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Clues to Black Plague’s Fury in 650-Year-Old Skeletons
By NICHOLAS BAKALAR, The New York Times, January 29, 2008
Many historians have assumed that Europe’s deadliest plague, the Black Death of 1347 to 1351, killed indiscriminately, young and old, hardy and frail, healthy and sick alike. But two anthropologists were not so sure. They decided to take a closer look at the skeletons of people buried more than 650 years ago.
Their findings, published on Monday in The Proceedings of the National Academy of Sciences, suggest that the plague selectively took the already ill, while many of the otherwise healthy survived the infection.
Although it may not be surprising that healthy people would be more likely to survive an illness, it is not always the case. The Spanish flu of 1918 killed thousands of healthy people in their prime while sparing many children and the elderly, whose weaker immune systems did not overreact to the infection. Sexually transmitted infections like H.I.V. disproportionately affect the strongest and healthiest, for the obvious reason that they are the most sexually active.
Plague is caused by a bacterium called Yersinia pestis, and it is usually transmitted to humans by fleas; flea-infested rats caused the 14th-century epidemic. The bacteria invade the bloodstream, causing internal bleeding that leads to shock and death.
In the new study, the researchers examined 490 skeletons exhumed from the East Smithfield cemetery in London. The site, like many other cemeteries, was set up to bury victims of the Black Death and was almost certainly used for no other purpose.
The scientists determined the victims’ state of health when they died by counting bone lesions, defects that suggest previous infections and other existing health problems. The researchers also estimated age at death by noting dental development and using other established methods. As a comparison, they analyzed the bones of 291 genetically and culturally similar people buried in a Danish cemetery shortly before the plague began.
The aim was to find out whether the Londoners, who all died of the plague, were frail when the epidemic struck. In the nonplague Danish cemeteries, bone lesions were strongly associated with earlier death. If the Black Death killed without discrimination, such skeletal defects would not be associated with an increased risk of death in East Smithfield. Many of the victims would have had healthy-looking bones when the plague killed them.
But this was not the case. Among the East Smithfield plague victims, bone lesions were also associated with excess mortality. In other words, many of those people were already in poor health when the Black Death struck.
Most of the bone defects that the researchers found can be caused by malnutrition, and the scientists suggest that the findings may show effects of starvation on immune function. It is known from contemporary chronicles that many survived the plague, and they, the authors write, were probably well fed and healthy enough to mount an effective immune response.
“Even something as clearly deadly as the Black Death is still selective,” said Sharon N. DeWitte, a co-author of the study and an assistant professor of anthropology at the State University at Albany. The Black Death, she continued, is comparable in some ways to various emerging diseases of today like Ebola or SARS, and studying it “gives us some insight into who might be at highest risk for these new diseases.”
The authors acknowledge that their findings are not conclusive. The samples used were from two geographic areas, and similar lesions could have been caused by diseases of varying severity in the two areas.
Still, the authors write, the fact that a pattern of excess mortality was associated with different kinds of lesions suggests that the plague more often killed the weak than the strong.
Books: A Fight for Life Consumes Both Mother and Son
By ABIGAIL ZUGER, M.D., The New York Times, January 29, 2008
Swimming in a Sea of Death: A Son's Memoir. By David Rieff. Simon & Schuster. 180 pages. $21
“A good death” may be one of the emptiest phrases in the English language. Research has confirmed that no two people use it to mean exactly the same thing. Even the premise is unclear; for whom, exactly, is that death supposed to be good? Many would prefer a swift, sudden and painless exit for themselves — but a little warning when it comes to friends and relatives, with time to prepare and to say goodbye.
“A bad death” is another matter. We all know those when we see them, the miserably protracted and painful affairs that overwhelm everyone — the deceased and survivors alike — with panic, guilt and bitter regrets.
And now we have a new benchmark of bad. The writer Susan Sontag’s death, as set out in this short and immensely disturbing account by her son, David Rieff, must rank as one of the worst ever described.
For starters, it took a long time. Ms. Sontag was diagnosed with breast cancer metastatic to the lymph nodes in 1975, at 42. She survived the draconian treatment and the years spent expecting her unlikely remission to end, only to develop unrelated uterine cancer in the late 1990s. Again she survived, and again she developed a new cancer: this time myelodysplastic syndrome, a virtually untreatable variant of leukemia, probably related to the treatment for the first two. She died in 2004.
Three decades of having cancer, being treated for cancer or waiting for cancer to recur might bring out the inner philosopher in some. In Ms. Sontag, an inner adolescent seems to have emerged instead, with each battle and victory strengthening her determined appetite for life and her conviction that she was immortal. Intellectually, of course, she knew otherwise, but she balanced that age-old contradiction with the insouciance of a helmetless 18-year-old on a snowboard. “She believed in her own will, and, grandiose though it may seem, in her own star,” Mr. Rieff says in his book. “My mother came to being ill imbued with a profound sense of being the exception to every rule.”
To watch that kind of arrogance and bravery succeed is marvelous; to watch it fail, dreadful. For an elderly woman with a body weakened and deformed by prior surgery and bones oozing new malignant cells, failure was pretty much a foregone conclusion.
Such was the strength of Ms. Sontag’s giant personality, however, that apparently no one in her coterie of friends, family or physicians was willing or able to help her along the path to accepting the inevitable. She took them with her instead, on the snowboard heading straight for a cliff.
During the nine months before the final plunge Ms. Sontag embarked on an all-out campaign to cure an incurable disease. She experienced gruesome mental and physical suffering before and after a bone marrow transplant that predictably failed: recurrent hospitalizations, dire infections, wild mood swings, bouts of confusion — all punctuated by desperate Internet searches for more and better treatment. She never admitted she was dying.
“Obviously,” Mr. Rieff says, “there is no comparison between the sufferings of a person who is ill and the sufferings of those who love them.” Still, one suspects he got the worst of the deal, for despite what he describes as a tense relationship with his mother, he was cast in the role of head cheerleader. His job was to enthusiastically endorse her struggle, always to be optimistic and supportive and never, ever, to talk about death.
“What she wanted from me was an adamant refusal to accept that it was even possible that she might not survive,” Mr. Rieff writes. Ms. Sontag “might be covered in sores, incontinent and half delirious,” but Mr. Rieff would “tell her at great and cheerful length about how much better she seemed to look/seem/be compared to the day before.”
Months of this duplicity left him guilty and miserable, obsessively revisiting every decision again and again, even — and especially — after she died. On the one hand, Mr. Rieff acknowledges, “she was entitled to die her own death.” On the other: “Did I do the right thing? Could I have done more?”
Poor Mr. Rieff wound up entangled in the single biggest dilemma in medicine: how to calculate the dose of hope, that most powerful of all medications, to be dispensed in hopeless cases. The professionals stumble here all the time. No child could or should be asked to get it right for a parent.
It is small wonder that Mr. Rieff finds all the usual compromises inadequate. He is equally upset by the platitudes in a brochure trying to make a bad disease seem not so bad, by a doctor who pulls no punches in announcing how bad it actually is, by friends who maintain against all reason that Ms. Sontag is going to survive and by doctors who suggest that she should settle for smaller goals than survival.
Mr. Rieff’s misery as a son is so palpable that it seems petty to wince at some of the decisions he makes as a writer. This is a jagged, strangely shapeless work, as if the author were determined not to smooth any part of it with standard narrative tools. Ms. Sontag’s story is told only glancingly; his own whirling emotions take center stage. For a journalist (Mr. Rieff is a contributing writer to The New York Times Magazine), he chooses some odd locutions, with jarring “dear reader” interjections and annoying neo-verbs like “vigilize.”
Most frustrating of all is that Mr. Rieff maintains an unflagging admiration for Ms. Sontag’s primary physician, yet the reader never learns the exact words this doctor chose to counsel his famous, courageous and deluded patient as the months passed. Would uninvolved observers find them inspiring, or problematic? It is hard to know.
When it comes to dying writers, William Saroyan said it best: “Why am I writing this book? To save my life, to keep from dying, of course. That is why we get up in the morning.” Desperate as she was to live, Ms. Sontag knew perfectly well that she was bound to live on in her work.
Mr. Rieff has now guaranteed her a second immortality. He and his mother will undoubtedly survive for a long time to come in medical school courses on death and dying — as a case study in how not to do it.
Observatory: 120 Million Years Old, Fossil Shows Divergence of Platypus and Anteater
By HENRY FOUNTAIN, The New York Times, January 29, 2008
The platypus tops many people’s oddest mammal list, what with its ducklike bill and beaverlike tail. Its closest relatives, the echidnas, don’t get the press the platypus gets, but they are pretty weird, too, and are the only other monotremes, or egg-laying mammals, around.
There is not much of a fossil record of monotremes, so it has never been clear when the platypus and the echidnas (also known as spiny anteaters) diverged. Most estimates using genetic analysis — looking at the rate of mutations — suggest that they split perhaps 20 million to 30 million years ago, although a few stretch that from 80 million years.
Now Timothy Rowe of the University of Texas and colleagues report in The Proceedings of the National Academy of Sciences that the divergence may have occurred long before that. They used X-ray computer tomography to examine a 120-million-year-old fossil, Teinolophus trusleri. It is an ancestral platypus, they say, with some similar morphological features, in particular a canal in the jaw that the researchers say is evidence that Teinolophus had a duckbill.
The researchers conclude that the platypus and echidna branches of monotremes were already distinct at that early date. The findings also suggest that monotremes diversified at a slower rate than the other mammals.
By NICHOLAS BAKALAR, The New York Times, January 29, 2008
Many historians have assumed that Europe’s deadliest plague, the Black Death of 1347 to 1351, killed indiscriminately, young and old, hardy and frail, healthy and sick alike. But two anthropologists were not so sure. They decided to take a closer look at the skeletons of people buried more than 650 years ago.
Their findings, published on Monday in The Proceedings of the National Academy of Sciences, suggest that the plague selectively took the already ill, while many of the otherwise healthy survived the infection.
Although it may not be surprising that healthy people would be more likely to survive an illness, it is not always the case. The Spanish flu of 1918 killed thousands of healthy people in their prime while sparing many children and the elderly, whose weaker immune systems did not overreact to the infection. Sexually transmitted infections like H.I.V. disproportionately affect the strongest and healthiest, for the obvious reason that they are the most sexually active.
Plague is caused by a bacterium called Yersinia pestis, and it is usually transmitted to humans by fleas; flea-infested rats caused the 14th-century epidemic. The bacteria invade the bloodstream, causing internal bleeding that leads to shock and death.
In the new study, the researchers examined 490 skeletons exhumed from the East Smithfield cemetery in London. The site, like many other cemeteries, was set up to bury victims of the Black Death and was almost certainly used for no other purpose.
The scientists determined the victims’ state of health when they died by counting bone lesions, defects that suggest previous infections and other existing health problems. The researchers also estimated age at death by noting dental development and using other established methods. As a comparison, they analyzed the bones of 291 genetically and culturally similar people buried in a Danish cemetery shortly before the plague began.
The aim was to find out whether the Londoners, who all died of the plague, were frail when the epidemic struck. In the nonplague Danish cemeteries, bone lesions were strongly associated with earlier death. If the Black Death killed without discrimination, such skeletal defects would not be associated with an increased risk of death in East Smithfield. Many of the victims would have had healthy-looking bones when the plague killed them.
But this was not the case. Among the East Smithfield plague victims, bone lesions were also associated with excess mortality. In other words, many of those people were already in poor health when the Black Death struck.
Most of the bone defects that the researchers found can be caused by malnutrition, and the scientists suggest that the findings may show effects of starvation on immune function. It is known from contemporary chronicles that many survived the plague, and they, the authors write, were probably well fed and healthy enough to mount an effective immune response.
“Even something as clearly deadly as the Black Death is still selective,” said Sharon N. DeWitte, a co-author of the study and an assistant professor of anthropology at the State University at Albany. The Black Death, she continued, is comparable in some ways to various emerging diseases of today like Ebola or SARS, and studying it “gives us some insight into who might be at highest risk for these new diseases.”
The authors acknowledge that their findings are not conclusive. The samples used were from two geographic areas, and similar lesions could have been caused by diseases of varying severity in the two areas.
Still, the authors write, the fact that a pattern of excess mortality was associated with different kinds of lesions suggests that the plague more often killed the weak than the strong.
Books: A Fight for Life Consumes Both Mother and Son
By ABIGAIL ZUGER, M.D., The New York Times, January 29, 2008
Swimming in a Sea of Death: A Son's Memoir. By David Rieff. Simon & Schuster. 180 pages. $21
“A good death” may be one of the emptiest phrases in the English language. Research has confirmed that no two people use it to mean exactly the same thing. Even the premise is unclear; for whom, exactly, is that death supposed to be good? Many would prefer a swift, sudden and painless exit for themselves — but a little warning when it comes to friends and relatives, with time to prepare and to say goodbye.
“A bad death” is another matter. We all know those when we see them, the miserably protracted and painful affairs that overwhelm everyone — the deceased and survivors alike — with panic, guilt and bitter regrets.
And now we have a new benchmark of bad. The writer Susan Sontag’s death, as set out in this short and immensely disturbing account by her son, David Rieff, must rank as one of the worst ever described.
For starters, it took a long time. Ms. Sontag was diagnosed with breast cancer metastatic to the lymph nodes in 1975, at 42. She survived the draconian treatment and the years spent expecting her unlikely remission to end, only to develop unrelated uterine cancer in the late 1990s. Again she survived, and again she developed a new cancer: this time myelodysplastic syndrome, a virtually untreatable variant of leukemia, probably related to the treatment for the first two. She died in 2004.
Three decades of having cancer, being treated for cancer or waiting for cancer to recur might bring out the inner philosopher in some. In Ms. Sontag, an inner adolescent seems to have emerged instead, with each battle and victory strengthening her determined appetite for life and her conviction that she was immortal. Intellectually, of course, she knew otherwise, but she balanced that age-old contradiction with the insouciance of a helmetless 18-year-old on a snowboard. “She believed in her own will, and, grandiose though it may seem, in her own star,” Mr. Rieff says in his book. “My mother came to being ill imbued with a profound sense of being the exception to every rule.”
To watch that kind of arrogance and bravery succeed is marvelous; to watch it fail, dreadful. For an elderly woman with a body weakened and deformed by prior surgery and bones oozing new malignant cells, failure was pretty much a foregone conclusion.
Such was the strength of Ms. Sontag’s giant personality, however, that apparently no one in her coterie of friends, family or physicians was willing or able to help her along the path to accepting the inevitable. She took them with her instead, on the snowboard heading straight for a cliff.
During the nine months before the final plunge Ms. Sontag embarked on an all-out campaign to cure an incurable disease. She experienced gruesome mental and physical suffering before and after a bone marrow transplant that predictably failed: recurrent hospitalizations, dire infections, wild mood swings, bouts of confusion — all punctuated by desperate Internet searches for more and better treatment. She never admitted she was dying.
“Obviously,” Mr. Rieff says, “there is no comparison between the sufferings of a person who is ill and the sufferings of those who love them.” Still, one suspects he got the worst of the deal, for despite what he describes as a tense relationship with his mother, he was cast in the role of head cheerleader. His job was to enthusiastically endorse her struggle, always to be optimistic and supportive and never, ever, to talk about death.
“What she wanted from me was an adamant refusal to accept that it was even possible that she might not survive,” Mr. Rieff writes. Ms. Sontag “might be covered in sores, incontinent and half delirious,” but Mr. Rieff would “tell her at great and cheerful length about how much better she seemed to look/seem/be compared to the day before.”
Months of this duplicity left him guilty and miserable, obsessively revisiting every decision again and again, even — and especially — after she died. On the one hand, Mr. Rieff acknowledges, “she was entitled to die her own death.” On the other: “Did I do the right thing? Could I have done more?”
Poor Mr. Rieff wound up entangled in the single biggest dilemma in medicine: how to calculate the dose of hope, that most powerful of all medications, to be dispensed in hopeless cases. The professionals stumble here all the time. No child could or should be asked to get it right for a parent.
It is small wonder that Mr. Rieff finds all the usual compromises inadequate. He is equally upset by the platitudes in a brochure trying to make a bad disease seem not so bad, by a doctor who pulls no punches in announcing how bad it actually is, by friends who maintain against all reason that Ms. Sontag is going to survive and by doctors who suggest that she should settle for smaller goals than survival.
Mr. Rieff’s misery as a son is so palpable that it seems petty to wince at some of the decisions he makes as a writer. This is a jagged, strangely shapeless work, as if the author were determined not to smooth any part of it with standard narrative tools. Ms. Sontag’s story is told only glancingly; his own whirling emotions take center stage. For a journalist (Mr. Rieff is a contributing writer to The New York Times Magazine), he chooses some odd locutions, with jarring “dear reader” interjections and annoying neo-verbs like “vigilize.”
Most frustrating of all is that Mr. Rieff maintains an unflagging admiration for Ms. Sontag’s primary physician, yet the reader never learns the exact words this doctor chose to counsel his famous, courageous and deluded patient as the months passed. Would uninvolved observers find them inspiring, or problematic? It is hard to know.
When it comes to dying writers, William Saroyan said it best: “Why am I writing this book? To save my life, to keep from dying, of course. That is why we get up in the morning.” Desperate as she was to live, Ms. Sontag knew perfectly well that she was bound to live on in her work.
Mr. Rieff has now guaranteed her a second immortality. He and his mother will undoubtedly survive for a long time to come in medical school courses on death and dying — as a case study in how not to do it.
Observatory: 120 Million Years Old, Fossil Shows Divergence of Platypus and Anteater
By HENRY FOUNTAIN, The New York Times, January 29, 2008
The platypus tops many people’s oddest mammal list, what with its ducklike bill and beaverlike tail. Its closest relatives, the echidnas, don’t get the press the platypus gets, but they are pretty weird, too, and are the only other monotremes, or egg-laying mammals, around.
There is not much of a fossil record of monotremes, so it has never been clear when the platypus and the echidnas (also known as spiny anteaters) diverged. Most estimates using genetic analysis — looking at the rate of mutations — suggest that they split perhaps 20 million to 30 million years ago, although a few stretch that from 80 million years.
Now Timothy Rowe of the University of Texas and colleagues report in The Proceedings of the National Academy of Sciences that the divergence may have occurred long before that. They used X-ray computer tomography to examine a 120-million-year-old fossil, Teinolophus trusleri. It is an ancestral platypus, they say, with some similar morphological features, in particular a canal in the jaw that the researchers say is evidence that Teinolophus had a duckbill.
The researchers conclude that the platypus and echidna branches of monotremes were already distinct at that early date. The findings also suggest that monotremes diversified at a slower rate than the other mammals.
