In 2005, a historian named Jason Emerson opened a steamer trunk that had been sitting in a lawyer’s attic for forty years. The trunk belonged to Robert Todd Lincoln’s personal attorney. Robert, Mary Todd Lincoln’s only surviving son, had spent decades trying to suppress every document that touched his mother’s mental health history—letters, court records, correspondence from the asylum where he had her committed in 1875. He wanted them destroyed.

His attorney had instead locked them in a trunk and forgotten about them, or perhaps decided not to forget. Inside the trunk were twenty-five letters. Twenty of them had been written by Mary Todd Lincoln herself, from inside the asylum, from her exile in France, and from the last years of her life when she could barely leave her darkened room. They had been assumed lost.

They had been assumed destroyed by a dutiful son protecting a family reputation. They were not destroyed. They survived. Those letters became the foundation of the most serious modern reassessment of Mary Todd Lincoln’s medical history, a reassessment that eventually drew in a cardiologist who had spent years consulting on the television show House M.

D. , a psychiatrist who had studied her case for a decade, and a debate in the pages of Perspectives in Biology and Medicine that is still ongoing today. At the center of it all is a question that DNA science has made newly urgent and newly honest about its own limits. What was actually wrong with Mary Todd Lincoln?

And what can modern genetics tell us—and what can it not—about a woman who has been diagnosed, rediagnosed, and misdiagnosed for 150 years by people who never met her? The accepted story of Mary Todd Lincoln’s health is that she was mentally ill. That story was built across a century of historical writing, and it rests on three foundations. First, her behavior.

The historical record documents mood swings so severe they alarmed everyone around her, explosive rages in the White House, extravagant spending that consumed the government’s entire four-year furnishing budget in a single year, and fits of weeping so prolonged she could not attend her own son’s funeral. After the assassination, her behavior escalated into paranoia, auditory hallucinations, and delusions that everyone around her was stealing her money or trying to harm her. These are not contested in the historical record. They are documented in her own letters, in newspaper accounts, and in the recollections of friends.

Second, the formal legal determination. In May 1875, a Cook County jury found Mary Todd Lincoln legally insane after a proceeding that lasted less than a day. Her son Robert had orchestrated the hearing, brought in five doctors who testified to her condition, and had her committed to Bellevue Place Sanitarium in Batavia, Illinois. She was there for four months before friends intervened to secure her release.

Third, the retrospective psychiatric consensus. Beginning in the 1990s and reaching its most systematic form in historian Jason Emerson’s 2007 book The Madness of Mary Lincoln, which was based partly on those rediscovered letters, modern psychiatrists consulting on the historical record argued she displayed symptoms consistent with bipolar disorder—the cycling between high-energy, impulsive, expansive states and prolonged, devastating depressions. Emerson’s psychiatric consultant, Dr. James S.

Brust, concluded that her pattern of manic spending, relentless anxiety, fierce temper, and deep grief was a textbook presentation. The consensus, then, was that Mary Todd Lincoln was mentally ill. The debate has been about what to call it and whether that illness was treatable. Until Dr.

John Sotos opened her medical history with a different instrument entirely. Here is the detail the mental illness consensus cannot cleanly explain. The symptoms do not all fit. The ones that do not fit are the physical ones, the ones that psychiatric diagnoses, even accurate ones, cannot account for on their own.

Mary Todd Lincoln’s documented medical complaints across thirty years of adult life included a persistent sore mouth noted in letters as early as 1852, pallor, paresthesias—the sensation of being stuck by needles in her extremities—fatigue so severe it periodically confined her to bed, fevers without clear infectious cause, progressive weakness that worsened decade by decade, a gait disturbance in her later years, visual impairment, resting tachycardia, edema, and finally, in the last years of her life, a complete physical collapse. She could barely move, could barely speak, and in her final months communicated primarily by blinking. She died in 1882 at the age of sixty-three. Her doctors attributed her death to a slight apoplexy.

Bipolar disorder, even severe untreated bipolar disorder, does not cause progressive physical deterioration of the nervous system. It does not explain sore mouth, pallor, paresthesias, and ataxia accumulating over thirty years. It does not explain why a woman described by contemporaries in the 1840s as a ball of fire ended her life unable to speak. Something was happening in Mary Todd Lincoln’s body, something that the psychiatric framing, however accurate it might have been about her mood episodes, was not designed to see.

Why did no one put this together before? Three structural reasons, each compounding the others. First, the political economy of her reputation. Mary Todd Lincoln entered American historical memory as a problem to be explained.

She was expensive, difficult, erratic, and ultimately committed to a psychiatric institution, all of which made her easy to dismiss and hard to take seriously as a medical subject. For most of the nineteenth and early twentieth centuries, the dominant framework for understanding women with her symptom profile was straightforwardly moral, not medical. She was high-strung, hysterical, or simply not suited to the pressures of her position. Historian Jean Baker, who wrote the most important modern biography of Mary Lincoln, noted that she has been described as the reverse of Teflon.

Every medical diagnosis has been postulated about her. That saturation of speculation made careful analysis harder, not easier. When everything is a theory, nothing gets verified. Second, the destruction and suppression of her medical records.

Robert Todd Lincoln spent years actively suppressing documentation of his mother’s health. He burned letters. He pressured friends to destroy correspondence. He almost succeeded in destroying the very trunk Emerson found in 2005.

The only formal medical records that survived from her entire life are the notes kept during the four months of her institutionalization—four months out of sixty-three years. A physician trying to construct her medical history was working from a record that had been deliberately dismantled by a man with strong reasons to keep it incomplete. Third, the limits of retrospective diagnosis as a methodology. Brian Casey and David Casey, writing in Psychiatric News in 2019, made this point with precision.

The historical record may be incomplete or distorted, and the reporters may be biased. Manifestations of psychiatric disorders may change over time as cultures evolve. Applying DSM-5 criteria to a woman who died in 1882 is not the same as applying them to a living patient. The diagnostic categories themselves did not exist.

Kraepelin’s concept of manic depression, the intellectual ancestor of the modern bipolar diagnosis, came decades after her death. Every retrospective diagnosis of Mary Todd Lincoln says something about the clinical framework being applied, not only about Mary herself. These three conditions together explain why a simpler, more physical explanation went unexplored for so long. The mental illness framing was already in place.

It was politically convenient. And the evidence needed to challenge it had been locked in a trunk. In 2015, Dr. John Sotos, a cardiologist, formerly an adjunct professor of medicine at the University of North Carolina and for some years a medical technical consultant on the television series House M.

D. , published a paper in Perspectives in Biology and Medicine, the journal of the Johns Hopkins University Press, titled “What an Affliction: Mary Todd Lincoln’s Fatal Pernicious Anemia. ”

The methodology Sotos used was not DNA testing. It was something both simpler and more painstaking: systematic symptom mapping across the historical record.

He assembled approximately one hundred historical sources—678 letters, photographs, newspaper accounts, and the surviving institutionalization records—and mapped every documented physical symptom against the known progression of a single disease. That disease was pernicious anemia, and understanding why it matters here requires understanding what pernicious anemia actually is, because most people today have never encountered it. Pernicious anemia is not primarily a blood disease, though it affects the blood. It is an autoimmune condition in which the body attacks the cells that line the stomach that produce a protein called intrinsic factor.

Without intrinsic factor, the body cannot absorb vitamin B12 from food, regardless of how much B12 that food contains. And without B12, the body cannot maintain its DNA synthesis, cannot produce adequate red blood cells, and cannot maintain the myelin sheath that insulates nerve cells throughout the body and brain. Vitamin B12 is not a supplement that produces minor improvements in energy. It is structural.

It is part of the molecular machinery that keeps nerve cells intact. Without it, those cells degrade slowly, progressively, over years and decades. The brain shrinks, peripheral nerves lose their insulation and begin misfiring. The result in advanced untreated cases is a constellation of symptoms that looks exactly like what psychiatrists would call a severe psychotic disorder: paranoia, hallucinations, delusions, with a strange internal consistency.

The hallucinations feel utterly real to the person experiencing them. And running alongside the psychiatric picture is progressive physical deterioration—weakness, gait disturbance, visual impairment, cardiovascular symptoms, a body dismantling itself from the inside. Pernicious anemia was not identified in English-language medical literature until 1874, eight years before Mary Todd Lincoln’s death. In her lifetime, it was simply invisible as a diagnostic category.

When she described tingling in her extremities or a persistent sore mouth, no physician would have known what those symptoms meant together. They would have treated them separately, ineffectively, or attributed them to her nerves. There is one more piece. Sotos noted in his paper that pernicious anemia has a documented genetic predisposition, and that the predisposition is geographically clustered.

Studies conducted in the 1960s found unusually high rates of pernicious anemia in populations from specific regions of Scotland. Mary Todd Lincoln’s parents were cousins—consanguineous, in the technical language—with ancestral roots in Scotland. That ancestry, combined with the pattern of her symptoms across thirty years, is what Sotos argued constituted a coherent medical diagnosis that no previous scholar had attempted. Here is what the evidence suggests.

Mary Todd Lincoln almost certainly was not primarily mentally ill. She was almost certainly a woman with a progressive hereditary biochemical disease that destroyed her nervous system over thirty years. A disease that in its advanced stages produces a psychiatric picture so convincing that her contemporaries, her physicians, and a Cook County jury all concluded she was insane. A disease that did not have a name in her lifetime.

A disease that today is caught by a routine blood test and treated with a monthly injection of vitamin B12, typically with full reversal of symptoms if caught early enough. The woman who was found legally insane in 1875, who was committed to an asylum by her own son, who was mocked in the press and dismissed by Congress and written off by historians for more than a century, was in all probability not insane. She was sick in a way no one around her had the knowledge to understand. Sotos’s analysis shows a temporal coherence that psychiatric explanations cannot replicate.

The symptoms he documented in Mary Todd Lincoln’s historical record track the known natural history of untreated pernicious anemia with unusual precision. Early-stage B12 deficiency produces fatigue, pallor, mood instability, and peripheral tingling. Mid-stage deficiency adds cardiovascular symptoms, cognitive changes, and the beginning of paranoid ideation. Late-stage deficiency produces frank psychosis—hallucinations and delusions clinically indistinguishable from schizophrenia or severe mania—alongside progressive physical collapse, weakness, ataxia, and visual failure.

Her documented symptom progression followed exactly this sequence, beginning with the sore mouth notation in 1852 and ending with her near total immobility in 1882. That thirty-year arc is the signature of a progressive organic disease, not a primary psychiatric disorder. Sotos’s analysis also rules out the simpler explanations proposed previously. Bipolar disorder, even untreated across decades, does not cause the physical symptom cluster.

The paresthesias, the gait disturbance, the progressive visual impairment, the ataxia—these are neurological findings. They require a neurological cause. Chloral hydrate overdose, a theory suggested by some because recently found letters mention her use of the sleep medication, can cause neurological symptoms, but would not produce a thirty-year progressive pattern without acute crises. Spinal stenosis and diabetes, also suggested in the scholarship, cannot explain the full symptom picture.

The Lhermitte’s symptom she appears to have experienced—an electric shock sensation running down the spine on neck flexion, documented in her letters without her knowing its name—is pathognomonic of posterior column damage in the spinal cord. It is the precise kind of damage B12 deficiency causes. No other proposed diagnosis accounts for it. The implications extend well beyond one woman’s biography.

Sotos argued that his diagnosis means Mary Todd Lincoln’s behavior during the White House years—the spending, the mood swings, the explosive outbursts—was not the willful misconduct of a difficult woman, but the early-stage manifestation of a progressive neurological disease that was in her era completely invisible to medicine. A great deal of historical analysis has treated Mary as a liability Lincoln had to manage. Sotos’s diagnosis reframes that entirely. She was not a liability.

She was a patient in a world where patients with her condition had no diagnosis, no treatment, and no vocabulary to describe what was happening to them. The genetic dimension implies something else. If pernicious anemia has a documented hereditary component, clustered in specific populations, then her ancestry was not merely biographical context. It was, in a medically meaningful sense, part of the mechanism of her illness.

The Scottish ancestry she and her consanguineous parents carried, from regions with elevated pernicious anemia prevalence, may have carried the genetic predisposition for the autoimmune attack that killed her nervous system over thirty years. In this case, DNA is not a bloodline mystery. It is a disease vector. Sotos’s diagnosis has not been accepted without challenge.

There are serious objections, and the scholars making them deserve to be heard. The most significant comes from biographer Jean Baker, whose 1987 biography Mary Todd Lincoln: A Biography remains the standard scholarly reference on her life. Baker is not convinced. She points to Mary Lincoln’s enormous energy in her early and middle years.

She was described repeatedly as vivacious, intellectually aggressive, socially tireless—all inconsistent with a disease that progressively depletes the body. Sotos’s response is that pernicious anemia is a slowly progressive disease. Early stages do not typically sap energy, and the depletion accelerates as damage accumulates. But Baker’s objection is legitimate.

The retrospective diagnosis depends on a selective reading of the symptom record, and the symptom record itself is incomplete by design, because Robert Todd Lincoln destroyed so much of it. Psychiatrist Brian Casey, writing in Psychiatric News in 2019, raised a methodological objection that applies to every retrospective diagnosis, including Sotos’s. Applying DSM-1, 2, 3, 4, or 5 criteria may yield different opinions as to whether Mary Todd Lincoln did or did not have bipolar disorder. The same caveat applies to applying modern medical criteria to an 1882 death.

The diagnosis of pernicious anemia relies on symptom pattern matching, not laboratory confirmation. No blood sample from Mary Todd Lincoln exists. No tissue sample exists. The genetic predisposition Sotos invokes—the elevated prevalence of pernicious anemia in Scottish ancestry populations—is a population-level statistical association, not evidence that any specific individual carried the relevant susceptibility.

Without a direct biological sample, the diagnosis remains, as Dr. Christopher Kenner of the University of Kansas Medical Center described it, “medically plausible”—a carefully different phrase from “medically proven. ”

These objections matter for how we understand who Mary Todd Lincoln was and what she survived. A pernicious anemia diagnosis is more sympathetic than a psychiatric diagnosis.

Sotos explicitly said he hoped it would lead historians to see her as a woman with a biochemically injured mind. But the desire for a more sympathetic reading of her life, however justified that desire might be, is not itself evidence. The historical record can support the diagnosis. It cannot confirm it.

The history of how people have tried to explain Mary Todd Lincoln is itself a story about what we want from the past. Every generation has applied its own diagnostic framework. Nineteenth-century physicians applied the language of hysteria and feminine weakness. Early twentieth-century biographers applied the language of nervous breakdown.

Late twentieth-century psychiatrists applied the language of bipolar disorder. Twenty-first-century medical scholars have applied the language of autoimmune disease and genetic predisposition. Each of these framings reflects something true about its own moment in the history of medicine and culture, not only something true about her. The DNA angle—the part that draws people to this subject—is the part to be most careful about.

Pernicious anemia has a genetic component, and that component is real and documented. But having a genetic predisposition is very different from saying DNA revealed a hidden truth about her bloodline. The second framing implies that who she really was could be decoded in her cells, that her ancestry is the key to understanding her suffering. That is a seductive idea.

It is also one that medicine does not support and that history does not require. What Mary Todd Lincoln’s case actually reveals about DNA science is more valuable than a bloodline story. It reveals what population genetics can legitimately do, what it cannot do, and what it has been used irresponsibly to claim. Pernicious anemia today is largely invisible, not because it has been cured, but because it is caught before it becomes catastrophic.

A routine complete blood count will flag macrocytic anemia, which triggers a B12 level test. A B12 deficiency triggers treatment—a monthly intramuscular B12 injection or high-dose oral supplementation. If caught early, the damage to the nervous system is reversible. If caught late, the neurological damage is permanent, but further progression stops.

In Mary Todd Lincoln’s America, none of this existed. The disease was not named until 1874. The first effective treatment—eating half a pound of raw liver daily, as developed by George Whipple, George Minot, and William Murphy—was not discovered until 1926. The three researchers shared the Nobel Prize in Medicine in 1934 for that work.

The injectable treatment used today was not developed until 1948. The population genetics piece matters here in a specific clinical way. Pernicious anemia is an autoimmune disease, and autoimmune diseases have documented genetic risk factors that cluster in specific ancestral populations. Genome-wide association studies have identified variants in the HLA region—the human leukocyte antigen system that governs immune response—that elevate risk for pernicious anemia.

Some of these variants are more common in northern European ancestry populations, particularly those from Scotland and Scandinavia, precisely the populations Sotos pointed to in Mary Lincoln’s family history. This is population genetics used responsibly, identifying disease risk at the community level without claiming individual certainty. Ancestry matters not as a matter of identity, but as a matter of medical probability. A patient of northern European descent presenting with fatigue, mood instability, and tingling extremities should have B12 levels checked.

The genetic ancestry does not diagnose the patient; the blood test does. But it can help a physician know which tests to order. Mary Todd Lincoln had none of these tools available. She died from the slow collapse of a system her doctors could not see, because medicine had not yet learned to look for it.

Here is what the historical record tells us about who Mary Todd Lincoln actually was beneath the diagnoses. She taught herself French at a time when most women in Kentucky were not expected to read beyond the Bible. She read Voltaire, Pascal, and Victor Hugo in the original. She had strong, informed opinions about politics—sharper, by multiple contemporary accounts, than many of the men who surrounded her husband in the White House.

She was the first wife of a sitting president to be referred to as First Lady during her own tenure. She buried three of her four sons. Eddie died at three. Willie died at eleven in the White House while she was First Lady, while her husband was prosecuting a war that would decide the fate of four million people.

Tad died at eighteen, six years after she watched her husband’s skull destroyed from arm’s length in a theater box. She outlived them all. She was committed to a psychiatric institution by her own son, denied legal representation at her own hearing, and found legally insane in a proceeding that lasted less than a day. She secured her own release through the intervention of two friends, James and Myra Bradwell, who believed she was being railroaded.

She spent four years in France, largely alone, before returning to die at her sister’s home in Springfield. The letters Jason Emerson found in that trunk in 2005 showed a woman who was not, in the clinical language, delusional about everything. She was furious. She was fighting for her reputation and her freedom with the cognitive resources she had left—resources that a progressing neurological disease was gradually destroying.

“Everyone is trying to steal my money,” she wrote from the asylum. Modern psychiatrists consulted by Emerson concluded this was a delusion. But it is worth noting that Robert did, in fact, take legal control of her finances. The line between delusion and reality in her case was thinner than the diagnosis suggests.

There is a version of DNA history that promises to reveal the hidden truth behind every famous person—the real ancestry, the secret bloodline, the genetic key that unlocks who someone really was. That version is almost always wrong, not because genetics is unreliable, but because it is being asked to do something it cannot do. DNA does not contain identity. It does not encode who a person was or what their life meant.

It is a molecular record of evolutionary and demographic history carried forward without intention or narrative. What DNA science can genuinely do, when used carefully and with appropriate humility for the questions it was actually designed to answer, is illuminate the biological mechanisms behind human experience. It can identify disease risk. It can trace population movements across millennia.

It can establish paternity and descent. It can help explain why certain people get certain diseases and whether their descendants should be tested. The Mary Todd Lincoln case is a precise illustration of both sides of this. A sensationalist DNA framing asks: Who were her real ancestors?

What were they hiding? An honest scientific framing asks: What genetic predispositions ran in her family, and what did those predispositions cost her? The second question has a real answer. It is documented in a peer-reviewed paper by a cardiologist who spent years assembling 678 letters and photographs to build a case.

It is not exciting in the tabloid sense. It is genuinely important in the medical and historical sense. The difference between those two kinds of questions is the difference between using DNA to tell a better story and using DNA to tell the truth. What is remarkable is not that her medical history was misunderstood.

What is remarkable is that the evidence survived to be reread. Robert Todd Lincoln spent decades trying to make sure it didn’t. He burned letters, suppressed records, and pressured those who knew his mother’s story to stay silent. He very nearly succeeded.

For most of the twentieth century, historians worked with a deliberately incomplete record and built a portrait of Mary Todd Lincoln that, while not entirely wrong, was shaped as much by absence as by presence. Then a lawyer in Chicago failed to carry out his client’s final instructions, and a historian named Jason Emerson, researching a separate project, opened a trunk he almost didn’t open. Inside were twenty-five letters from a woman who had been told her words were worthless, who had been told her mind was broken, who had been told the story was over. The letters disagreed.

They insisted on their own existence. They survived the way things survive that have no reason to survive—not through strategy or protection, but through the random persistence of matter against the wishes of the people who wanted it gone. A cardiologist who consulted on a television medical drama, reading 678 letters in search of a pattern no one had looked for, may have finally found what was actually wrong with her. It is not a bloodline reveal.

It is something more useful: a cause, a mechanism, and a name for what she survived for sixty-three years. The specific, empirically resolvable question that remains is this: Could a tissue sample be recovered from Mary Todd Lincoln—from hair, from a preserved artifact, from the Lincoln tomb itself—sufficient to test for the HLA variants associated with autoimmune B12 malabsorption? The technology exists. Ancient DNA extraction from nineteenth-century biological material is now routine.

The question is not technical, but institutional: whether the Lincoln family estate, the Abraham Lincoln Presidential Library, and the relevant historical societies would consent to and cooperate with such a study. If the test returned positive—if the specific autoimmune susceptibility variants were present in her recovered DNA—Sotos’s retrospective diagnosis would shift from medically plausible to medically supported. The Cook County verdict of 1875 would need to be reassessed by the scholars who have relied on it. The history of Abraham Lincoln’s presidency would need to be reread with a different understanding of what the woman beside him was managing.

And one more thing would change. The way we ask questions about historical figures and DNA. Not what secrets her bloodline hid, but what her body was trying to tell her in a language medicine had not yet learned to read. That is the question worth answering.

That is the question that is still open.