projects, the focus of her talk at the conference was cryonics.

My prior knowledge of the topic consisted of liking Futurama and holding a vague certainty that Walt Disney’s head is frozen in a vault somewhere. (Fun fact: This is apparently an urban legend. Walt Disney was cremated, and it’s an example of the Mandela effect that so many of us think otherwise.) The actual father of cryonics was Robert Ettinger, born in 1918 and himself cryopreserved in 2011. Similar to Deming, he was smitten with the idea of longevity while still quite young. In his case, he fell in love with the stories published in the classic science fiction magazine Amazing Stories.

Ettinger assumed that by the time he grew up, scientists would discover the secret of immortality. He was already frustrated by what he saw as a lack of progress when he stumbled on reports of a French research team exploring cryopreservation. He began to advocate for the idea that everyone should be cryopreserved for reanimation by a later generation with more advanced medical technology, writing long letters at random to individuals selected from Who’s Who in America. Eventually, he published a book (The Prospect of Immortality) that captured the attention of Isaac Asimov, among others, and rocketed him to media fame.

In her talk, Deming called Ettinger’s plan “an ambulance to the future.” Her case is a compelling one. “One year of medical progress,” she argued, “can increase patient survival from 6-9 months to 10+ years.” And in specific disease cases, like metastatic melanoma or cystic fibrosis, dramatic recent advances mean that people born a year or two apart have dramatically different life expectancies. An ambulance to the future could mean a cure. Her current work is focused on a more proximal goal: cryopreserving organs to extend their viability and enable more transplants. Researchers have already demonstrated that a rat kidney that had been frozen, thawed, and then transplanted into a rat can regain full function. Human trials seem likely.

What’s next?

Most of my writing focuses on the history of medicine and innovators who found cures and solutions to problems that we barely remember today. To sit for four days with people who are so focused on the future, so committed to the next frontier, was an exciting departure. To pursue longevity, not survival — to target aging itself, not a specific disease — is to shift the paradigm of medicine. A transition from less disease to more life. The science is still in its early days, and it’s happening largely along non-traditional paths and with non-traditional funding and support models. In that, it keeps company with many of the true medical breakthroughs in history.

Coming out of the conference, I look forward to seeing frozen organ banks that enable more transplants, gene therapies that target cellular senescence, and pharmacological interventions that we can take like vitamins to extend the lives of our cells (and ourselves). But my main takeaway from wandering through gardens with longevity researchers? A reminder that human life is an unqualified good. More life is better, and the frontier of medical science is premised on that understanding.

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Early Life

Like so many other brilliant people, Montessori started life as a bad student. She was so inattentive, in fact, that she failed the first, third, and fourth grades. She faked illnesses, forgot assignments, missed tests. At home, when her parents tried to make her finish her work, she would fake migraines and confine herself to bed. When she finally passed the primary school exams, she was thirteen, looking in class photos like the older sister of her ten-year-old classmates.

But as luck would have it, her delayed graduation meant that she finished primary school just in time for Italy to open the door to secondary school for girls. To the surprised delight of her parents, she declared her intention to continue her studies. With her academic record, she couldn’t get into a classical school, so she enrolled instead in the Royal Technical School of Rome. As one of the first ten girls admitted, Montessori saw school with new eyes. No longer an imposition from the outside, she became fiercely committed to earning her place in the new world.

“I know I shall become a doctor of medicine.”

If going to secondary school was daring, going to medical school was unheard of. For a woman in Italy in 1890, it was not simply a matter of completing the application and earning admission. Montessori needed to find someone with the power to change society. She started with the head of the Board of Education, Dr. Bacelli, who informed her in no uncertain terms that the idea was impossible. She responded by standing up, shaking his hand, and calmly remarking: “I know I shall become a doctor of medicine.”

Eventually, she appealed to the Pope himself, and his intercession enabled her to enroll at the University of Rome.

Once admitted, her path was not a smooth one. As the only woman in her class, her male colleagues embarked on a campaign of intimidation. She, however, refused to be intimidated. When the men whistled or hooted at her in the hallways, she would reply, “Blow away my friends! The harder you blow, the higher up I shall go.”

But not all indignities were as easily ignored. She later recalled her first anatomy lesson, when a professor lifted a sheet to reveal a female cadaver— the only other woman in a room full of men. Her fellow students turned to stare at her, and one of them began to grope the corpse’s breasts. She completed the rest of her anatomy dissections alone, after hours, by candlelight. She even hired an assistant to sit next to her and smoke, in an attempt to overwhelm the smell of formaldehyde.

But with each obstacle, with each challenge, she persevered. And she made good on her promise: becoming the first woman to graduate as a medical doctor from the University of Rome.

Asylums and Animus

Montessori’s first job after graduation was as an Assistant in a Psychiatric Clinic in Rome. At the time, asylums frequently mixed children with adults, and developmental disorders with psychiatric disorders or even criminality. When she started, the nurses warned her to avoid the children. They were, she was assured, little more than feral animals. As evidence, the nurses pointed to the children’s behavior after mealtime: crawling around on the floor under the tables, scrabbling for crumbs and bits of food.

Montessori, however, found herself observing them intently. They were on the floor, and they were looking for crumbs, but they weren’t eating them. They were using the crumbs to build small piles, to play small games, to make patterns in the dust. In the absence of any toys, education, or meaningful interaction, they were starving not for food but for intellectual stimulation. She began to advocate for disabled children, and a few years later was appointed as director to a state school. She called the experience, “my first and only true degree in pedagogy.”

“Like Buds Destined Never to Bloom”

In 1906, the neighborhood of San Lorenzo in Rome became the focus of various charitable organizations. San Lorenzo had been called in the papers “the shame of Italy” for its poverty, lack of resources, and high crime rate. The tenement apartment buildings housed whole families in single rooms, so crowded that children sometimes shared sleeping space with prostitutes receiving visitors. In one dramatic episode, a San Lorenzo man chased his wife out into the street and murdered her in broad daylight, watched intently by the neighborhood’s children.

It was in this place that Montessori opened her very first school. In describing San Lorenzo, she recalled an impression of overwhelming darkness:

“Whoever enters, for the first time, one of these apartments is astonished and horrified. [Here are] many who have no ‘casa,’ [home], but only ghastly walls within which the most intimate acts of life are exposed upon the pillory. Here, there can be no privacy, no modesty, no gentleness; there is often not even light, nor air, nor water!” (Maria Montessori, The Montessori Method)

She looked on the children born and raised in darkness, without education, nourishment, or stimulation, and wrote that they were “like buds that seemed never destined to bloom.”

For these children, Montessori built her first school. She built for them a casa- a home. The “Casa dei Bambini,” or Children’s House. Outside its walls, all was dirt, and violence, and fear, and darkness. Inside, she built a world of peace, order, fairness, and purposeful work. And her children began to bloom.

The Montessori Method

Montessori started her school from a place of pure curiosity. She started with empty tables, a clean room, and minimal assumptions about what young children should or could learn. She observed: watching the children, seeing what they did without adult intervention, seeing what they gravitated towards. She remembered her small patients in the state hospital, scrabbling for crumbs. She received donations for the school, and provided the children with toys, dolls, games, and learning materials. And she watched.

She saw her children transform in the ordered, clean, and beautiful environment around them. Sparse as her first classroom was, it was a haven of peace compared to the children’s prior experiences. She watched as they began to like the cleanliness and order, even to enforce it on their parents at home. She saw her students, repeatedly, choose the learning materials over the dolls, the carefully ordered blocks instead of the games. They were drawn to order, they appreciated cleanliness, they began to rejoice in repeating a task over and over until it was done with proficiency.

Her students’ mothers saw the transformation, too. They began to come to Montessori with a new request. If so much was possible, if their children were capable of so much growth, was it possible to give them that one gift that would truly open the world for them? Could Montessori, perhaps, teach their children something the mothers themselves had never mastered? Could she teach them to read? Conventional wisdom at the time said no. Children under the age of 6 were incapable of reading. But when the mothers, illiterate themselves, made the request, Montessori knew she had to try.

She began bringing in an alphabet and teaching letter sounds, not expecting much. She discovered, instead, an “explosion into writing.” Coming back the following week, she found her pupils writing whole words with sticks in the dirt, covering walls with chalk letters. She began writing messages on the chalkboard, things like, “If you can read this, come and give me a kiss.” For days, the children seemed to ignore the missives, until a small girl came up to her one day and said, matter-of-factly, “Here is your kiss!”

She watched as children exploded into reading, just as they had taken so readily and joyfully to writing. An accomplishment previously thought impossible, in a place labeled unsalvageable, for children declared unteachable.

A world at war

By 1910, public schools in Italy and Switzerland had adopted Montessori’s methods, with new schools planned in Paris, London, Argentina, Australia, the United States, and more. Montessori began to teach, and to write. She published a dozen books on her educational methods. She trained hundreds of teachers who opened their own classrooms and schools.

In the 1920s, her rise to popularity attracted the attention of another rising Italian: Benito Mussolini, the founder of Italy’s Fascist Movement and newly appointed Prime Minister. Initially, Mussolini endorsed Montessori. He served as the Honorary President of the Montessori Society of Italy, and encouraged her to open a teacher’s training college. But the gulf was widening, as Montessori’s pacifism— grounded in her experiences of World War 1— clashed with Mussolini’s ambitions. In 1931, things came to a head when Il Duce demanded that Montessori require her teachers to take a loyalty oath. She refused, and Mussolini responded by closing all Montessori schools in Italy. Maria herself was forced to flee Italy in 1934 to escape the threat of imprisonment.

She moved to India, where— living in exile— she founded schools and teacher training programs, and continued to write about her method. When the war ended, she returned not to Italy but to Amsterdam, where she died at the age of 81 on May 6, 1952.

Her experience of war profoundly impacted her philosophy. It would have been easy, perhaps, for her to conclude that humanity was fundamentally flawed, that the future was a dark one, and that the work she was doing— so much of which had been destroyed by Mussolini— was for naught. Instead, she renewed her commitment to education as the most profound means of building a brighter tomorrow. She also renewed her belief that the better tomorrow she imagined was possible.

“If help and salvation are to come, they can only come from the children, for the children are the makers of men. The child is endowed with unknown powers, which can guide us to a radiant future. If what we really want is a new world then education must take as its aim the development of these hidden possibilities.” - Maria Montessori, Education for a New World

A personal note

Montessori, in reflecting on her first Children’s House and the dramatic changes she saw in her students, wrote:

“I changed my whole life. I was nearly 40. I had in front of me a doctor’s career and a professorship at the University. But I left all, because I felt compelled to follow [the children], and to find others who could follow them, for I saw that in them lay the secret of the soul.”

Those of you who have read this Substack might know why this resonates so powerfully for me. I, too, changed my whole life, at nearly 40. With a doctor’s career and a professorship at a university in front of me, I found myself following my students (I started with surgical residents) backwards, younger and younger, and finding through them a path to Montessori, and through Montessori, a new view of humanity, of children, and of the world. A new vision of what is possible for the future.

So: for anyone who might be curious about what I do when I’m not writing stories about medical history, three weeks ago I launched a brand-new Montessori elementary program in Austin called Montessorium. Our first model classroom is one of the most beautiful spaces I have ever seen, run by some of the most talented teachers I have had the pleasure of working with. We are combining Montessori pedagogy and curriculum with cutting-edge digital tools and systems. For every student who joins the class, we make three promises: students will love school, they will excel academically, and they will gain independence. It is everything I would have wished for in a school, and everything I have wanted to give to a child since starting on this education journey.

And you’re all invited!

If you’re in Austin, come check it out in person. If you’re not in Austin, follow along with photos and videos. And if you don’t care about any of that, but want to learn more about Maria Montessori (because you should!), here’s my favorite biography.

I was interning with a research group on cardiac surgery that semester, and images filled my mind of what he might be going through: a sternal saw to crack open the breast bone; a bypass machine to take the blood out of his body and oxygenate it; the heart itself naked and exposed to the outside world. After the surgery, the bone being forced back into position and held together with actual wires, thick as a piece of spaghetti. Weeks in the hospital, months of rehab. So imagine my surprise when, five days later, he showed up to class complaining about late papers.

His emergency procedure was not the open-heart surgery I imagined, but a coronary angiography with stenting. A needle was inserted in his groin, and a small flexible catheter advanced under fluoroscopy into his heart. Contrast dye was injected to identify the blocked arteries, and a small metal cage- a stent- was placed to hold the artery open and keep the blood flowing. The procedure took less than an hour. He was awake throughout and went home the next morning. He was back to lecturing, in apparent good humor, less than a week later.

My professor was one of the more than one million people who undergo a coronary angiogram every year in the United States. And whether he realized it or not, he was the end of a long line of advancements that had as one of its earliest stepping stones a brash, unapologetic German surgeon named Werner Forssmann.

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Operating on Myself

In his memoirs, Werner Forssmann recalls being told by a mentor that surgery was “the method of healing which uses mechanical means to rectify mechanically accessible disorders.” It’s a good definition, and for much of surgical history, the challenge has been to find a way to make more problems, more organs, mechanically accessible. Forssmann rose to that challenge, and set his sights on the heart. In the 1920’s, the options for investigating the heart were limited: percussion, auscultation, x-ray, and electrocardiogram. Forssmann recalls that “time and again our clinical diagnoses differed inexcusably from the pathologist’s post-mortem findings.”

While still a student, Forssmann discovered the work of French physiologists Claude Bernard and Etienne-Jules Marey. The pair had performed experiments on horses, inserting catheters “as thick as a finger” into the jugular vein and from there, into the horse’s heart. By inflating rubber balloons into the ventricles, they created graphs that provided an unprecedented understanding of the actual functioning of the heart. Forssmann immediately saw the potential of the technology: what it could do to medical care, which relied so much on guesswork regarding cardiac physiology; what it might do to surgical treatment of heart-related illnesses. He was transfixed.

The procedure had been completed successfully in animals, so Forssmann immediately jumped to the need to test it in humans. He presented the proposal to his supervisor, the idea of introducing a catheter into the vein of a patient in order to interrogate his or her heart. No anesthetic was needed, he assured his boss; it was not really surgery, after all, but closer in kind to a routine blood draw! The suggestion was rejected on its face. Forssmann was told to start with animals. He objected for two reasons: first, clearly the French had already proven the safety on animals! And second, more compellingly, he had no funding. In those days, physicians funded their own research, and he had no money to spare to purchase lab animals. Patients were cheaper.

He was instructed to abandon the project. He went another way. He decided to try the experiment on himself, but to do that, he needed the support of Nurse Gerda Ditzen who held the keys to the supply closets. He succeeded in convincing her that the experiment he proposed would change the world, and she agreed to assist him if he would let her take the risk as the first subject. After she helped him gather the materials, he asked her to lie down on an exam table and submit to restraints. It required such delicate technique, he explained, that she needed to be tied to the table so she would not disturb the procedure by moving. In his memoirs, she agrees readily. Once she was restrained, he stepped out of her line of sight and quickly made an incision in his own left elbow and inserted a urinary catheter into his own antecubital vein. When it was a foot inside his body, he released poor Nurse Ditzen from her bonds and instructed her to please call the x-ray nurse.

What happens next deserves, if there is any justice in the world, a Hollywood reenactment at some point. Nurse Ditzen was furious at the deceit and refused to call the x-ray team; instead, she ran into the hospital and spreads the news of what Forssmann had done. Forssmann decided, under the circumstances, to simply walk to radiology, the catheter dangling from his arm beneath a hastily draped sterile sheet. He arrived, only to find another physician appalled at his presumption and ready to pull the catheter out. They have an actual fist-fight in the x-ray room, which Forssmann won, the tube still dangling. He advanced the catheter further into his own arm, and then into his chest and finally his heart. He managed to take some x-rays before the rest of the hospital arrived and all hell broke loose.

In some historical descriptions, biographers claim that Forssmann’s mentor abandoned him, discredited him, even fired him, leading to a lifetime of relative scientific obscurity. In truth, after venting his not inconsiderable spleen, Forssmann’s mentor supported his work and acknowledged its importance. Together, they quickly prepared and submitted a manuscript to Germany’s preeminent medical journal of the day, Klinische Wochenschrift. It was this paper which would establish his place in the history of cardiac physiology. The response from the German medical establishment was not surprising. There was excitement, but also accusations of unethical experimentation, questions regarding the validity of the results, and various claims made that someone else had achieved the same result first.

It was not a lack of support, or mentorship, or funding, that curtailed Forssmann’s promising research career. Those were challenges, but they were the kind of challenges a man like Werner Forssmann was absolutely guaranteed to overcome.

His life was redirected by much broader forces. While Forssmann was busy threading a catheter into his heart, the Nazi party was steadily gaining power. By 1933, Hitler was appointed Chancellor. In 1934 he declared himself Fuhrer, and by 1939, World War II had begun. Whatever future Forssmann might have had, whatever story might have been told of the daring young upstart who operated on himself, it was overwritten by the story of a nation, a continent, and a world, at war.

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Memoirs of a Surgeon in Germany

Forssmann was 25 when he became the first person to successfully visualize the inside of the human heart. Over the next five years, while he struggled with the early career challenges of departmental politics and funding, he also bore witness to Hitler’s rise to power. In his memoirs, he is casual in his recollections of these years: an off-handed mention of a surgeon asked to leave his position because he was Jewish, who responded by killing himself and his wife in 1930. Or the collapse of the German urological societies in 1933, because such a high percentage of German urologists had been Jewish. Recollections of “eugenic sterilizations” of mental patients as an unpleasant but required task, similar to how a physician today might recall being asked to sit on a dull committee.

A member of the Nazi party and an officer in the German army, Werner Forssmann was not a war criminal. He joined the army as a means of avoiding conscription into the Nazi paramilitary organizations, the SS (Schutztaffel) or the SA (Sturmabteilung). He did not participate in the atrocities of the concentration camps, and he rejected offers of Nazi-funded labs and the promise of unlimited research subjects. When confronted with direct orders to harm innocents, he disobeyed— like when a young enlisted man in his company was revealed to be Jewish. Forssmann received an order to send the man to Berlin, and instead was able to falsify records and help him escape.

But he was also not a hero, and makes no attempt to paint himself as one in his autobiography. He ignored the early dangers of the Third Reich, joining the Nazi party to advance his career while watching Jewish colleagues lose theirs. Despite his later renown, his is the story of an everyman who sought a pragmatic path to survival. As Thoreau tells us, “the mass of men serve the State thus, not as men mainly, but as machines, with their bodies.” Such men make up the armies, fight in the wars, and suffer from them. It is strange to think of our innovators, the individuals who advance the cause of science, technology, and medicine, as Thoreau’s “posse comitatus.” The ability to think outside the box in one field does not necessarily translate to any special genius in others; and the Nobel Prize winners of medicine can still serve as the standing army of the state.

When the war ended, Forssmann reunited with his beloved wife and six children, who all survived. His history of party membership barred him from returning to surgical practice, and he toiled in relative poverty and obscurity for the next two decades while the science of cardiology advanced without him in America. He had found a degree of tranquility in small town life when, in 1956, he received a phone call from a reporter asking him how he felt about being on the short list for a Nobel Prize. He shared the award that year with Andre Cournand and Dickinson Richards, who had worked to establish heart catheterization as the standard for cardiac diagnosis and treatment. He described the unexpected award as equivalent to “a parish priest who suddenly became the pope overnight.”

Copies of Forsmann’s autobiography, “Operating on Myself: Memoirs of a Surgeon in Germany” are hard to find today. He is a straight-forward and compelling storyteller, even if the narrative could have benefited from a skilled editor. There is no Kindle version, and no one has yet reviewed it on Goodreads. But the forgotten memoir hits with surprising relevance today, not simply as an opportunity to revisit the evolution of cardiac surgery, but as the story of a middle-class professional in Germany and the choices he made as he survived the second world war.

What guilt, if any, does Werner Forssmann carry for being born German, for living through World War II, and for being a brilliant innovator who joined the Nazi party? He confronts, in his foreword, the “sharp dividing line between communal guilt and individual criminality,” and the gulf he sees developing between his countrymen and the rest of the world. What guilt does he bear for the crimes committed by his country, and how should his pre-war decisions be viewed in the light of history? It is a question he grapples with throughout the book, and a question for which we as readers can find no easy answer.

1. Forssmann, Werner. Experiments on Myself: Memoirs of a Surgeon in Germany. New York: St. Martin's Press, 1974.

2. Thoreau, Henry David. Civil Disobedience. Originally published 1849. Reprinted in Walden and Civil Disobedience. New York: Penguin Classics, 1983.

Perl shared her own contribution to the game, whispered into the ears of starving women wearing lice-infested rags inside a death camp:

“I am a lady- a lady doctor in Hungary. It is morning, a beautiful, sunny morning and I feel too lazy to work... I ring for my assistant and tell her to send the patients away, for I am not going to my office today… What should I do with myself? Go shopping? Go to the hairdresser? Meet my friends at the café? Maybe I’ll do some shopping. I haven’t had a new dress, a new hat in weeks…”

Perl depicts the horrors of Auschwitz with unflinching clarity: the physical depravations, the loss of freedom, the mass murders and torture. She also exposes the deepest perversion of the Nazi death camps, the worst potential outcome for its surviving victims. Auschwitz was designed to transform its inmates into what the Germans claimed them to be: subhuman. In unthinkable conditions, facing the most horrifying of choices, inmates devolved into theft, prostitution, even murder. Having torn from its victims every possession, every personal tie, every life-sustaining or supporting aid, Auschwitz tried to take their fundamental humanity. And how can any sane observer, staring into that abyss across the span of time, find blame?

But despite the conditions, Perl and the women around her found a way to keep a sense of self. Throughout her memoir, Perl spotlights individual women and girls who fought back. Not with weapons, as they had none; not even with words, at least not directed towards their captors. And sometimes, not successfully. But they fought back with spirit, with a refusal to see themselves as the Nazis painted them and pushed them to become. Night after night, in darkness and filth, they reminded themselves: I am a lady. I am a person. I am human.

Before the war, Gisella Perl was a lady doctor in Hungary: the only woman, and the only Jew, to graduate from secondary school in her small hometown. She studied medicine in Berlin because, at the time, the city had a particularly large population of Jewish doctors. She spoke Hungarian, Romanian, German, French, and Yiddish. She worked as a gynecologist alongside her husband, Ephraim Krauss, who was a surgeon, and together they had two children. She played the violin.

Before the war.

“Obliterate the biological basis”

In March of 1944, the German army invaded Hungary. Perl and her family, like the rest of the country’s Jewish population, were forced into an overcrowded ghetto where they hoped they might stay until the war’s end. By then, it was clear that worse fates than the ghetto were possible. But within months, the family was in a cattle car traveling towards Auschwitz where they were met with “the smoke of the crematory… the air full of the nauseating smell of burning flesh.”

The 400,000 Hungarian Jews who arrived that year to Auschwitz were sorted as they came through the gates, first women from men, and then life from death. Joseph Mengele, the camp doctor who would later come to symbolize for the world the worst atrocities of the Holocaust, stood at the front of the line ordering people to the right, towards the rat-infested barracks and a temporary chance at life, or to the left, towards the crematories.

Perl, along with four other doctors and four nurses, was ordered to establish a hospital for the camp. They treated everything from broken bones to broken skin, from tuberculosis to typhus. It was medicine without medication, without instruments, without even basic nutrition or running water. Perl lanced abscesses and set bones without anesthetic. With no ointments to help relieve the rashes and sores resulting from parasites and poor hygiene, she started using the margarine from their meager dinner as a salve to cover the wounds. And when nothing else was possible, she talked with her patients, reminding them of the past and painting for them the possibility of a future.

Early in her time at Auschwitz, Mengele ordered Perl to report any pregnancies directly to him. These women, he said, would go to a different camp and receive double rations. Many prisoners, desperate to escape starvation, rushed to declare their pregnancies. Perl discovered the lie when she witnessed a group of pregnant women being beaten and attacked by dogs before being thrown alive into the crematorium.

The goal of Auschwitz, as camp commandment Rudolf Hoess recorded in his autobiography, was no less than to “obliterate the biological basis of Jewry.” An infant was a potential future; a fertile woman, a threat. Initially overwhelmed by what she saw, Perl recalls that “gradually the horror turned into revolt,” and she made the decision that no more pregnancies would be revealed to the Nazi doctor.

The decision was heroic in its aim and gut-wrenching in its execution. Many women arrived at the camp already pregnant; others became pregnant through prostitution or what Perl delicately called “love” with guards or prisoners. When Perl found that a woman was expecting, she explained what discovery would mean: a painful death for the baby and the mother. She then helped the woman to conceal, and eventually terminate, the pregnancy.

For women who were only a few months along, she manually dilated the cervix to remove the fetus with her fingers— an operation done “in the dark, always hurried, in the midst of filth and dirt.” The mother’s abdomen was bandaged, and she went back to roll call the next morning. For women who were closer to delivery, she ruptured the membranes (caused the water to break) to accelerate spontaneous delivery. If the child was stillborn, she buried it among the heaps of corpses that littered the camp. If the child was born alive, she had a harder task.

She is unflinching in her recollection of an infant, born alive, who she knew faced torture and experimentation if discovered:

“I took the warm little body in my hands, kissed the smooth face, caressed the long hair- then strangled him and buried his body under a mountain of corpses waiting to be cremated.”

Pregnancy in Auschwitz was a death sentence. By ending pregnancies, she offered the mother a chance “to come out of this death camp not only alive but in a condition to have other children — later.”

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“You owe me a life, a living baby.”

Seven months after her arrival, Perl was sent away from Auschwitz- potentially because of her intimate knowledge of Mengele’s torture chamber laboratories and what occurred there. She was transferred to Bergen Belsen, a place that was even more horrific:

“Bergen Belsen can never be described, because every language lacks the suitable words to depict its horrors. It cannot be imagined, because even the most pathological mind balks at such a picture. One must have heard those unearthly screams of agony which continued through the day and the night, coming from hundreds of throats, unceasingly, unbearingly…”

In this hellscape, Gisella Perl was put in charge of “Block III,” the maternity ward. With no equipment, no medication, no water, she treated hundreds of women. Starving, lice-infested, typhus-ravaged, the outcomes were rarely positive. “And yet,” Perl wrote, “the doctor in me never gave up even when the human being reached the limits of its endurance. I fought on with bare hands, cut my shirt into rags to wipe the hot, moist, soiled faces of my patients, tried to smile at them through the layer of filth that covered my own face.”

On April 15, 1945, Perl was in her maternity ward at Bergen Belsen helping Marusa, a young Polish woman from the Warsaw underground movement, give birth. Around them, the camp buzzed with rumors of liberation. The allies are coming! Will the Germans destroy the camp, with all of us in it, to destroy the evidence of what they have done? Or is freedom within reach?

As the British forces entered Bergen Belsen, Marusa’s baby offered up its first screams of life to mingle with the cries of thousands of newly liberated prisoners. The first free child of the camp was born. But Marusa was hemorrhaging dangerously, and Perl lacked even the most basic tools to stop the bleeding. She ran from the tent to beg the arriving troops for water, for disinfectant, for help. Supplies in hand, she returned to perform a hysterectomy on her knees, in the dirt, with battle-hardened Brigadier General Glyn Hughes kneeling beside her, tears running down his face. Marusa and her baby survived Bergen Belsen.

After the war, Perl testified to the Nazi atrocities she had witnessed and experienced, raising money for survivors and refugees. “I didn’t want to be a doctor,” she confessed, “I just wanted to be a witness.” She credited Eleanor Roosevelt with releasing her back into the world. After one of Perl’s lectures, Mrs. Roosevelt invited her to lunch and urged her: “Stop torturing yourself; become a doctor again.”

Perl was granted US Citizenship in 1951, and set up a practice at Mount Sinai Hospital as a gynecologist specializing in infertility. When she discovered that her daughter was still alive, she moved to Israel with her and worked at the Shaare Zedek Medical Center in Jerusalem. She practiced another 43 years, until her death in 1988, delivering roughly 3,000 healthy babies after the war. And every time she entered a delivery room, she offered the same prayer.

1. Perl, Gisella. I Was a Doctor in Auschwitz. International Universities Press, 1948.

In my first week of medical school, I sat with 300 classmates in an echoing auditorium heavy with history and anticipation. I felt like Hippocrates was looking down at me, maybe holding out a phantom hand, whispering to me: all of this is yours, now. I’m not one to overlook an opportunity for wonder, and I felt it in spades. The oil paintings on the walls, the polished wood podium, it was all just the way it was supposed to be. Up to and including the white-bearded, white-coated lecturer who stood at the front and told us the same joke he had clearly told every new class for the past two decades:

Welcome to medical school! In the next four years, half of what we’ll teach you here is going to be false. We just don’t know which half yet!

He winked, offering a touch of showmanship up the rows of seats, and 300 nervous first years erupted into laughter.

I didn’t laugh.

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I was 22, and very naïve, and very over-awed. And I believed that I was stepping into a field that had things figured out. Not cured, you understand. I knew, of course, that there were lots of things we couldn’t fix. But I hadn’t made the conceptual leap from “unable to fix” to “not understood.” Knowing that we can’t cure cancer is very different from realizing we don’t fully understand it. And recognizing that our understanding is incomplete is only the first ice floe in the ocean of epistemological realizations. The second jump is when you recognize that some of what we do know will be overturned with new knowledge. As that realization hit me, I felt like some part of the foundation of my world had cracked, just a little.

I didn’t yet appreciate that I was entering into a tradition built on incomplete understanding. If Hippocrates had any message to pass down to me, this was it. My professor may have overestimated the percentage, but he was sharing a fundamental truth about our new field. The world does not wait for human omniscience; patients present with diseases long before doctors know how to treat them. And what then? In our earliest histories, people used plant-based pharmacology to treat the symptoms with a heartfelt appeal to the unknowable divinities who were believed to cause the problem. The earliest healers relied on their senses for anatomy and pharmacology. For physiology, they looked to the gods.

It was in Ancient Greece that the search for reasons transitioned from the supernatural to the natural. While Hippocrates is remembered today largely for his eponymous (and mistranslated) oath, he earned the title “Father of Medicine” for bringing the field from the ordained to the observable. Unlike his contemporaries, he rejected divine punishment or demonic possession as an explanation for illness. He focused, instead, on what could be perceived with the senses, and he pushed his students to do likewise. Before radiology, before germ theory, before microscopes— Hippocrates did not yet understand the cause of any specific disease. But he put the nature of health and illness into the realm of the understandable, and medicine began. Aristotle, although speaking of himself, described the impact of Hippocrates as well when he said:

Mine is the first step and therefore a small one, though worked out with much thought and hard labor. You, my readers or hearers of my lectures, if you think I have done as much as can fairly be expected of an initial start... will acknowledge what I have achieved and will pardon what I have left for others to accomplish.

The early explanations of health and disease, physiology and pathophysiology, often sound absurd to our modern ears. Take, for example, the pneumatic theory of circulation, first proposed about 150 years after Hippocrates by the Greek anatomist Erasistratus. This theory prevailed for more than 1500 years- until William Harvey famously cut open a pig on a lecture hall stage to disprove it. Among other things, the pneumatic theory argues that there is a ‘pneuma,’ or vital spirit that is essential to health, that travels in the arteries. In this theory of circulation, blood enters the lungs through the pulmonary artery and, by the time it leaves the lungs again, transforms into the invisible pneuma. That pneuma travels throughout the bloodless arterial system, where it enables thought, feeling, and function.

How did the greatest minds of Ancient Greece reach a conclusion so misguided? Especially since they were proponents of a natural, observable theory of disease, and “the gods did it” was no longer an accepted answer. They drew conclusions based on what they knew. The first thing they knew was that the arteries were empty of contents. Unlike veins, which carried blood, the arteries must have some unseen purpose. Hence the concept of the unseeable pneuma. So how could Hippocrates, Aristotle, and Erasistratus know that arteries are empty, when every school child today knows they are full of blood? Their source of information was, primarily, the body after death. In a corpse, the thick-walled arteries drain quickly of blood, which pools and collects in the thin-walled and expandable veins. The result is that when our early anatomists conducted an autopsy, they found a system of empty tubes.

These empty tubes- the arteries- connected to the lungs. The lungs connected to the outside world via the trachea, or windpipe. Open your mouth and take a deep breath. It’s obvious that you take in air through the windpipe. As anatomists dissected the heart, they found a similar contradiction: the thick-walled left side of the heart is empty of blood in a corpse more than a few hours old, as it quickly pools in the lower pressure right side. The observers saw a system of veins full of blood, and a system of empty arteries. They concluded- reasonably!- that the visible blood, once it entered the lungs, must transform into the invisible substance that filled the arteries. Pneuma.

You might be thinking: “That’s all well and good, ancient anatomists, but surely one of you must at some point witness a living person who receives an arterial injury? Or even butcher an animal? You must see the blood spurt forth and realize that arteries are not full of air?” They noticed that, too, and had an explanation for it. Nature, Aristotle himself explained, abhors a vacuum. When an artery in a living being is opened, the negative pressure pulls blood from nearby veins to draw it into the damaged space. This explains why the empty arteries can bleed, and why the pressure of that bleeding is so much higher than a cut vein.

I wonder if, when students sat at Hippocrates’s feet and began to study with him, he told them gently, “My students, half of what I will teach you may be false. I don’t know yet which half.” Perhaps they laughed. Perhaps one of them was shocked. The reality of medicine is a need to act in a world of incomplete knowledge. An absolute need in the absence of absolute truth. So all students of medicine learn that lesson eventually, and all of the great minds that have pushed medicine forward encounter it constantly. Surgeons, it is said, are “sometimes wrong, but never unsure.” They cannot afford to be unsure, when the disease is certain; they cannot afford doubt, when the choices are absolute. Cut, or don’t cut; the structure bleeds, or it doesn’t. Sometimes what we know is proven wrong. Sometimes what we don’t know is proven essential. Sometimes people die in that space of the unknown. And the surgeon’s task is to accept, and start again the next day. For the anatomists who move the world forward, it’s fuel: not for uncertainty, not for doubt, but for a better understanding of the world tomorrow than we have today.

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So how does a single operation carry a 300% mortality rate? Imagine with me an operating theater: a literal theater of the old school, with tiers of benches for students, professionals, even curious laypeople off the street to watch the action from above. Onto the stage strides Robert Liston—6’2” tall, with a booming voice and a showman’s appreciation of his audience. He was known to call out to onlookers as he started, “Time me, gentlemen. Time me!” And he meant that literally, as the students in the audience would pull out pocket watches. This was an era before anesthesia, when speed was everything. Liston, made famous for removing a leg in less than 30 seconds, enjoyed the moniker “The Fastest Knife in the West End.”

On this fateful day, Liston approached the table to begin the amputation of a badly injured lower leg. He drew his scalpel and, in a smooth motion, cut through skin and muscle. As he switched from scalpel to bone saw, he was moving so quickly that his swipe went through the hand of his assistant, struggling to hold the fully awake patient to the table. One version of the story claims that an onlooker was so horrified, he suffered a fatal heart attack in the gallery. Later, both patient and assistant would die from wound infections.

The only known operation with a 300% mortality rate.

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So who was this swashbuckling surgeon, this attention-seeker, this dangerous daredevil with a blade? Not many years later, the Nobel Prize-winning thyroid surgeon Emil Theodor Kocher would offer a pointed criticism of this kind of bravado:

Surgeons who take unnecessary risks and operate by the clock are exciting from the onlookers’ standpoint, but they are not necessarily those in whose hands you would by preference choose to place yourself.

In Victorian England, when Robert Liston served at the University College Hospital in London, surgery took place without anesthesia, without antibiotics, and with a roughly 50/50 chance of the patient making it out of the hospital. The most a surgeon could offer to a patient by way of comfort was alcohol, opium, or a bullet to bite on—and speed. If you can imagine the pain of enduring a limb amputation fully awake and aware, perhaps you can understand why Liston’s skills were so sought after. He was a giant in his own time; contentious, perhaps, and cantankerous, but widely acknowledged as a technical virtuoso. Today, he is more often a punchline than a protagonist in the annals of medical history.

The infamous tale of the 300% mortality rate is not the only cautionary (and possibly apocryphal) story told of Liston’s breakneck speed. In another story of botched amputation, he went so quickly through a patient’s thigh that he included the man’s scrotum in the cut. And once, he tried to lance an abscess that turned out to be a carotid artery aneurysm, causing the child to bleed out in front of him. In today’s emergency rooms, the story of the abscess-that-wasn’t is used to remind residents to get imaging. A simple ultrasound probe ensures that no one ever makes that error again. But in Victorian England, there were no ultrasound probes. No CT scans. No anesthetic, no numbing medication.

The roll call of Liston’s errors is a long one. While it is truly said that the only surgeon without complications is the one who doesn’t operate, not all complications are created equal. It is hard not to classify some of these outcomes as “things that should never happen.” And to classify Liston himself as a blowhard who, as Kocher put it, took unnecessary risks as he operated by the clock. And yet.

And yet, in an era when average surgical mortality rates hovered around 40%, Liston took the tough cases and boasted a mortality rate of 10%. And yet, in the preface to his textbook Elements of Surgery, he implored surgeons to embark on a study of anatomy in order to know when not to operate, for when they understood “the functions and structures of parts… mutilation is more rarely required—and operations are dispensed with.” And yet, when he found the notorious grave robbing anatomist Robert Knox creating a lewd display with the corpse of a young homeless woman, Liston punched Knox unconscious and paid for the young woman’s burial.

Perhaps most compellingly, on December 21, 1846, Liston performed Europe’s very first operation under anesthesia. Ether gas became popular initially as a recreational drug, fueling “ether frolics” that caused ordinary people to behave in extraordinary ways. American surgeon Crawford Long saw its potential in medicine when he realized that his trips and falls under the drug’s influence were pain-free. His American colleagues quickly appreciated the potential. But physicians are nothing if not conservative, and in Europe, many argued against the use of ether by claiming that the excruciating pain of a surgical procedure enhanced the healing process.

The argument was nonsense, rooted not in observation or physiology, but in a dogmatism that feared to upset the status quo. For a surgeon like Liston, who built his career and his name on the double-edged sword of speed, anesthesia was an advancement that threatened the source of his fame. He might, with his colleagues, have rejected the new technology. Instead, he embraced it fully, with the bravado he was known for. As his first ether-supported operation concluded, he declared to the room, “This Yankee dodge beats mesmerism hollow!” In Europe, the anesthetic du jour was mesmerism, a form of hypnotism that worked exactly as well as you would expect it to work. Recognizing a game changer when he saw one, Liston tipped his hat to the Americans and brought his country into the age of anesthesia.

Today, Liston is often remembered as a footnote in surgical history. His Liston amputation knife is still used, among other tools and techniques he developed; but his most enduring legacy is usually a sort of surgical ghost story. “Have you heard the one about the 300% mortality? The one about the amputated scrotum?” And yet. And yet, he was someone who stood up for his patients because he saw their humanity. A surgeon who tried not to operate if a better option existed. And a man who, fiercely and outstandingly competent in his field, was ready to make his competence obsolete in pursuit of a better way. He was flawed, and flamboyant, and probably insufferable to work with. And he pushed the world forward for all of us.

If you don’t know the story of Antigone, it’s not a complex plot: most of the action takes place off stage. Antigone is a daughter of Oedipus (yes, that Oedipus). The play starts when the Trojan War ended, and both of Antigone’s brothers have been killed. Unfortunately, while one brother (Eteocles) fought for the winning side and was buried with military honors, the other (Polynices) died fighting for the losing side. King Creon of Thebes declares that Polynices will rot on the hillside, “to be a sweet treasure for [vultures’] eyes and beaks.”1 Antigone, early in the play, makes the daring choice to disobey the King and bury her brother. The remainder of the play is mostly taken up with Antigone being sentenced to death, preparing for death with several fantastically angry and righteous speeches, and then ultimately being led off to die. You can’t beat the Greeks for tragedy.

It might feel like an odd plot in the modern world— especially for a cast of mostly 20-something atheists. Antigone was willing to die rather than have her brother’s body go unburied. She did die, for the crime of covering his corpse. How compelling can that conflict possibly be in today’s world? For Antigone, or others who view bodily integrity after death as a key to entry into the afterlife, perhaps the motivation sings more instinctively. But for those of us who have the organ donor heart proudly displayed on our driver’s license? Who find cremation a practical and admirable funerary practice, and would rather see ashes scattered than sit morbid in an urn?

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There are things I would die for— although of course, that resolve remains untested in my life to date. But the treatment of a corpse, even the corpse of a beloved, is not high on the list. Still— it is not hard for me to understand the outrage, the righteous anger, that runs through Antigone when she declares:

“I will bury him myself. And even if I die in the act, that death will be a glory.”

The way we treat our dead is part of what defines humanity; what separates us from other species. When we hear that elephants, for example, dig graves— it is profound information that shakes our concept of the animal. The idea of desecration or violation of a corpse or a grave is deeply disturbing at a visceral level; perhaps because there is no state more helpless than death. And if you imagine yourself in Antigone’s place, with a brother, a friend, a loved one, condemned to humiliation and desecration after death, the anger and the outrage and the horror is easier to understand.

But this is a story about anatomy, not afterlife. And as I think back on Antigone, her furious speeches and her emotionally moving sacrifice, I find myself drawn to a strange comparison with the anatomists whose stories I’ve sworn to tell. How do we reconcile the gothic and the gruesome with the heroic and the hard-fought?

The history of medicine is no stranger to horror. I will, one day, tell the full story of the anatomy murders of Burke and Hare. But it is just one part of the fascinating back-and-forth legality of human dissection that influences and underlies the history of anatomy. The Murder Act of 1752 made it legal for medical schools to dissect the cadavers of executed criminals- but only those. As medical schools and private anatomy labs expanded, demand quickly outstripped supply for cadavers. The market solved, as it so often does, with the cottage industry of Resurrection Men: glorified grave robbers, who dug up corpses and delivered them to dissecting room back doors.

Burke and Hare cut out the middleman, so to speak. William Burke and William Hare owned a lodging house, and when a lodger died with a debt unpaid, they sold the corpse to Dr. Robert Knox, a well-known anatomy teacher. They quickly realized the untapped potential of the market, and started creating their own supply by killing more than 15 of their lodgers. Ironically, after Burke was found guilty and hanged in 1829, his body was donated to the medical school for dissection— in fact, his skeleton is still on display at the University of Edinburgh Medical School.

The history of anatomy is not for the faint of heart.

But Burke and Hare were not anatomists. They were more aligned with Creon, the king who thought punishing a corpse was a valid means of political action, than with Antigone. Because what really drove Antigone? What inspired her to action, what made her willing to die for her principles? She has been compared to Joan of Arc, a French peasant girl canonized after her death for her willingness to die for God and country. But I don’t see Antigone as a childlike token of man or deity. Her love is not for duty, but for humanity, as personified by those she loves. In fact, after Creon sentences her to death, Antigone retorts:

“It is no shame to pay respect to one’s own flesh and blood. I was not born to share in hatred, but in love.”

The anatomists are united in love, not hatred. A deep, unshakeable love of the truth, and of humanity. Put yourself in Antigone’s shoes. The dark of night, a lonely hillside, the vultures sweeping overhead. Around you, corpses— your enemies and your countrymen. You come in search of a brother who, when you find him, is not the brother you remember. He is a dead thing, broken and putrefying. Your task is unpleasant in the extreme, even putting aside the mortal danger, and yet you persevere. Antigone, without a doubt, had the soul of an anatomist. What is it that unites every individual who has ever— in pursuit of truth— defied the edicts of society, of tyranny, and of the gods themselves, to do what many think immoral, indecent, or simply unsavory? It is the belief that there is nothing in the world more noble than understanding. Nothing more crucial than the truth. And nothing more enticing than the knowledge of who we are as human beings.

Antigone— the Greek heroine who died rather than suffer desecration of her brother’s corpse— in this way joins the ranks of every anatomist who has ever risked censure by exploring the mysteries of the dead or living human form. They were not born to share in hatred, but in love.

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Charlene, still unbuckled, was ejected through the window and died instantly. James and his children, buckled to their seats, were injured. But James was an orthopedic trauma surgeon, and he knew the immediate dangers the family faced. Putting aside his own pain and fear, his first concern was fire. He managed to drag his children away from the plane and into the dark Nebraska night before searching the forest for his wife. He found her- dead- about 300 feet from the aircraft. And then he began to wait. His three younger children were in and out of consciousness; his oldest couldn’t move his right arm, and he himself had facial fractures that left him nearly blind. With the fear of fire resolved, the fear of hypothermia and head injury came to the forefront.

As the minutes became hours, Styner decided that help wasn’t coming. At around 2 in the morning, he left Christopher, his oldest, to watch the other three children and slowly walked towards the road. Bloody and staggering, looking in the dark night like something out of a horror movie, he began trying to flag down a passing car or truck. Incredibly, the third vehicle to pass him stopped. With the driver’s help, he loaded his children into the car and they drove to the town’s hospital.

As they pulled up to the hospital, James exhaled in relief- gratitude washing over him for the proximity to help. He was quickly disillusioned. They had crashed down in Hebron, Nebraska, a town of less than 2000 people. The hospital was not just small: it was closed. The night nurse who opened the door initially refused them entrance, citing protocol that demanded a doctor be present for any admission. Finally, the town’s two general practitioners were roused and arrived, and the family was taken in for treatment. Things did not improve once inside.

The hospital’s staff were clearly inexperienced with trauma and overwhelmed by the arrival of five bleeding, concussed patients. Their assessment and treatment of the family was haphazard and without method. James would later recall with particular clarity watching a physician carry his 8-year-old son to the x-ray area in a cradle carry- an arm under his knees and shoulders, the child’s head dangling with no thought to a potential neck injury.

James Styner knew what excellent trauma care looked like. He was horrified by the contrast to what he saw his children receiving. He began frantically calling his partners, working to arrange emergency transportation to his own hospital- barring the Hebron providers from any further contact with his children as they waited. Finally, a helicopter was arranged, and the five Styners arrived at Lincoln General Hospital. A team of emergency personnel stood waiting for them, and immediately sprung into action. Styner, finally able to hand over the care of his children and receive much-needed treatment himself, recalled the feeling of “coming out of a hostile dark hell into civilization.”

The family was eventually discharged, and they spent the next year recovering physically and emotionally. They grieved the loss of Charlene. Their wounds slowly healed. But Styner found himself unable to move past the accident- focusing not on the losses, or even the plane crash itself, but the horror he felt when he realized that the hospital did not know how to help his family.

Defining the Problem

It would have been easy to focus on who messed up. Styner himself was flying the plane, and then, to arrive at a hospital where a nurse barred entry, and a physician ignored basic principles of care, leaves a great deal of room for blame. Styner had a different perspective. He was familiar with the trauma bays of Lincoln, a large city with busy hospitals that might see a dozen traumas on an average night. He also understood the urgency of trauma: what is known as “the golden hour.” Half of all trauma deaths occur within 60 minutes of the initial injury. His own family had survived the golden hour, but what if they had a more urgent problem? Patients injured far from a metropolitan center did not always have the luxury of time to wait for a transfer. How could a rural physician, who saw a major trauma only once or twice in their career, or a small town hit by a natural disaster, respond to the unexpected with competence? What they needed, Styner realized, was a method. A protocol or an algorithm for how to approach these situations.

The idea was not entirely novel. Another Nebraska surgeon, Steve Carveth, had only recently developed the protocols and algorithms known as “ACLS” – Advanced Cardiovascular Life Support. ACLS helped physicians move quickly when faced with a heart attack. Similar algorithms were being increasingly used for the treatment of a variety of chronic and acute illnesses— from medication choice in asthma, to diagnosis and treatment of stroke. But these algorithms focused on one specific disease or disorder. The same markers, the same diagnostic criteria and tests, the same treatments. Could it be possible to build a protocol for trauma? Trauma is as wide as the world. It’s a plane crash and a gunshot to the abdomen; a laceration and a lost limb; it’s a trip-and-fall and a three-car pile-up. How do you build an algorithm for the unknown?

The Birth of ATLS

Styner put together a team of experienced nurses and physicians. They analyzed how they themselves responded when a trauma arrived; the protocols and practices they followed but had not yet codified. The things that were normal and natural for busy trauma centers, but unknown to the rural physician.

In some ways, they created nothing new. The team was not trying to develop a new diagnostic test or a more effective treatment. Their focus was on ensuring that every patient, at every hospital, received the best treatment already available. What they created was an approach. An algorithm.

Today, when a trauma patient arrives at the hospital, regardless of their injury, they are met by a team poised and ready. Because today, every member of that team is most likely trained in Advanced Trauma Life Support. Which means that regardless of injury, every patient who rolls into an emergency room after an accident is met with the A, B, C’s.

Let me take you to the trauma bay for a moment. Imagine that you’ve just survived a car accident, and the ambulance has transported you to the nearest hospital. As you’re rolled into the trauma bay, you’re met with a team who slides you from the stretcher onto a hospital bed. There’s a person at the head of your bed, whose face looks down at yours.

“What’s your name, sir?”

That’s “A” – for airway. It’s not really a polite inquiry; they want to know if you’re able to speak. If you answer (“My name is Joe!”), your airway is clear. A gurgle, choke, or silence in response means that your airway may be compromised- and nothing else matters until the problem is resolved. Nothing else matters because a blocked airway means no oxygen is getting to the brain, the heart, the kidneys, the gut. The patient is minutes away from permanent brain damage. The airway is cleared, or nothing else happens. “A” is always first.

But now that you’re speaking, a stethoscope is brought to your chest- rise and fall, rise and fall. Are there breath sounds on both sides? This is “B” – breathing. Are the lungs expanding? If not, the team stops until the problem is identified and resolved. At which point they move on to “C” – circulation. What’s Joe’s heart rate? His blood pressure? Does he have a pulse? If there’s a pulse in the carotid artery at the side of the neck, that’s good; if there’s a pulse in the radial artery in the wrist, even better. A pulse all the way down in the dorsalis pedis artery, on the top of the foot? Better still- the heart is strong enough and full enough to get blood as far away as it needs to go.

A, B, C comes first because these are the things that kill trauma patients in the golden hour. It might seem obvious: if someone isn’t breathing, their broken leg is unimportant. But when Joe arrives with his thigh bone protruding at a grotesque angle through his skin, it is very hard to realize that there could be a problem that is more urgent but less apparent.

The physician or team who responds to a trauma prepares for everything, expects anything. What Styner and his team created was a mental model; a process; a path. A rhythm that keeps everyone in the room dancing to the same beat, and prevents them from missing the potentially lethal injury in the face of the more immediately obvious.

Airway. Breathing. Circulation.

An algorithm for the unknown.

The Impact

The American College of Surgeons adopted the ATLS protocol (originally called “the Nebraska protocol”) soon after its development. It was expanded upon, reviewed, and taught- first in Nebraska, then throughout the United States, and now, around the world. Researchers have found that preventable trauma deaths are cut roughly in half after hospital or city-wide ATLS training, with the biggest impact in the hospitals for whom the protocol was developed: rural centers, small hospitals, and developing nations.[1][2][3]

Change is often slow, and not every innovator receives recognition in their own time. Even fewer see the impact of their work fully realized. Styner is one of these few. Before his death in 2024, more than 1 million physicians in 86 countries were trained in ATLS. It has become not just the standard of care for trauma, but a language in its own right, connecting trauma providers across cultures and communities. Styner saw the power of that language first-hand when he joined a medical mission to Peru. Two Peruvian marines were injured in a gunfight and rushed to a small field hospital. The local team and their patients spoke only Spanish. The visiting American doctors spoke only English. But “the common thread was the ATLS ‘language’ that was used by both groups,” and the result was a team working in concert: coordinated, organized, efficient, and effective.

Styner had transformed his personal tragedy into a systems-based solution. And the results are visible around the world.

Emil Theodor Kocher, Chair of Surgery in Bern, Switzerland, changed what was considered possible by making thyroid surgery technically feasible. He had decades of successful patients to look back upon. But success, in surgery, in the 19th century, was very much defined as getting the patient off the table. The really ambitious surgeon aimed for getting patients out of the hospital. Kocher had changed what was considered possible— but he hadn’t changed the definition of success. Not yet.

The Letter

In 1883, Kocher was 42 and at the height of his career. He was widely acknowledged as the best technical surgeon in Europe, if not the world. And it was at this point that he received a letter from a local physician in a small neighboring town. The physician asked if Kocher happened to remember a patient named Maria Richsel, a girl whose thyroid he had removed nine years earlier when she was 11 years old.

By this time, Kocher had removed more thyroids than any surgeon alive. Maria was one case among thousands. Her primary doctor reported that since the operation, she had undergone “a complete and substantial change in the nature of her character.” Before the surgery, she had been maturing normally. But now, while her younger sister “has now grown up to a blossoming young woman of very pretty looks, the sister operated on [Maria] has remained small and exhibits the ugly looks of a semi-idiot.”

The family doctor asked: is there any chance that the thyroid operation caused this change in her? She had stunted growth, altered facial features, and her once-normal intellectual abilities were severely limited. The changes seemed to date from the time of her operation.

Conservative opinion of the time was a definitive no: the operation was not to blame for the alterations. Others had noticed a possible connection between the thyroid and a collection of symptoms that included growth retardation. But it was rarely reported, sometimes disbelieved or dismissed as a coincidence, and in those who did see a connection, assumed to be the end-stage result of the original thyroid disease. In other words, the thyroid was clearly diseased and had become enlarged as a goiter. Taking it out should have prevented these symptoms, but if you see them anyway, maybe you operated too late.

French physiologist Claude Bernard described it this way in 1879:

We know absolutely nothing about the function of the [thyroid], we do not even have an idea of its utility and of the importance it may have, for its removal has not told us anything about this, and anatomy alone remains absolutely silent.

The thyroid is widely believed to be useless in health, and dangerous only when diseased. And its removal— if technically possible— should be pursued.

So what does Kocher do when he gets this message? He told the story very plainly in his own words, looking back:

It was the influence of just one case, on whom I had operated in 1874 (that changed my opinion on the nature of the thyroid) and about whom a doctor mentioned that the girl in question had since undergone a complete and substantial change in the nature of her character. This was so important to me, that I now took all pains to see the girl with my own eyes. I was astonished to a great extent by the conspicuous looks of the individual in question. I immediately sent invitations to all my patients on whom I had operated for goiter asking them to present themselves for examination.

This is what’s known as a “single surgeon case series.” Today, it’s the lowest level of clinical evidence: it’s one step above an anecdote, because it’s a series of anecdotes. In the 1800s, it was a nearly unheard-of level of review.

Surgeons in the 1800s were not looking back on their cases for long-term outcomes. The goal of a surgeon was to finish the operation. His patients left the hospital. From what he knew, they were happy and healthy and living their lives. To ask people, sometimes years later, to come back and see how they were getting on is an appreciation of physiology that is completely novel in medical history to this point. Kocher’s response was an epistemological landmark in a field that needs epistemology badly. It was the recognition that what was thought absolutely true yesterday— the thyroid does not have a necessary function— must immediately be called into question today upon the appearance of new data.

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Kocher sent invitations to his last hundred patients; 60 of them responded. Of these, 28 had only a partial removal of the gland. These patients, he reported, “enjoy the best of health and are very happy with and grateful for the success of the operation.” The results in 34 patients who had a total removal of the gland were entirely different: “Of the patients who presented themselves for examination, only 2 showed unchanged or improved general status.”

On April 4, 1883, Kocher reported his findings to the German Society of Surgery in Berlin. It was a long lecture, including a 15-page description of his findings and theories. He described each of his patients with their outcomes in detail. Those who had their whole thyroid removed had a slow physical and mental decline over months and years. They stopped growing, with puffy, swollen hands and faced and pale, thick skin. Kocher called it cachexia strumipriva, or “wasting away resulting from the lack of a goiter.” Today, the condition resulting from severe lack of thyroid hormone is called “myxedema.”

Kocher concluded that the thyroid clearly had a crucial function, even if the anatomy couldn’t demonstrate what that function might be. He described it somewhat poetically as the task “to paralyze the influences which produce stupidity.” And it’s possible to imagine that he must have felt much like his students, at the bedside of a wound infection, desperate to beat his breast and exclaim, “I have sinned!” He wrote later:

In technical terms, we have certainly learned to master the operation for goitre. We can deal with bleeding and prevent loss of speech. But something else happened… removal of the thyroid gland has deprived my patients of what gives them human value. I have doomed people with goitre, otherwise healthy, to a vegetative existence. Many of them I have turned to cretins, saved for a life not worth living.

The Pursuit of Truth

A surgeon is a strange type of person. He or she must be willing to stake their livelihood, and someone else’s life, on their knowledge of the world. I used to tell medical students: there are no subjectivists in the operating room. Anyone who has held a scalpel knows that you cut, or you don’t; the structure bleeds, or it doesn’t. It is a thing, definite, and the consequences are apparent. You learn to trust your senses and your conclusions. You need to trust your own mind, because if you don’t, you become paralyzed, unable to act. Surgeons, it is said, are sometimes wrong— but never unsure. So what happens when the state of knowledge changes? When what was absolutely true yesterday is called into question today?

Ironically, it was probably Kocher’s unparalleled precision that allowed him to so clearly demonstrate the purpose of the thyroid. Other surgeons attempting to remove the thyroid gland were less absolute in their anatomy and their methods. Theodor Billroth, an equally famous name in the history of surgery, worked with Kocher on some of the technical and antiseptic advancements that enabled safe thyroid surgery. But when he followed Kocher’s example and reviewed the results of his own operations, he found a much lower incidence of symptoms. William Stewart Halsted, in his 1920 book on the history of goiters, explained the difference:

I have pondered the question for many years and conclude that the explanation probably lies in the operative methods of the two illustrious surgeons. Kocher, neat and precise, operating in a relatively bloodless manner, scrupulously removed the entire thyroid gland doing little damage outside its capsule. Billroth, operating more rapidly and, as I recall, with less regard for the tissues and less concern for hemorrhage, might easily have left fragments of the thyroid behind.

Kocher’s precision, his competence, his uncompromising dedication to excellence— his very merits— were what exposed his error.

He spent the rest of his career searching for an explanation for his findings. His ideas on the physiology and pathology of the thyroid gland caused controversy, as any new ideas must do. He did not discover thyroid hormone; that happened after his death. But he did experiment with oral and injected extracts of thyroid tissue as a treatment, an early precursor to transplantation and hormone replacement therapy. And he was adamant that surgeons should not remove the whole gland.

Importantly: he continued to operate, and he continued to operate on the thyroid. He completed more than 5000 thyroid surgeries in his career. After seeing Maria, he removed only half or three-quarters of the gland, noting that this partial removal resulted in no long-term consequences.

And he remained a giant in his field. He was awarded the Nobel Prize in 1909, in recognition both of his technical advances and his work on thyroid physiology that eventually did lead to the discovery of thyroid hormone. Today, hormone replacement for hypothyroidism is common, and many types of thyroid cancer are completely curable with a total resection. For that, we thank Kocher.

And as we thank him, it’s worth reflecting on the nature of his accomplishments, which go beyond the technical or the anatomic. In his middle age, at the height of his career, Kocher faced the possibility that his life’s most important work to that point— the technical perfection of thyroid surgery— was causing disastrous harm. Rather than flinch from the possibility, rather than deny, deflect, or despair, he flew into action, with a need to understand that overrode all other considerations.

Kocher’s story, when it is told (usually in an operating room, by an endocrine surgeon, to either bore or entertain a medical student), is told as a story of achievement, advancement, and innovation. A timeline of discovery after discovery, invention after invention, a testament to meticulous attention to detail and a creative mind.

But his real contribution, which carries no eponym, is to medical epistemology: the study of how we know. It is the simultaneous ability to be so confident in your knowledge that you will stake lives upon it— and so aware of its limitations that you will question it in an instant, on a word. This is the true legacy of Emil Theodor Kocher, and it’s the one that you can take with you into whatever field you work in. Because all of us, in our own way, are doing new work, pursuing new insights, and developing new things. We all build a life upon our past work, build new knowledge on past knowledge. In medicine, new treatments give rise to new complications; in technology, potential innovations create new challenges; in culture, new movements surface new weaknesses.

Kocher’s story is the story of all human progress. It is the story of a fallible human being who, through exacting methods, unremitting toil, and moral courage, improved our understanding of the world.

The most common cause of a goiter in 19th century Europe, and indeed in the world today, is iodine deficiency. In Maria’s day, it was a fairly world-wide problem, and it was common to see men, women, or even children with the tell-tale bumpy neck. Today, it’s still endemic in some parts of the world, and coming back in others as people turn from iodinated table salt to various colorful Himalayan varieties.

Goiters, today as then, are unwelcome. The disfiguring bulge could impact someone’s likelihood of finding a spouse, or getting a job. If they grew big enough, they could even make it hard to swallow or to breath. So Maria’s family considered themselves lucky in living only a short distance from the hospital in Bern, Switzerland where 33-year-old Emil Theodor Kocher worked as Chair of Surgery. Kocher had pioneered the techniques that made it not only possible but safe to remove the thyroid gland. And in 1874, Maria’s parents brought her to Dr. Kocher, who saw her safely through the surgery. He removed her thyroid using all the modern advancements, including carbolic acid for disinfectant and ether for anesthesia. Maria sailed through the operation, with no bleeding, no infection, and almost no pain. She was up, happy, and home within days.

For the next ten years, Dr. Kocher continued his work, and if he thought of Maria at all, it was as one amongst many successful cases.

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Who is this surgeon?

Emil Theodor Kocher, born 1841 in a middle-class home in Switzerland, graduated at the top of his medical school class, which earned him the opportunity to travel throughout Europe and learn from the top physicians in the continent. In Berlin, he saw technical precision and beautifully sterile conditions. But when he applied to work in a lab there, he was denied- because they accepted only German applicants. He continued his travels to Paris instead, where the surgeons had not yet adopted the still-new theories of Joseph Lister, that pioneer of antisepsis. The French surgeons rarely washed their hands, let alone their instruments. Young Kocher saw the results: a dramatic difference in the rate of post-operative infection between the sparkling German theaters and the far less meticulous surgeries of Paris. The first antibiotic was still some 70 years away, and the most common outcome of a post-operative infection was death. Kocher returned to Switzerland a staunch supporter of sterility, near fanatical about following the best available practices for disinfection.

And he set to work.

This was the era of eponyms: every time a surgeon or scientist discovered something, he named it after himself. Medical students today hate this tradition, for what it’s worth. It’s never fun to explain to someone that they have Charcot Marie Tooth disorder, for example, which is a nerve disorder that has nothing to do with your teeth but is instead named after three people named Martin Charcot, Pierre Marie, and Briton Howard Henry Tooth. But whatever your feelings are on the validity of eponyms and their annoyance to the generations that follow, they are a means of mapping the impact of those who came before. And there are very few people with as many eponymous instruments, procedures, techniques, and signs as Kocher.

The “Kocher maneuver,” for example, is a simple three-step procedure for reducing a dislocated shoulder, developed after hours of manipulating joints in the local morgue. It’s still a common method used today. The “Kocher incision” is still used to remove gallbladders; the other “Kocher incision” is still used to remove the thyroid. The “Kocher clamp”— a surgical tool capable of holding delicate blood vessels closed without destroying the tissue- is still one of the most commonly called for instruments in operating rooms today. There are at least a dozen others. In an era when surgeons loved naming things after themselves, there are more Kochers in a textbook of surgery or anatomy than almost any other name.

His fame was not limited to his innovations. Operative results in his hands were dramatically better than the average surgeon of the time. At least part of the difference was due to his dedication to cleanliness and sterility, still a relatively new concept and not universally embraced in all operating rooms. But sometimes, even with his fanatical oversight, a trainee would break sterility and a patient would develop an infected wound.

When this happened, Kocher would require the student or junior physician responsible for the break in sterility to stand at the patient’s bedside, literally beating his breast and declaring for the ward to hear: “I have sinned!”

So this is Maria’s surgeon. A local boy made good, Chair of Surgery in his hometown hospital, close confidant to notables of the day, and revered in his own lifetime for his inventions, innovations, and precision. His operating technique was described as “infinite accuracy, infinite care, infinite patience that gave him results as near to absolute perfection as it is possible for surgery to go.”

Don’t touch the thyroid!

Kocher is technically as good as it gets. But it’s still the 1800s: and surgery is still in its infancy, or at least its early childhood. Throughout surgical history, the story of advancements is a story of what part of the body everyone generally agreed you can’t touch. Later innovators would question the maxim “don’t touch the heart,” or “don’t touch the pancreas.” But for Kocher and his contemporaries, the off-limits organ was the thyroid.

The thyroid gland, when healthy, is a fragile butterfly-shaped piece of tissue draping gently over the trachea (or windpipe) in your neck, just below the skin. You can, if you’re gentle, feel your own thyroid. Feel the indent on the top of your breastbone (the “sternal notch”), and slowly, gently, move your fingers up your neck, with one hand on each side of the windpipe. You’ll feel a soft, barely perceptible mass of tissue. That’s your thyroid! So what does this delicate butterfly organ do for us, other than get big and ugly if you abandon iodinated table salt?

Most organs were well understood in 1874. The details were fuzzy, but the function was clear. Except for these delicate, soft, and easy-to-overlook organs. Organs that blush pink in healthy, living tissue, but fade quickly to gray or yellow in a cadaver. The thyroid. The pancreas. The adrenal glands. What today we know of as “the endocrine system.”

The endocrine system is unique in the body’s systems. Its organs are isolated: they lay draped on top of other tissues, delicate and soft. Medical students in first year anatomy courses will sometimes struggle to even find the endocrine organs in their dissections, so well do they blend with surrounding tissues. Their function, we now know, is to produce and distribute hormones. Hormones are chemical messengers that travel in the blood stream and impact bodily functions far away from where they originate. There is no tube, no duct, no visible connection between the thyroid gland and the tissues impacted by thyroid hormone. And in the 1800s, no one had seen hormones. No one knew they existed. The word “hormone” (from the Greek, to set in motion) had not yet been coined.

So if you were an early anatomist, confronted with this disconnected pinkish gray lump, what would you assume was its function? Leonardo da Vinci, in 1511, created the earliest known anatomic drawing of the thyroid, and hypothesized that maybe its purpose was to hold the windpipe away from the sternum. Kocher himself, reflecting back on his early career, explained:

“Unfortunately the physiologists know next to nothing about the physiological significance of the thyroid gland, and this may have been the main reason for surgeons tacitly assuming that the thyroid gland had no function at all.”

The admonition not to touch the thyroid was not, then, due to its presumed importance. It was considered an overgrown bit of tissue in the neck that was likely useless in health, and became bothersome or even cancerous in its diseased state. Surgeons were eager to help sufferers and remove the goiters, but they soon learned caution. In 1866, American surgeon Samuel Gross summarized the general experience operating upon the thyroid:

Can the thyroid gland, when in a state of enlargement, be removed with a reasonable hope of saving the patient? Experience emphatically answers: NO. No sensible man will attempt to extirpate a goitrous thyroid gland. Every step he takes will be envisioned with difficulty, every stroke of his knife will be followed by a torrent of blood. And lucky will it be for him if his victim lives long enough to enable him to finish his horrid butchery.

A goiter is a life-changing problem for a man or woman in this era, leading not just to difficulty finding a marriage or job but also issues with infection, pain, eventually even trouble breathing. But the disease was often better than the cure: more than 50% of patients undergoing thyroid surgery died on the operating table or soon after from uncontrolled blood loss or infection. The French Academy of Medicine banned thyroid operations entirely in 1850.

Why was it so dangerous and deadly to remove the thyroid gland? The problem was three-fold: anesthetic, antiseptic, and anatomic. First, the only anesthetic option was short-acting ether. One of ether’s side effects is laryngeal spasm and coughing. Potentially okay if you’re operating in the leg; deadly in a delicate operation on the throat. Antisepsis- sterile procedure- is a novel and not entirely accepted practice. There are still physicians who move from the dissecting room to the operating room without a stop-over at the sink. And finally, the anatomic: the thyroid, especially when goitrous, is incredibly vascular. Dozens of tiny blood vessels supply the enlarged gland. Today, the options for stopping bleeding range from cautery, to hemostatic powders and glues, to fine sutures more delicate than a hair, and a choice of any number of hemostatic clamps and forceps. None of these existed in the late 1800s.

Three Problems

How did thyroid surgery transform from “horrid butchery” to a routine procedure? While not the only surgeon willing to dare the challenge, it was Kocher’s innovations and meticulous technique that truly enabled this transformation.

He tackled all three problems. He addressed the anesthetic challenge with specialized masks, delivering the ether below the level of the incision. He addressed the antisepsis challenge with his absolutely rigid adherence to best available sterile practices, dramatically reducing infection rates. But it was his technical advancements that truly revolutionized the field. These came in a wide variety of forms: he changed the type of incision used to access the thyroid, resulting in better visualization; he invented new instruments that held delicate blood vessels entirely closed without crushing or tearing; and he was beyond meticulous in his technique. One of his contemporaries wrote about him:

His operations numbered many thousands, and they represented scrupulous and minutely careful technical display; every tiniest detail was arranged, every difficulty gently overcome; there was no haste, no untidiness, no shedding of one drop of blood that could be spared.

The result of his work? The total removal of the thyroid gland, an operation so dangerous it was condemned by medical societies, became commonplace. In Kocher’s hands, the mortality of thyroid removal dropped from more than 50% to less than 0.5%. Remarkably, this is the same mortality that the procedure holds in experienced hands today. And for a time, that was the end of the story. Through precision, discipline, and innovation, Kocher changed the game for what was possible.

Until the letter came. About a girl named Maria.

Part two: He touched the thyroid

In the Royal College of Physicians in London, the 2^nd annual Lumleian Lecture on Anatomy is about to begin. The speaker is William Harvey: a small, dark man with penetrating black eyes and a quick, vivacious manner. Despite his presence on one of the most prestigious podiums of the day, Harvey is actually only a junior Fellow in the College— younger and less esteemed than most of the learned professors and physicians who fill the first rows of his audience. And despite the fact that the lectures were traditionally delivered in Latin (a language that the lay public and indeed most surgeons at the time could not understand), the hall is packed with onlookers of every class who are drawn by rumors that the lecturer has strange views, and stranger methods.

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Harvey is about to change the world. He is about to tell his audience that the Church, the venerable professors, and almost everyone in the College is wrong about the function of the heart, and the flow of blood in the body. He is about to reveal what medical historians will later call, “the greatest medical discovery of all time.” But to understand that discovery, we need to back up a bit and understand the era, the man, and the pivotal importance of what he’s about to do.

This is England during the Scientific Revolution. This is the Renaissance, the Enlightenment. It’s the century when Galileo will prove that the earth revolves around the sun, and Isaac Newton will describe the laws of gravity. But it’s also the century when Galileo is put under house arrest by the Catholic Church for his heretical theories. About 50 years before Harvey’s lecture, a man named Michael Servitus was burned at the stake as a heretic for contradicting the church’s teaching on the flow of blood. And it’s not just religion that impacts scientific progress: it’s also secular dogmatism. In all cultural areas, Europe— as it awakens from the Dark Ages— is looking with enchanted and deferential eyes to the past. The “rebirth” of the 17th century was not, initially, the creation of new art, culture, or philosophy. It was a renewed interest in, and emulation of, the art, literature, philosophy, and even science of classical antiquity.

What does this mean for medicine? It means the creation of the Cult of Galen. Claudius Galen, born in 131 AD at the height of the Roman Empire, was a physician to the emperors and a surgeon to the gladiators. He wrote extensively on human anatomy, producing hundreds of treatises. He also lived and worked in an era when human dissection was prohibited, raising the question: where did Galen get his data? Most likely, he had three sources. The first was other anatomists, either predecessors or contemporaries, including early Hindu and Chinese scientists. The second was likely his unique access to gaping wounds in the abdominal and thoracic cavities of the gladiators, giving him by dint of his position the ability to perform near-autopsies every week. The third source of data was that most commonly used by early anatomists: comparative anatomy. Galen performed countless meticulous dissections of pigs, apes, lions, dogs, and more— trying to determine which animal was closest to human for each body part.

Galen’s work led to real breakthroughs in understanding the human form. He was the first to describe many major nerves, for example, and he showed that urine was formed in the kidney, and traveled in tubes (ureters) to the bladder. He was also the first to discover the function of the heart: a pump to push blood through the arteries, those tubes that earlier anatomists believed carried air, rather than blood. But he also developed or perpetuated a number of misconceptions, some deriving from the differences between the animals he studied and the people he sought to describe. While his own observations on the function of the heart were a dramatic advancement, he still believed in the “pneumatic theory” of blood flow, handed down from Hippocrates. This theory argues that blood originates in the gut after each meal, then receives its vital force (the “pneuma”) from the liver, before heading back to the heart to be dispersed throughout the body. In other words, blood flows through the body in a one-way circuit away from the heart. It arrives at a final destination in the body (organs or limbs) and never travels back.

Galen was one of the most influential and prolific scientific writers of the Roman empire, and in the classical revival of the 1600s, his teachings were not simply rediscovered. They were canonized. One of his fiercest defenders was Jacobus Sylvius, a French anatomist. When presented with evidence of an error in Galen’s writings, Sylvius supposedly responded angrily:

“Then man must have changed his structure in the course of time, for the teachings of Galen cannot err!”

In 1616, both the Royal College and the Church had firm views on the nature of the heart and the flow of blood in the body. To question one was to commit secular heresy and risk career suicide; to question the other was to commit religious heresy and risk imprisonment or death.

And in that context, let’s return, to our unprepossessing lecture hall on a bright spring morning in 1616. William Harvey is about to take the stage— and dare both.

The Lumleian Lecture

Looking out on an audience who imbued theories on the flow of blood with both divine and political importance, Harvey must have known that he needed to overwhelm his audience with evidence. His lecture lasted the entire day. He referenced over 100 authors and performed a dozen experiments live on stage. The audience, largely, agreed with Galen and the pneumatic theory of one-way blood flow. Harvey told them they were wrong. And then he showed them.

First, he brought a live pig— squealing and thrashing— onto the stage. He took out a scalpel and slashed its neck, cutting first through the internal jugular vein, which resulted in a steady flow of dark mahogany. His next slash went through the carotid artery, spraying the stage with a geyser of brilliant crimson. With the two types of blood flowing in front of him, Harvey asked his audience: what explains the difference in pressure between the two types of vessels? Could it be, perhaps, that one system holds blood being forced away from the heart, pressured by each beat of the strong muscle, while the other more gently carries blood along the reverse journey?

His next demonstration went further. He invited on stage a large man with muscular forearms and generous veins. Harvey tied a tourniquet around the man’s upper arm, causing his veins to bulge out even more dramatically (you can see this in your own arm, if you ever have your blood drawn at the doctor’s). First, Harvey asked the audience to observe that the veins were not uniform: there were irregular swellings along their length. Valves, he argued. The swellings had been observed and described by Hippocrates, among others, but their function was unknown in 1616.

Next, Harvey used his finger to gently compress one of the veins in the middle of the man’s forearm. When he pushed gently, the vein disappeared between the place of obstruction and the next valve as though emptied of blood. He then used another finger to coax the blood out of the vein and down towards the hand. He was able to “milk” the vein in this way and compress it, collapsing the vein all the way down to the hand. According to the pneumatic theory, the hand was the blood’s final destination. If blood flows in a one-way circuit, he had simply sped up its journey. But when he released his finger, a startling revelation occurred: the blood rushed back into the vein, filling upwards from the hand and towards the tourniquet! The blood flowed through the vein TOWARDS the heart!

Blood, Harvey declared in conclusion, flows in two directions! It flows with high pressure through arteries going away from the heart, and then it returns from the tissues in the low-pressure veins going back towards the heart. It was a conclusion that flew in the face of Galen and his followers, and a conclusion the church considered heretical. Harvey had, in one lecture, fundamentally changed our understanding of how the body works— laying the groundwork for centuries of advancements to come. The preface of the English version of his book (originally published in Latin as De Motu Cordis) described it thus:

“Truly a bold man indeed, O disturber of the quiet of physicians! Who first of all durst oppose an opinion so confirmed for so many ages by the consent of all.”

Harvey was more blasé in his own reminiscences of the lecture, saying:

“These views as usual pleased some more, others less; some chid and calumniated me, and laid it to me as a crime that I had dared to depart from the precepts and opinions of all anatomists; others desired further explanation of the novelties.”

There were countless anatomic discoveries still to make after 1616, and some were made by Harvey himself. Others came from his students or the new schools that sprang up throughout Europe and the United States as anatomists shook off the shadow of Galen. The 1616 lecture— long, dramatic, and disturbing— was a first step towards many later advancements and discoveries. Its importance lies in its knowledge, true, but also in its methods. Harvey stepped on stage and defied his community, his country, his deity— in pursuit of truth. He put the observations of his senses and the conclusions of his mind above all else, and in return, he ushered in a new age: The Age of the Anatomists.

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As a child, I wanted to be a traveling storyteller. I was heartbroken to discover this wasn’t a viable career option.

As a young adult, I fell in love with medicine: with the intensity, clarity, and hope that is the soul of a hospital. I went to medical school, finished residency and fellowship training, and took a job as an academic surgeon. Later, I left medicine for education- which is a story for another day. But in that new field, I had the chance to teach, write curriculum, and reflect on how and why young people should learn history. I discovered Maria Montessori, and agreed with her when she said:

“History must be alive and dynamic, awakening enthusiasm … The history of human achievements is real, a living witness to the greatness of [humanity], and the children can easily be brought to thrill to the knowledge that there are millions of people like themselves, striving mentally and physically to solve the problems of life, and that all contribute to a solution though one may find it.”

- Maria Montessori, To Educate Human Potential

As I’ve been reflecting on my meandering path recently, I’ve been thinking about Steve Jobs’ observation that you can only understand your story looking backwards. Only at the end do the dots connect into a pattern. But as I look back on my choices, my changes, my chances, I’m wondering if my far-flung dots might be starting to come into alignment. Might be starting to show a pattern along the axis of storytelling, history, and medicine. So I’m revisiting “traveling storyteller” as the next entry on my resume.

I’ve named these posts “The Anatomists,” in honor of the first medical pioneers who captured my imagination and filled me with awe and admiration. These were the individuals who mapped the human body, making possible so many medical and surgical innovations to follow. And yet-- they’re almost entirely forgotten. I asked an incredibly well-read and well-educated friend the other day what he knew about Galen, and was shocked to hear he did not know the name. To my knowledge, there is no accessible, popular biography of William Harvey. Vesalius is absent in every history class I’ve ever taken. Even Hippocrates is a poorly translated oath, rather than a man.

The impact of the anatomists rivals that of Newton or Einstein; surely their courage matches that of Socrates or Galileo. And yet we do not teach them; we do not revere them; we do not tell their stories.

And here’s the thing. They are such GOOD stories! It’s not simply that justice seems to demand some narrator acknowledge their impact. It is that these are stories worthy of telling in their own right: they cut to the core of who we are as people; they are steeped in blood and intrigue; they are stories of individuals who defy the conventions of both man and god in the pursuit of truth. And along the way, they unlock for us the secrets of our own bodies.

So— in homage to my childhood self, in gratitude to the medical heroes I’ve studied, and in tribute to you, I present The Anatomists: tales of courage, discovery, and daring that changed our world.

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