As the image of populations at risk for diabetes shifted, so too did understandings of race.
At the turn of the twentieth century, most Americans remained certain that race was an established fact and that the divisions between races were fundamentally biological, although beyond that there was little consensus about whether biological meant unchangeable or even which populations properly made up a race.
The challenges to “race-thinking” that began with anthropologists in the 1930s and that exploded in the post, World War II period are part of a story well told in many excellent scholarly works.
The result was an attempt to abandon fixed racial typologies and to reimagine race as populations defined by differences in the frequencies of certain genes or traits.
Population genetics remains at the core of scientific understandings of race today, with evolutionary geneticists often preferring the language of “genetic ancestry groups.” This phrase addresses genetic differences between people, and the variation in gene frequencies among human populations.
Evolutionary geneticists, however, also acknowledge that the correlation between ancestry groups and the racial categories employed by the United States census is inexact at best, and so raises questions about what “race” actually means.
Contentious battles are fought today over whether race is a helpful category when it comes to understanding health disparities.
Those who argue that it is do not deny that current racial categories are only an approximation of an individual’s ancestry, but they still contend that further knowledge of race-specific genetic susceptibilities will ultimately improve health outcomes by permitting greater specificity in treatment protocols.
Those who oppose using race view it as a social convention that has little to do with ancestry (or a population’s genetic makeup) and everything to do with how a society chooses to distinguish among the people in its midst.
Their claim is that the focus on race ignores not only genetic diversity within groups but also other factors, such as poverty, that might better explain differences in prevalence rates.
Their fundamental concern is that racial stereotyping risks constraining diagnostic and treatment options in ways that can do harm.
Some who reject the use of race as a substitute for ancestry, including me, still view it as a powerful lens through which to understand health and disease.
From this perspective, race has a direct effect on someone’s health, but genetic differences, which may or may not exist, are not the primary reason for health disparities.
Rather, health disparities reflect far more the racism that populations experience because of the meanings ascribed to different skin colors and other physical attributes.
Racial discrimination can lead to inadequate access to quality health care, as well as exacerbate the social conditions of poor health, such as high levels of unemployment, inadequate housing, and underfunded neighborhood schools.
It can also generate ill health by producing pathological responses to the stress of living in a society in which white skin color is endowed with privileges denied to others.
Racism, in other words, can make people sick.
In this way, racism, not race, becomes a fundamental cause of differential disease rates, making it impossible to draw a sharp line between what is biological and what is social.
Previous works have explored the central role of race and racism in the history of disease. Syphilis, tuberculosis, smallpox, plague, malaria, HIV/AIDS, sickle cell anemia, and heart disease are just some of the diseases whose histories have revealed the subtle and not so subtle ways that race and racist attitudes have shaped the spread of disease, the experiences of those who fall ill, and the theories that medical, public health, and civic leaders put forth to account for the unequal distribution of disease.
Three studies in the past fifteen years have looked in particular at startling shifts over the course of the twentieth century in the populations imagined to be most at risk for cancer, schizophrenia, and fetal-alcohol syndrome. In each case, the disease was transformed from one associated with middle-class whites to one believed to afflict mostly racial minorities. And in the process, descriptions of those who suffered from the disease became far more judgmental.
Diabetes builds on these studies as it charts a similar racial transformation of a disease.
The story, however, is complicated, because diabetes went through not one but multiple such transformations over the more than one hundred years covered in this book.
Beginning in the late nineteenth century and extending to the present, professional and popular writers alike consistently evoked race to explain the uneven distribution of diabetes, but the populations considered most at risk have been, at various times, Jews, whites, Native Americans, African Americans, Mexican Americans, and Asian Americans.
Race, and class to some extent, has thus been a persistent presence in writings on diabetes, even as the racial group considered most vulnerable changed with time and even as definitions of race proved highly unstable.
It is striking that at times when more than one race was considered at risk of developing diabetes, race did not have a single meaning.
For example, in the 1980s, when a government task force on health disparities singled out five races for their high rates of the disease, it emphasized genetics for only two populations; for the others it pointed to behavior, stress, and acculturation.
In addition to race, professional and popular writers also noted the strong link between diabetes and obesity. Joslin even labeled diabetes “a penalty of obesity” back in 1921, and few questioned his assertion. Yet diabetes did not become almost synonymous with obesity until the 1990s, when multiple publications began generating alarm about the impending arrival of an “obesity epidemic,” even coining the term “diabesity.” Before then, and certainly well into the 1970s, medical researchers considered obesity to be just one factor among many responsible for driving up diabetes rates.
Also on their list were heredity, nervous strain, emotional shock, and infections, to name just a few. Researchers certainly mentioned obesity frequently, but they rarely used obesity to explain why some populations had higher rates of diabetes than others. To answer that question, they turned most often to race.
The centrality of race to the history of diabetes explains why I have organized each chapter around a population considered at one time to have had the highest prevalence of the disease. The book is thus loosely chronological, beginning with Jews, who were widely believed around the turn of the twentieth century to have a diabetes mortality rate between two and six times greater than that of the rest of the population, and ending with Native Americans, African Americans, and Mexican Americans, who today are the groups believed to be most at risk of becoming diabetic. I also occasionally disrupt this chronology to chart more fully the rise and fall of a given population’s close association with the disease.
In exposing the fraught relationship between disease and race, I am not arguing that race should be abandoned as an analytical category. A disproportionate number of people live in poverty, are denied opportunities, and confront racism because of their skin color, and each of these factors increases one’s chances of becoming ill. Race is, thus, intimately connected to health outcomes. As such, it occupies a place at the nexus of social conditions and biology.
I am also not claiming that differential morbidity and mortality rates have been fabricated or are only culturally determined.
In the past, Jews may have suffered disproportionately from diabetes, and today statistically significant studies show that the rate of diabetes is higher among American Indians, African Americans, and Hispanic Americans than among whites as a whole.
The critical question is: how have those rates been explained?
The answer I offer is that among the many risk factors, which include age, gender, and economic status, none has figured as prominently in explanations of observed health disparities as race.
This focus has led to a shift of resources away from efforts to address inequalities in income, education, employment, and social capital, as well as blame being placed on those suffering from the disease.
“I Have Diabetes. Am I to Blame?” This opinion piece, published in the New York Times on October 12, 2016, was penned by a woman who described herself as young, black, fat, and struggling with type 2 diabetes.
Simply posing the question in such a prominent forum is a reminder that, in our culture, disease has carried social, political, and racial meanings that have in turn reinforced tropes, misled researchers and clinicians, and misdirected resources. My father had his faults, but no one blamed him for his diabetes.
Diabetes: A History of Race and Disease
DIABETES
Diabetes: A History of Race and Disease
Judenkrankheit , a Jewish Malady
When the Jew is thirsty, he has his sugar tested; when the Christian is thirsty, he drinks.
Albert A. Epstein, 1919
The reason the Jew has more diabetes is not that he is a Jew, but that he is a fat Jew.
E. P. Joslin, 1924
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 percent of the more than two hundred patients he had seen in the previous fifteen 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 percent would have been unusual enough, given that Jews constituted just over 2 percent of the overall population in Europe.
That they comprised one-quarter of his patients suggested that something unusual was going on.
Seegen’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 twentieth 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 two hundred 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 two-and-a-half 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.”