I was surprised that rumors of contagion seemed to multiply, rather than subside, as time wore on and as people in Belize became more familiar with the illness and observed it more closely in their own communities. Public health authorities often emphasize education about the causes of diabetes as one of the most important tools to curb its spread. But in this case, it was not that people had never received diabetes education; it was that the one-size-fits-all biomedical education from abroad often did not fully square with the realities they saw with their own eyes. Diabetes moved like an epidemic. It killed like an epidemic. In the Stann Creek District, diabetes affected at least ten times more people than HIV/AIDS,33 and everyone knew that AIDS was an epidemic. Diabetes was spreading quickly, and a “non-transmissible” disease is not supposed to spread.
Map of global diabetes deaths, shown at community forum in Dangriga.
As historian Allan Brandt notes, “The problem of causation is critically important because it reflects directly on the fundamental moral issue of responsibility for disease.”34 This point hit home more concretely for me when I gave a public presentation on an early version of this project’s findings to a small crowd in Dangriga. The audience came mostly from local branches of the Belize Diabetes Association and HelpAge, a local organization providing supportive care across generations. I began our conversation that day with a cursory slide showing the World Health Organization map of diabetes deaths. I had assumed that larger context was the part everyone would already know, but the global map seemed to be the only image I showed that surprised anybody. People raised eyebrows at each other. Wait, versions of this are happening across the world? Some people later reflected that they had gotten so used to stories attributing the Belizean rise in diabetes to their personal responsibility or local “cultural foods” that it shook up their perspectives just to take a step back and think of diabetes as an epidemic—a much bigger story, whatever that might mean.
There is a lot on the line in “explaining epidemics,” as Charles Rosenberg once put it.35 Global aid resources tend to move according to the moral rationales of humanitarian “crisis.”36 This kind of intervention “has come to define itself through exception,” Peter Redfield aptly observes, though that framing quickly “loses its transcendent magic” when “diseases prove chronic.”37 One woman in Belize named Nel described how a team of U.S. medical students visiting her village had been fascinated by her ankle wound when they believed she had leishmaniasis (a tropical disease caused by sandfly-borne protozoa parasites), but stopped visiting when it turned out to be a diabetic ulcer. Senses of medical urgency (or nonurgency) also remain deeply contoured, as Priscilla Wald describes in Contagious, by “how both scientists and the lay public understand the nature and consequences of infection, how they imagine the threat, and why they react so fearfully to some disease outbreaks and not others at least as dangerous and pressing.”38
The “entwined histories . . . of tropical medicine and racial thought” continue to shape how health issues get perceived, Warwick Anderson argues, together underpinned by colonial notions of contagion. 39 A cursory glance into the archives yields more than fifty years of ignored calls for a response to diabetes in the world. “Diabetes is no longer a rare syndrome in the tropics, and in many parts is being diagnosed with increasing frequency,” Dr. Silas Dodu wrote in the British Medical Journal in 1967. Returning home to Ghana after medical school in London, Dodu linked the phenomenon he observed to the spread of “white man’s food.”40 Several years later, the Pan American Health Organization (PAHO) sounded another alarm. “Right now the seriousness of the problem is reflected by the large number of diabetics who suffer, die, or become invalids,” reads their 1975 diabetes report, “fatalities considered largely preventable because effective treatments for these diseases were known.”41 Their astute and progressive policy recommendations are disturbing today, because they detail precise knowledge and actionable suggestions for policies to prevent diabetes injuries from spreading further—published before HIV/AIDS ever became legible as an epidemic, and before most people described in this book were born.
Although wider diabetes policy responses largely stagnated after PAHO’s 1975 call to action, other aspects of diabetes knowledge have grown more robust over the decades that followed. In addition to studying industrialized diets, more scientists now also track the ways that diabetes risks can be amplified by environmental exposures and chemicals. Some molecular pathologists call this “the new toxicology paradigm of endocrine and metabolic disruption” that reframes diabetes and related autoimmune conditions as a “hidden cost” to polluted landscapes.42 This phenomenon first became clear through industrial accidents: for example, diabetes rates in a small town in Italy spiked in the twenty years after its chemical plant exploded.43
Altered atmospheres also get absorbed: a recent long-term study of 1.7 million U.S. veterans estimated that about 14 percent of diabetes cases may be associated with air pollution, regardless of what diets individuals ate.44 Foods are impacted by air changes, too: crops such as wheat have less protein and more carbohydrates when grown in high-carbon atmospheres,45 while rice can absorb heavy metals like mercury (which also contribute to diabetes risk) if the rice patties are fed by polluted water.46 Chemicals used to protect crops also get inside humans: a study of 3,080 farmworkers in India reported that exposure to organophosphate chemicals significantly increased diabetes risk, apparently because insecticides meant to kill pests also interact with the microbes crucial to metabolic balance inside people’s digestive tracts.47 This is only one of several mechanisms by which endocrine-disrupting chemicals contribute to diabetes, which is a disease of the endocrine system.48
“We are porous selves within microbiomes and with microbes, sharing social lives even when we may not want to,” notes Juno Salazar Parreñas.49 Exposure to viruses can also trigger certain forms of diabetes and cancer.50 In addition to the microbial life within us, there has also been more scientific attention being paid to the plasticity of human biology—including metabolic absorptions that connect human bodies and larger environs,51 hunger- and stress-related epigenetic modulations,52 and ideas of “infective heredity.”53 The notion of “situated biologies” proposed by Margaret Lock reflects these puzzles—Lock initially used the name “local biologies” to consider such contingent effects on each individual body, yet the worldwide patterns in rising chronic conditions presented her with a paradox: How are “local biologies” of individuals changing in such patterned ways across global scales?54
In this view, human eating is only one dimension within “nested metabolisms.”55 Bodies exchange matter through “metabolic landscapes,”56 such as the paradoxical “choices” that Elizabeth Hoover examines in The River Is In Us when studies revealed that local fish and waters contain diabetes-causing toxics.57 Chemicals also impact industrial farm animals and plants, as Hannah Landecker examines in “Food of our Food,” which become part of human digestion as well when people eat them.58
Amid so many complex interactions, diseases are not binary either-or conditions. So how did our terms for addressing them come to be? It is worth taking a step back to ask how diseases came to be framed in such a dualistic paradigm to begin with.
The old paradigm of environmental miasma comes from an ancient Greek word meaning “pollution” (muíασμα), which framed disease as coming from “morbid material” in contaminated local environs. In the nineteenth century, germ theory replaced miasma paradigms with a stricter dichotomy. Dominant models today still hold that there are two basic ways to think about diseases: they are either “communicable” or “non-communicable.” In this binary schema, infectious diseases need to be addressed in terms of interrupting contagion between people, vectors, and environments via specific exposures to disease-specific germs or biological pathogens. Meanwhile, since non-communicable diseases are by definition not being transmitted between bodies, they are typically analyzed via the individual’s own inborn genetic constitution