To approach chronic disease patterns, we need ways to recognize and publicize potential exposures of processed diets and industrial toxicants, as well as biological germs—an epidemiology of what Adia Benton has called “connectors,” rather than vectors alone.61 That requires attention, Michael Fischer notes, to “the bioecologies at play” between porous boundaries and reactive membranes, commodity flows, and human and ecological health.62
In light of these gray zones, the either-or labeling of “contagious” versus “non-communicable” disease appears insufficient to describe the prevalence of human-made diseases now becoming visible around the world.63 Diabetes is not an exception to, but very much iconic of growing chronic epidemics—such as cancer clusters64 or the soaring prevalence of asthma and other autoimmune conditions.65
When I talked with public health practitioners and policy makers about such exposures, I found it helpful to have a working name for this in-between. I came to describe it as para-communicable—chronic conditions like diabetes that may be materially transmitted as bodies and ecologies intimately shape each other over time, with unequal and compounding effects for historically situated groups of people. Focusing on para causalities—the products and exposures changing alongside (para) people’s bodies—draws attention to the imperative to acknowledge and rework those systemic harms. Exploring this approach also became a way to translate across different spaces of knowledge making—such as academic conferences where keywords to describe exposures were abundant, and the arenas of practice where they were often illegible or quietly fell out of frame.
This is not a return to miasmatic thinking, though. As historians have observed, cloudy causalities are indeed frequently part of what it feels like to live amid ongoing exposures—but confusion is difficult to regulate, and industries bank on this.66 Nor can chemicals simply be reframed as contagious—they too do not follow a neat binary pattern. They have their own intervals of low-dose “latency.”67 Current regulatory paradigms that contribute to so many toxics on the loose are in part flawed for exactly this reason. Germ theory informed the ways in which chemicals were tested in the laboratory, but these simplified models of disease have often failed to recognize the complex ways a chemical can still cause harm.68
Sugar and food industries have also attempted to intentionally produce confusion, akin to techniques described in books like Merchants of Doubt.69 Marion Nestle examined how Coca-Cola, for example, has paid doctors to back suspicious studies and run ad campaigns focused on how individuals with chronic health issues need to exercise more.70 These corporate strategies raise special challenges for scholarship dealing with uncertainty. The key theorists of syndemics—a widespread model describing how multiple epidemics interact—recently expressed concern that the term can take on a miasma-like cloudy quality if it is taken up imprecisely or without follow-up steps to trace specific pathways and signatures of responsibility.71 Anthropologists like Elizabeth Roberts72 are seeking ways to build a counter-science, through sustained collaborations and a grassroots-guided “science of the in-between.”73
Thinking back to “diabetes multiple,” policy interventions (or their absence) may actually produce biologically different versions of diabetes, on the population level as well as for individual bodies. What an epidemic is is different—not just in scale, but potentially in its mechanisms and forms of transmission. The first two cases of drug-resistant bacteria documented in the United States both occurred in diabetic ulcers—apparently from separate instances of horizontal gene transfer, by which bacteria can nearly instantaneously swap genes with other living or dead bacteria.74 One study of 150 diabetic ulcers in India found that “91% of the bacteria were resistant to three or more antibiotics,” including feared bacteria like MRSA.75 In cases where people live for months or years walking in sandals with open diabetic wounds on their feet, it is also possible that horizontal gene transfer occurred directly between the bacteria infecting lower limb ulcers and the bacteria living in local soils.
This tendency for unchecked diabetes injuries to foster drug-resistant bacteria may have implications for future antibiotic efficacy and diseases of all kinds. Yet if drug-resistant bacteria sound like an urgent global issue in a way that the foot ulcers fostering them do not, that is another example of why the diabetes epidemic will continue to grow.
GEOGRAPHIES OF BLAME
Media analysts report that a “full 73 percent of articles that mention the poor, African Americans, or Latinos blame obesity on bad food choices, compared to only 29 percent of articles that do not mention these groups.”76 As Paul Farmer has noted of the common figure of a blame-worthy patient, “All too often, the notion of patient noncompliance is used as a means of explaining away program failure.” He related this to “immodest claims of causality”—how patient noncompliance is commonly assumed and made persuasive without evidence, but any alternative explanation requires a great deal of evidence for policy makers to find it convincing.77 Looking at tuberculosis cases, Farmer asked how people with TB could be labeled “noncompliant” with treatment when 50 percent don’t even know they have it. This is the same percentage of people with diabetes globally that the International Diabetes Federation today estimates have never been diagnosed.78 These patterns resonate with the “geographies of blame” that anthropologists have documented around the politics of labeling “noncompliance” elsewhere: “Throughout the world, those least likely to comply are those least able to comply.”79
“How am I going to make a diet? There is only one kind of food here,” I often heard patients tell the visiting Cuban physician, who would laugh kindly but never really had an answer. In nearby Guatemala, Emily Yates-Doerr has described the ways nutritional experts carefully avoided talking about problems of macro-infrastructure that neither they nor their patients could change, since that advice could easily have registered as cold or uncaring.80 The caregivers I met likewise avoided initiating conversations about “social determinants of health” directly with patients, in hopes of generating a healthy sense of optimistic possibility—focusing on the scale within their grasp. This mostly meant trying to equip patients to negotiate existing foodways. But who will rework larger food systems?
Some preliminary studies have proposed that diabetic foot ulcers could be better treated if patients were also provided with supplies of nutritious food.81 Scholars such as Harvard economist Michael Porter have argued that such investment would be beneficial for health systems, which spend thousands of dollars each time they amputate a diabetic injury. That money could be better invested in nutrition programs to help prevent amputation.82
Yet even the food baskets that accompany HIV/AIDS treatment programs often contain cheap grains, such as white rice, which are precisely the kinds of high-carbohydrate foods that people with diabetes are discouraged from consuming. What would be in a diabetes food basket? (And should it be in the HIV/AIDS food baskets, too, considering how many patients with HIV/AIDS are also getting diabetes as a side effect of their drug treatments?83) Trying to imagine a food basket’s hypothetical contents only highlights the bigger issue: to actually curb the rise in diabetes, healthy foods need to exist for sale at affordable prices in grocery stores, not just dispensed in baskets for those with already sick bodies or imperiled limbs.
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