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 twentieth 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 twentieth 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 nineteenth 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 roller-made 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 non-infectious 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 twentieth 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 twentieth 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 seventeenth 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 nineteenth 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 twentieth 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 nineteenth 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 percent 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.