The year was 1870. Josef Seegen had been seeing patients at the Carlsbad baths in Bohemia since the summer of 1854, tending primarily to individuals who suffered from diabetes. Over the years, he had become convinced that drinking and bathing in the spa’s mineral waters were helping his patients assimilate carbohydrates and thereby reduce the glucose that passed into their urine. What he could not ﬁgure out was why over 25% of the more than 200 patients he had seen in the previous 15 years were Jewish. “This percentage is immense,” he declared, even if Jews tended to visit spas more frequently than Christians. In a book he published on diabetes in 1893, he commented that 10% would have been unusual enough, given that Jews constituted just over 2% of the overall population in Europe. That they comprised one-quarter of his patients suggested that something unusual was going on.
Segen’s publication was just the beginning. As clinicians and medical researchers all over Europe noted that the number of diabetes cases increased as deaths from infectious diseases declined, they conﬁrmed his ﬁnding that Jews suffered disproportionately from the disease. These studies also revealed that mortality rates were every bit as troubling as morbidity rates. Jews seemed to be dying of diabetes at a rate two to six times greater than the rest of the population. In the German-language literature, diabetes even came to be known as the Judenkrankheit, or “Jewish disease.”
Such views made their way across the Atlantic. “There is no race so subject to diabetes as the Jews,” proclaimed one New York City physician in 1904. William Osler, perhaps the most famous American clinician of the early 20th century, noted that “Hebrews seem especially prone to it.” A physician with the U.S. Public Health Service concurred, insisting that the tripling of the diabetes mortality rate between 1888 and 1912 in New York City could be explained only by the rapid growth of the city’s Jewish population. And roughly 200 miles away, in Boston, a Jewish physician concluded from his study of the city’s death certiﬁcates that the rate of diabetes deaths among Jews was 2.5 times greater than among “their neighbors.” By 1916, Elliott P. Joslin, the foremost diabetes specialist in the nation, could write with conﬁdence in his highly acclaimed textbook that “the frequency with which diabetes occurs in the Jewish race is proverbial.” The association between Jews and diabetes would not be seriously challenged until the 1930s, and would not disappear until well after World War II.
What was going on? Might Jews have suffered disproportionately from diabetes around the turn of the century? Perhaps. Jewish immigrants who had ﬂed poverty and hunger in Eastern Europe tended to eat better in their new land, and this may have increased their chances of putting on a lot of weight and thus of developing the disease. Even the poor, who during lean times ate little more than herring, dark bread, and some carrots and beets, usually had plenty of potatoes. One immigrant remembered eating “Sunday, potatoes, Monday, potatoes, Tuesday and Wednesday, potatoes, Thursday and Friday, potatoes, and on the Sabbath you get a potato kugel.” Clearly the chronic starvation that had marked the lives of Jews in Eastern Europe had ended. Moreover, as immigrants slowly assimilated to their new lives in America, their ability to provide for themselves and their families improved. Fish and meat were no longer conﬁned to the Sabbath meal; butter, schmaltz (animal fat), preserves, and strudel also became regular fare. To be able to eat—and eat a lot—became not only a sign of success, but also a great joy. “It was lovely here—so much food,” recalled one woman who settled in Pittsburgh. “Cake for breakfast!” commented another, adding that “the very idea of serving cake for breakfast struck me as an extravagant fancy.”
Of course, plentiful food does not necessarily lead to increased rates of diabetes. Nor does being fat. Most overweight individuals do not have diabetes. But being overweight can increase one’s risk of developing the disease, and a daily fare that included ample portions of butter and schmaltz, and that led Jews to gain weight, could have increased their chances of becoming diabetic. So, too, might their experiences as recent immigrants. Studies of migration and disease have provided ample evidence that immigrants, especially those who have escaped lives of hardship and hunger, can develop high rates of diabetes after moving to a new environment. Why this is so remains unclear. Until recently, researchers had focused most on the consequences of a sudden introduction to a “Western lifestyle,” with its abundance of dense-energy foods and low levels of physical exercise. In the past decade or so, however, some scholars have begun to examine how the various stresses immigrants face as they adapt to a new home might increase insulin resistance not only by affecting dietary choice (cravings for “comfort food”), but also by triggering inﬂammatory responses in the body. This suggests that in the early decades of the 20th century, Jews might have suffered high rates of diabetes in part because of their immigrant status.
Yet as suggestive as these possibilities might be, there are ample reasons to be wary of assertions in the early 20th century linking Jews and diabetes. For one, most writers who mentioned this link rarely provided statistics to back up their claims. They simply repeated what everyone else was saying. And those who did offer up numbers and patterns offered statistics that were often unreliable. Not only did physicians usually draw on select populations, whether from their own private practice, the patient population of a speciﬁc hospital, or those seeking relief at expensive spas, but it was not always clear how to determine whether someone was Jewish—especially when calculating mortality rather than morbidity rates. One Jewish physician complained that New York City’s death certiﬁcates had no information about the religious afﬁliation of the deceased, although that did not prevent him from counting as Jewish anyone buried in a Jewish cemetery or whose personal name, parent’s name, or place of birth suggested that they were “of undoubted Jewish origin.” Physicians at the time even commented on the tenuous nature of the data available to them. Albert A. Epstein, a Jewish physician who practiced in New York City, was so skeptical of the evidence linking Jews and diabetes that he claimed that statistics showing the Jews’ predisposition to the disease only taught us how easy it is to “prove anything by statistics not sufﬁciently analyzed.”
To add to this confusion, the exact nature of diabetes remained a mystery. By the ﬁnal decades of the 19th century, the medical community may have known that the pancreas was the damaged organ and that its islets of Langerhans, the site of insulin’s production, had the greatest impact on the disease, but no one was sure what caused the islets to malfunction. (This remains unclear even today.) Even the discovery of insulin in 1921–1922, which radically transformed the management of the disease, did little to clarify its fundamental cause. Instead doctors pointed to a wide range of possibilities, including heredity, obesity, dietary excesses, a strenuous life, nervousness, infection, viruses, mental shock, and co-morbidities including arteriosclerosis, syphilis, acromegaly, gout, and Bright’s disease (today called nephritis, or inﬂammation of the kidneys). One author even blamed diabetes on processed foods, condemning in particular “the patent rollermade ﬂour, which is deprived of all the coarser part of the ﬂour.” As an exasperated physician summed up the conundrum in 1919: “Unlike many other morbid states, the immediate cause of this disease is unknown.”
Medical practitioners were clearly feeling frustrated in their efforts to bring a level of certainty to the diagnosis and treatment of diabetes. If only diabetes could be understood as well as the infectious diseases! Buoyed by recent discoveries of the bacterial and viral causes of many infectious diseases, by the beauty and simplicity of the model “one germ, one disease,” and by the development of effective treatments such as diphtheria antitoxin, physicians, patients, and popularizers alike wondered whether noninfectious diseases might also stem from a single cause. By the late 1920s this impulse would lead to increased interest in genes, which were imagined as the “cause” of noninfectious diseases in the same way that “germs”caused infectious diseases. In fact, the idea that diabetes was transmitted as a single recessive Mendelian trait was ﬁrst suggested in the 1920s, although at that time nearly every discussion of the etiology of diabetes began with the caveat that its cause was “still debatable.”
Even more challenging, especially for those intent on improving the care they offered their patients, was the lack of standardized tests for determining whether someone had diabetes. Nineteenth-century physicians may have had chemical tests to detect the presence of sugar in the urine without relying on their taste buds (as their predecessors had done), but the lack of uniformity in testing meant that results from different examinations could not be properly compared. Besides, glycosuria (sugar in the urine) was not always thought to signify diabetes: Physicians believed that a high sugar diet, an overly active thyroid, liver disease, or even a normal pregnancy could all cause it. One solution to this lack of certainty was to treat any patient who had sugar in the urine as though he or she had diabetes mellitus, at least, as Joslin suggested, “until the contrary is proven.” But clearly anyone who followed the diabetes specialist’s lead would ﬁnd more diabetes in the populations they examined than someone who worked with a more restrictive deﬁnition.
Fortunately for those who preferred not to treat all their patients with glycosuria as diabetic until proven healthy, blood glucose tests became available in the early 20th century. Yet even then there was considerable room for interpretation. There was no agreement, for example, on the concentration of blood sugar that should result in a diagnosis of diabetes. Nor did clinicians and researchers agree on the time of day to administer the blood test, how long a person had to fast before taking the test, how much glucose to administer during the test, or how quickly the individual’s blood sugar level had to return to normal for the person to be given a clean bill of health. What meaning, then, could be ascribed to a claim that Jews suffered disproportionately from diabetes, when “diabetes” was not clearly deﬁned?
The deﬁnition of “Jew” was equally ambiguous. Even putting aside the debates that took place in the early decades of the 20th century over whether Jews constituted a distinct race, the Jewish population in the United States was heterogeneous. Did claims that “Jews” had high rates of diabetes include Sephardim, who had emigrated from Spain and Portugal as early as the 17th century? Or did it refer only to Ashkenazi Jews, who had made their home in Europe following the diaspora? And if only the Ashkenazis, did that group include German Jews, who had started their migration to the United States in the 1830s and had achieved a level of wealth and accomplishment by the end of the 19th century? Or did it refer to the millions of Eastern European Jews, primarily from Russia, who had begun to arrive in large numbers in the 1880s and who frequently began their new lives in poverty? Only a few who commented on the high rate of diabetes among Jews made any distinctions among these groups, and among those who did, there was rarely agreement. To some, Russian Jews suffered most because of the particularly “cruel persecution” to which they had been subjected, while others claimed that German Jews’ greater wealth and “characteristic modes of living,” which included greater “mental exertion,” made them more susceptible to the disease.
In short, we cannot know for certain whether “Jews” did, in fact, suffer disproportionately from “diabetes” in the decades around the turn of the 20th century. Which Jews? Based on which statistics? Working with which deﬁnition of the disease? It is impossible to know whether they were overrepresented in the patient populations of those physicians who published statistical studies, or whether, as implied by Epstein’s joke about a thirsty Jew checking his sugar levels rather than taking a drink, Jews went to physicians more often than other populations when they were not feeling well. It is thus impossible to answer the question of whether Jews had a higher rate of the disease. But we can explore why, despite the highly ambiguous nature of the data—an ambiguity acknowledged at the time—virtually no one questioned the fundamental link between Jews and diabetes during the ﬁrst three decades of the century. Not even Epstein, who, despite drawing attention to the unreliability of the statistical evidence, conceded the likelihood that Jews were, in fact, more predisposed to diabetes. Better safe than sorry, he reasoned, as he recommended that Jews take proper precautions to prevent the onset of the disease.
Diabetes as a ‘Jewish Peril’
The seemingly high rate of diabetes among Jews in the United States ﬁrst attracted attention in the last decades of the 19th century, as diabetes rates in general appeared to be rising rapidly. Recognizing that improvements in public health and nutrition meant that more people were living into adulthood and developing a wide range of chronic diseases, health professionals noted two ways in which diabetes stood out. First, although many more people died from heart disease and cancer, the mortality rate for diabetes was increasing more rapidly than for these other ailments. According to one diabetes specialist, its rate had jumped 150% between 1850 and 1880. And second, Jews seemed to be affected disproportionately. In examining the relationship between the two, these writers ended up constructing racial narratives about the disease.
Some of these narratives were decidedly antagonistic toward Jews. J. G. Wilson, a surgeon with the U.S. Public Health Service, was particularly disdainful. In a study he conducted on “Jewish psychopathology” just a year after he wrote about diabetes, he referred to Jews as “a highly inbred and psychopathically inclined race.” Wilson made this claim while he was stationed at Ellis Island, the U.S. port of entry for most Eastern European Jews. His sense of discomfort with this group, whose clothing, language, and mannerisms seemed so alien to him, was clear in two ways: the speed with which he moved from correlation to causation, assuming that the simultaneous increase in both the mortality rate from diabetes and the Jewish population meant that Jews were responsible; and his insistence that Jews had such a high rate of this disease because of “some hereditary defect” exacerbated by “the practice of inbreeding.” Wilson’s decision to refer to the Jewish practice of consanguineous marriages—which was being hotly debated at the time by Jews and non-Jews alike—as “inbreeding” not only fed anxiety about the close-knit nature of Jews, but also tainted the diagnosis of diabetes with hints of incest.
Wilson was writing at a time of intense anxiety over the seemingly endless ﬂow of immigrants from Eastern Europe to the United States that had begun in the 1880s. In 1911, just a year before Wilson published his study of diabetes in New York City, a congressional committee known as the Dillingham Commission had produced a lengthy report recommending that immigration be curtailed. As part of its investigative work, the committee had prepared an analysis of the racial makeup of the existing immigrant population, a clear indication that race was to be a critical factor in deciding who among the “tired,” the “poor,” and those “yearning to breathe free” would be allowed to continue to enter the country. Working with standard anthropological classiﬁcations, the members of the commission began by dividing the immigrant populations into ﬁve major races—Caucasian (white), Malayan (brown), Mongolian (yellow), American Indian (red), and Ethiopian (black)—before separating them further into subgroups, alternatively referred to as “peoples,” “nations,” or, confusing matters further, “races.” In the end, and by employing a combination of biological, linguistic, and cultural characteristics, the Dillingham Commission identiﬁed roughly 600 “branches or divisions of the human family” throughout the world, 45 of which could be found in the United States. Jews, also referred to as Hebrews, were among them, along with Celtics, Alpines, Teutonics, Mediterraneans, Slavonics, and many others, but it remained unclear exactly who was related to whom and how. One of the questions that received considerable attention was whether Jews should be considered white.
This was not an academic question. The ﬁve major races were understood to exist in a hierarchy, with whites representing the most “civilized” of the groups and blacks and American Indians the most “savage.” According to the 1790 naturalization law, only “free white persons” could apply for citizenship, and in the early years of the American republic this included Jewish immigrants, who hailed primarily from Germany. But later in the century, the inﬂux of millions of Eastern European Jews, with their strange language, clothing, and overall appearance, cast doubt on this classiﬁcation. A group of radical nativists jumped into the fray, going to great lengths to cast the latest inﬂux of Jews as “thoroughbred Asiatics.” As strange as that may seem today, the question of whether Jews were fundamentally “oriental” or “occidental” dates back at least to the Middle Ages, when Christian writers often depicted them as turbaned and oriental as a way of highlighting their otherness. According to radical nativists, Jews still bore the imprint of their years wandering in the desert when they were little more than a nomadic tribe. Describing them alternately as primitive, tribal, and “Mongoloid,” some claimed that they had descended from the Khazars, a Turkic people who allegedly converted to Judaism in the eighth century. Whatever the speciﬁc allegations, casting Jews as “oriental” raised the hope—at least for the nativists—that Jewish immigrants seeking entry might be denied under the terms of the 1882 Chinese Exclusion Act, which barred Chinese laborers from entering the United States.
The members of the Dillingham Commission did not join the radical nativists in questioning whether Jews were white. But they evidently struggled with the degree of Jews’ whiteness, revealing their embrace of early 20th-century beliefs that some groups were whiter than others. This was apparent in their criticism of the Bureau of Immigration’s previous classiﬁcation of Jews as “Slavonic” and thus as “Aryan,” and their reclassiﬁcation of them as “Semitic,” which placed them lower on the race ladder. Given the widespread belief that Semitic peoples stemmed originally from Africa, this change raised further questions about Jews’ whiteness. Indeed, although never a popular belief, some considered Jews to be “essentially Negro in habits, physical peculiarities and tendencies,” possessing both “Mongoloid” and “Negroid” traits. The motivations behind this change became evident when the commission concluded its work in 1911 and recommended that the government enact a restrictive immigration law. It took another decade, but the commission’s report ﬁnally bore fruit: In 1921, and again in 1924, with the passage of the Johnson-Reed Act, the government put in place restrictive immigration laws that reduced the number of Jews entering the United States from a record high of 120,000 in 1921 to just 10,000 three years later. As the eugenicist Charles Davenport, who had advised the Dillingham Commission, wrote to a friend shortly after the legislation passed: “Our ancestors drove Baptists from Massachusetts Bay into Rhode Island, but we have no place to drive the Jews to. Also they burned the witches but it seems to be against the mores to burn any considerable part of our population. Meanwhile we have somewhat diminished the immigration of these people.”
A decade before Davenport penned these words, J. G. Wilson, the surgeon with the U.S. Public Health Service, had voiced related concerns. The same year the Dillingham Commission published its ﬁnal report, and one year before he blamed rising diabetes rates on the inﬂux of Jewish immigrants, Wilson had published an article in Popular Science Monthly on “The Crossing of the Races.” This was Wilson’s opportunity to articulate the criteria he believed the government should employ as it crafted its immigration policy, and his message was clear: There are good immigrants and bad ones, and Jews belonged to the bad group. Notably, Wilson did not base this determination on biological race, despite the title of his article. Unlike his peers who spread widespread panic about the effects of race mixing on the vigor of wholesome American stock, Wilson believed that “racial amalgamation” had long been a part of human history and should be embraced, at least as long as it took place “between different branches of the white races.” In fact, he believed that some racial crosses, such as between Teutons, Britons, and Celts, had produced positive results, and he could well imagine future intermarriages between “real Americans” and select immigrants that would be similarly beneﬁcial. What worried him was not the biological mixing of the races, but their moral mixing. He wanted the government to restrict entry to those immigrants who would have a positive impact on “our habits of thought, upon our morals, and upon our institutions,” in short, on “our spiritual selves.”
Wilson claimed that history provided the best clue to an immigrant group’s moral mettle, so he proceeded to offer a brief lesson about each of several populations, reading their past to see what it revealed about the group’s character and whether they would be capable of adopting “those Anglo-Saxon habits of thought which we must insist upon as necessary to good citizenship in a great republic.” His conclusion was that Italians, Magyars, Poles, and other Slavs had all demonstrated their ability “to adopt the ways of western civilization.” Jews, on the other hand—he referred to them as “the other type of immigrant”—had failed the test. In his interpretation of their history, Jews had been welcomed in many different lands from biblical times to the present, and each time they had begun by being treated as equals. Invariably, however, they had drawn others’ wrath by insisting on “certain special privileges” and keeping to themselves. This “clannishness,” Wilson insisted, reinforced by Jews’ refusal “to intermarry with those of other religions,” worked against ensuring that immigrants adopt, rather than obliterate, “our inherited Anglo-Saxon ideals.” Diabetes, Wilson may well have thought, was a just punishment for Jews’ insistence that they “breed” only among themselves.
The hostility that Wilson evinced in his discussion of Jews and diabetes was, however, the exception rather than the rule. Far more common in the diabetes literature was subtle trafﬁcking in negative stereotypes. Thus one physician attributed Jews’ high rate of diabetes to the love of the “Hebrew race” for “high living,” adding that “they are given to parties, they congregate together and have frequent and irregular meals.” William Osler wrote of Jews’ particularly “neurotic temperament.” A journalist weighed in, blaming Jews’ “racial tendency to corpulence.” And Haven Emerson, professor of preventive medicine at Columbia’s College of Physicians and Surgeons, and a previous commissioner of health for the city of New York, put the onus on Jews for spreading what he called “this great luxury disease.” In doing so, he drew on not only widespread fears of the drastic changes shaking the foundation of American society in the interwar years, but also negative images of the Jew as the embodiment of much that was wrong with modernity.
Emerson honed his argument in an article titled “Sweetness Is Death,” published in 1924 in The Survey, the leading journal of the social work profession. In the ﬁrst two-thirds of his article, Emerson did not even mention Jews. Instead he drew in his reader by presenting disturbing statistics about the 15-fold rise in the annual death rate from diabetes between 1866 and 1923, and by targeting the social, economic, and cultural changes that were making the trend difﬁcult to reverse. Emerson mentioned, for example, the way the new “motorized and mechanistic existence” reduced the need for physical labor and thereby reduced the number of calories a person burned. But what truly disturbed him were challenges to the moral ﬁber of the nation. These included the growing “self-indulgence,” the increase in “lazy comforts,” the “sugar coating” of meals, the desire for little more than “the satisfaction of … caprice.” Indeed, if anything, Emerson’s diatribe in the ﬁrst pages of his article was against “the idle rich” and their embrace of conspicuous consumption, not Jews per se. Diabetes rates were going up, he ranted, because Americans had become “the grossest feeders among the nations … bulging with the money bags of the world, fairly oozing with wealth, eating every day much more than any of our allies or opponents of the war … and, as it were, dying of overeating.”
“Sweetness Is Death” is clearly about more than diabetes. It is also Emerson’s denunciation of so many of the changes taking place in the years following the Great War. Labeling diabetes “a great luxury disease,” he expressed deep anxiety about the transformation of fundamental aspectsof American life: The economic prosperity that stemmed from the mass production of consumer goods, including clothing, radios, cars, and magazines; the rise of print culture and advertising, which encouraged citizens to support the new consumer culture; and a credit economy that allowed working-class and middle-class individuals to participate in new leisure activities, whether they had the means or not. New cultural activities also took shape during the “roaring twenties,” with the proliferation of dance halls, movie theaters, and jazz clubs, offering venues where traditional gender roles and staid sexual mores could be ﬂouted publicly. To Emerson, diabetes was symbolic of all that he loathed; “a disease of wealth and feeding and fatness,” it provided physical evidence of what was, in essence, moral turpitude. And nowhere, he added, is this “better shown than in the story of the races.”
This was Emerson’s segue to his discussion of diabetes’s prevalence among Jews. In support of his argument that diabetes and wealth went hand in hand, he claimed that tuberculosis, “a disease always fostered by poverty, low standards of living and food shortage,” barely affected Jews, whereas diabetes ran so rampant among them that it was “commonly known in Europe as the ‘Judenkrankheit.’” Yet Emerson’s explanation for this proclivity did not ﬁt the picture he had just painted, for he described Jews as “merchants, storekeepers, [and] needle workers,” who were “abundantly though cheaply fed.” In other words, by his own account they were not the “idle rich.” Still, by deﬁning Jews as the most at risk of developing “this luxury disease,” and by linking the disease to “wealth and feeding and fatness,” Emerson reinforced an image of the rich and fat Jew, hoarding his money and indulging himself while the rest of the world struggled with hunger and deprivation.
This image was ﬁnding particular resonance in the early decades of the century, when the “fat Jew” became a potent symbol, in one historian’s words, of “the potential for disease and decay” associated with modernity. The fears to which Emerson gave voice in his essay—that self-indulgence and hedonism were replacing self-discipline and asceticism as the social values to which one should aspire, and that the “American way of life” was rapidly coming to an end—reﬂected the changing meaning of fat from a marker of afﬂuence and inﬂuence to a symbol of gluttony and decadence.
In this context, the fat—and diabetic—body of the Jew became one important site where these anxieties played out.
Excerpted from Diabetes: A History of Race and Disease by Arleen Marcia Tuchman, published by Yale University Press. Copyright © 2020 by Arleen Marcia Tuchman. Reprinted by permission of Yale University Press. All rights reserved.
Arleen Marcia Tuchman is professor of history at Vanderbilt University. She is the author of Diabetes: A History of Race and Disease; Science, Medicine, and the State in Germany; and Science Has No Sex: The Life of Marie Zakrzewska, M.D.