“Miasma” is from the Greek miainein, meaning “to pollute.” Medical experts gave the term its notoriety, particularly during the nineteenth century, when they dismissed the idea of invisible pathogens in favor of miasmas: vaporous exhalations from patients or the environment that were assumed to cause disease.In The Conquest of Epidemic Disease, Charles-Edward Amory Winslow remarked, “It is fascinating to note how, for two millennia, laymen were generally contagionists and physicians were miasmatists.” Winslow’s observation was perceptive, but his rationalization was not: “The physician, knowing more, was quite correct in denying that any then-available theory of contagion could explain the facts.” Actually, the theory of contagion available throughout the nineteenth, eighteenth, seventeenth, and most of the sixteenth century, could explain the facts. Winslow’s observation therefore raises questions that are pressing today because there are modern counterparts of miasmas, vaguely defined factors that are offered as causes of disease.Why have experts in health care been slow to recognize infectious causation? Why do they still tend to dismiss hypotheses of infectious causation out of hand and then only gradually warm up to them? My physician, for example, seems like a particularly thoughtful and conscientious practitioner of healing and disease prevention. He keeps abreast of current thinking and tries to keep up with the literature.When I talked with him in 1998 about infectious causation of chronic diseases, he seemed interested. He agreed that peptic ulcers were caused by infection and thought that infectious causation of atherosclerosis was reasonable and perhaps even likely. But when I pushed the envelope just a bit further, to possible infectious causation of breast cancer, prostate cancer, and schizophrenia, that was too much. He stopped his probing, moved backward, his body language mirroring his intellectual response, gave a not unpleasant but self-assured chuckle, and said, “Now, that’s going too far!” I went on making a pest of myself discussing the evidence, but without any discernible impact.The answer to Winslow’s puzzle seems to stem more from human nature than from human knowledge. Humans generate their biases from their everyday experiences and need to struggle continually to recognize them. Physicians may need to struggle even more than the rest of us because they are trusted as the experts in health care, because they are expected to have the answers, because the systems they work with are very complex, and because ethical considerations restrict the normal options for definitive resolutions of uncertainties.What is it that creates a bias against infectious causation, especially among such highly trained people? Physicians, like everyone else, base their opinions on their experience. Before the microscope was trained on human pathogens, their experience argued against some solid organism causing disease by moving from person to person. Had they been able to see the organisms, the ideas of infection and contagion would undoubtedly have been accepted almost immediately. After all, physicians had been accepting the idea that worms cause disease for more than two thousand years. They could see the worms with their unaided eyes. Mesopotamian physicians could extract the worms that cause dracunculiasis manually, by cutting through the skin and twisting the worms around sticks; and ancient Egyptian physicians purged intestinal worms from patients using drugs. After the worms were removed the patients got better.The microscope generated widespread acceptance of infectious causation of most acute infectious diseases because by extending the visual sense, it allowed physicians to see the small organisms and associate them with the diseases they saw in everyday practice. The research and ideas of Pasteur, Koch, and their fellow microbe hunters put microscopes in hospitals and physicians’ offices. With microscope eyeglasses, the daily experiences of physicians reinforced rather than weakened many hypotheses of infectious causation, particularly for acute infectious diseases.Chronic diseases are different. Even with microscopes, the daily experiences of physicians do not reinforce infectious causation of chronic diseases unless the chronic disease develops from an acute infectious disease, as with syphilis and tuberculosis. In fact, daily experience must have done, and must still be doing, just the opposite. A physician does not contract cancer, stroke, dementia, or a heart attack soon after visiting a patient with one of these diseases.By relying on surrogates, some physicians avoid the bias against accepting infectious causation. For instance, antibiotic treatments can sometimes aid vision much the way microscopes aid vision. The physicians in New York City hospitals who were treating and curing peptic ulcer patients with antibiotics during the late 1940s were using the antibiotics to glimpse infectious causation. The daily experience of those physicians accorded with infectious causation of peptic ulcers because their antibiotic-aided eyes could see the infectious causation of ulcers more clearly than the eyes of physicians who had not been using antibiotics to treat ulcer patients.Physicians are still considered society’s experts on human diseases, and if we want an opinion in the absence of hard evidence, we seek an expert opinion. Winslow would not disagree on that matter. But in contrast with Winslow’s interpretation, history does not suggest that physicians are slow to accept infectious causation because they know too much; rather, what they know has been biased against the idea of infectious causation.Winslow’s particular opinions are not widely circulated. Aside from some medical historians, hardly anyone even remembers Charles-Edward Amory Winslow, Yale professor of medicine. The importance of the observation quoted here lies in its persistence. Winslow made his generalization about the slowness of physicians’ acceptance of infectious causation as a way of explaining attempts during the nineteenth century to understand acute diseases. With our clarity of hindsight, we can see that the bias against infectious causation has never been eliminated. It still masquerades as expertise.The causation of cancer provides an eye-opening illustration. Infectious causation of cancer was demonstrated by Francis Peyton Rous, who in 1910 published his discovery that an infectious agent can cause cancer in chickens. Rous, in his 30s, received flak from experts who knew that cancers were not infectious. The criticism led Rous, in his 40s, to shift his research away from infectious causation of cancer. The 87-year-old Rous, however, received a Nobel Prize in 1966 for the work he had done more than a half century earlier. That recognition gave a boost to the small cadre of researchers who were pursuing the possibility of infectious causation of cancer in labs scattered around the world. When Nixon’s War on Cancer generated a flush of funding, research was supported in both the infection camp and the not-infection camp. Not surprisingly, physicians were more heavily represented in the not-infection camp, though there were plenty of exceptions. When the funding dried up, the not-infectionists received the lions share of what was left, just at the time when the infection camp was poised to begin a long series of successes.From then until now, the not-infection camp has been unscientifically dismissing the infectious causation of cancer. With each new bit of evidence, they give up a bit of their argument, adamantly insisting on its general truth. In 1975 they granted that infectious agents cause cancer in animals, but almost never in humans. In 1985 they granted that infectious agents cause cancer in a tiny proportion of human cancers, but such cancers were portrayed as the rare exception. In 1995 they granted that infectious agents may cause about 15 percent of human cancers, but the vast majority of human cancers were caused by something else. In 2005? We can expect the percentage to have risen still higher. There is no sign of a slowdown in the discovery of infectious causation of cancer.During the last quarter of the twentieth century, researchers who made discoveries relevant to the genetic causes of cancer have received Nobel Prizes within several years after the publication of their research.I predict that historians in the middle of the twenty-first century will praise those who led the research effort into the infectious causes of cancer during this period at least as much as those who were contributing to our understanding of genetic causes. Harald zur Hausen, who has helped decipher the infectious causation of human cancer, will be praised as much as Nobel laureate Harold Varmus, who helped decipher the genetic causation of cancer. It has been about two decades since zur Hausen guided the health sciences toward an understanding of the infectious causes of cervical cancer. Using Peyton Rous as a model, one bit of advice can be offered to zur Hausen and the other pioneers of infectious causation of chronic disease, while waiting for their well-deserved call from Stockholm: Live a long life!*43\225\2*
“Miasma” is from the Greek miainein, meaning “to pollute.” Medical experts gave the term its notoriety, particularly during the nineteenth century, when they dismissed the idea of invisible pathogens in favor of miasmas: vaporous exhalations from patients or the environment that were assumed to cause disease.
In The Conquest of Epidemic Disease, Charles-Edward Amory Winslow remarked, “It is fascinating to note how, for two millennia, laymen were generally contagionists and physicians were miasmatists.” Winslow’s observation was perceptive, but his rationalization was not: “The physician, knowing more, was quite correct in denying that any then-available theory of contagion could explain the facts.” Actually, the theory of contagion available throughout the nineteenth, eighteenth, seventeenth, and most of the sixteenth century, could explain the facts. Winslow’s observation therefore raises questions that are pressing today because there are modern counterparts of miasmas, vaguely defined factors that are offered as causes of disease.
Why have experts in health care been slow to recognize infectious causation? Why do they still tend to dismiss hypotheses of infectious causation out of hand and then only gradually warm up to them? My physician, for example, seems like a particularly thoughtful and conscientious practitioner of healing and disease prevention. He keeps abreast of current thinking and tries to keep up with the literature.
When I talked with him in 1998 about infectious causation of chronic diseases, he seemed interested. He agreed that peptic ulcers were caused by infection and thought that infectious causation of atherosclerosis was reasonable and perhaps even likely. But when I pushed the envelope just a bit further, to possible infectious causation of breast cancer, prostate cancer, and schizophrenia, that was too much. He stopped his probing, moved backward, his body language mirroring his intellectual response, gave a not unpleasant but self-assured chuckle, and said, “Now, that’s going too far!” I went on making a pest of myself discussing the evidence, but without any discernible impact.
The answer to Winslow’s puzzle seems to stem more from human nature than from human knowledge. Humans generate their biases from their everyday experiences and need to struggle continually to recognize them. Physicians may need to struggle even more than the rest of us because they are trusted as the experts in health care, because they are expected to have the answers, because the systems they work with are very complex, and because ethical considerations restrict the normal options for definitive resolutions of uncertainties.
What is it that creates a bias against infectious causation, especially among such highly trained people? Physicians, like everyone else, base their opinions on their experience. Before the microscope was trained on human pathogens, their experience argued against some solid organism causing disease by moving from person to person. Had they been able to see the organisms, the ideas of infection and contagion would undoubtedly have been accepted almost immediately. After all, physicians had been accepting the idea that worms cause disease for more than two thousand years. They could see the worms with their unaided eyes. Mesopotamian physicians could extract the worms that cause dracunculiasis manually, by cutting through the skin and twisting the worms around sticks; and ancient Egyptian physicians purged intestinal worms from patients using drugs. After the worms were removed the patients got better.
The microscope generated widespread acceptance of infectious causation of most acute infectious diseases because by extending the visual sense, it allowed physicians to see the small organisms and associate them with the diseases they saw in everyday practice. The research and ideas of Pasteur, Koch, and their fellow microbe hunters put microscopes in hospitals and physicians’ offices. With microscope eyeglasses, the daily experiences of physicians reinforced rather than weakened many hypotheses of infectious causation, particularly for acute infectious diseases.
Chronic diseases are different. Even with microscopes, the daily experiences of physicians do not reinforce infectious causation of chronic diseases unless the chronic disease develops from an acute infectious disease, as with syphilis and tuberculosis. In fact, daily experience must have done, and must still be doing, just the opposite. A physician does not contract cancer, stroke, dementia, or a heart attack soon after visiting a patient with one of these diseases.
By relying on surrogates, some physicians avoid the bias against accepting infectious causation. For instance, antibiotic treatments can sometimes aid vision much the way microscopes aid vision. The physicians in New York City hospitals who were treating and curing peptic ulcer patients with antibiotics during the late 1940s were using the antibiotics to glimpse infectious causation. The daily experience of those physicians accorded with infectious causation of peptic ulcers because their antibiotic-aided eyes could see the infectious causation of ulcers more clearly than the eyes of physicians who had not been using antibiotics to treat ulcer patients.
Physicians are still considered society’s experts on human diseases, and if we want an opinion in the absence of hard evidence, we seek an expert opinion. Winslow would not disagree on that matter. But in contrast with Winslow’s interpretation, history does not suggest that physicians are slow to accept infectious causation because they know too much; rather, what they know has been biased against the idea of infectious causation.
Winslow’s particular opinions are not widely circulated. Aside from some medical historians, hardly anyone even remembers Charles-Edward Amory Winslow, Yale professor of medicine. The importance of the observation quoted here lies in its persistence. Winslow made his generalization about the slowness of physicians’ acceptance of infectious causation as a way of explaining attempts during the nineteenth century to understand acute diseases. With our clarity of hindsight, we can see that the bias against infectious causation has never been eliminated. It still masquerades as expertise.
The causation of cancer provides an eye-opening illustration. Infectious causation of cancer was demonstrated by Francis Peyton Rous, who in 1910 published his discovery that an infectious agent can cause cancer in chickens. Rous, in his 30s, received flak from experts who knew that cancers were not infectious. The criticism led Rous, in his 40s, to shift his research away from infectious causation of cancer. The 87-year-old Rous, however, received a Nobel Prize in 1966 for the work he had done more than a half century earlier. That recognition gave a boost to the small cadre of researchers who were pursuing the possibility of infectious causation of cancer in labs scattered around the world. When Nixon’s War on Cancer generated a flush of funding, research was supported in both the infection camp and the not-infection camp. Not surprisingly, physicians were more heavily represented in the not-infection camp, though there were plenty of exceptions. When the funding dried up, the not-infectionists received the lions share of what was left, just at the time when the infection camp was poised to begin a long series of successes.
From then until now, the not-infection camp has been unscientifically dismissing the infectious causation of cancer. With each new bit of evidence, they give up a bit of their argument, adamantly insisting on its general truth. In 1975 they granted that infectious agents cause cancer in animals, but almost never in humans. In 1985 they granted that infectious agents cause cancer in a tiny proportion of human cancers, but such cancers were portrayed as the rare exception. In 1995 they granted that infectious agents may cause about 15 percent of human cancers, but the vast majority of human cancers were caused by something else. In 2005? We can expect the percentage to have risen still higher. There is no sign of a slowdown in the discovery of infectious causation of cancer.
During the last quarter of the twentieth century, researchers who made discoveries relevant to the genetic causes of cancer have received Nobel Prizes within several years after the publication of their research.
I predict that historians in the middle of the twenty-first century will praise those who led the research effort into the infectious causes of cancer during this period at least as much as those who were contributing to our understanding of genetic causes. Harald zur Hausen, who has helped decipher the infectious causation of human cancer, will be praised as much as Nobel laureate Harold Varmus, who helped decipher the genetic causation of cancer. It has been about two decades since zur Hausen guided the health sciences toward an understanding of the infectious causes of cervical cancer. Using Peyton Rous as a model, one bit of advice can be offered to zur Hausen and the other pioneers of infectious causation of chronic disease, while waiting for their well-deserved call from Stockholm: Live a long life!
*43\225\2*
