Review of Heartsick: The Politics of Risk, Inequality, and Heart Disease. JanetShim New York: NYU Press, 2014, 277 pp.

Reviewed Book

Heartsick: The Politics of Risk, Inequality, and Heart Disease. JanetShim New York: NYU Press, 2014, 277 pp.

Who gets heart disease? Why do some groups seem to have it more than others? What risk factors best explain variance in disease rates? These epidemiological questions are part of complicated social and biophysiological dynamics at the root of Shim’s Heartsick. And, as the title indicates, heartsick is also used to describe social, legal, economic, historical, and other troubles, themselves nonrandomly experienced across and between groups. How might these life experiences explain heart disease? Yet epidemiology struggles, as do many other technoscientific approaches to human health and disease, with a set of logics that privilege the first set of questions and disables the second.

In Heartsick, Shim also deftly explores the sociology and politics of knowledge as a means to assess why social experiences are systemically erased from most epidemiological assessments of heart disease. Throughout, readers are treated to careful ethnography, thoughtful analysis, adroit argumentation, and pointed political realism commensurate with the best of sociocultural analytics of technoscientific claims-making enterprises.
Shim begins by introducing readers to the epidemiological trends for heart disease. The evidence is clear. Cardiovascular disease (CVD—hypertension, coronary artery disease, and stroke) is the leading cause of mortality in the United States. That is, if we ignore heartsickness. The disease is differentially experienced across groups of people ethnically categorized, across socioeconomic statuses (SES), and gender/sex spectra. Like most diseases, the poor, disadvantaged, racialized, excluded, and socially vulnerable (however defined) are disproportionately impacted and die sooner than people from groups with relative advantage.

Shim’s epistemological critique includes an erudite and clear explanation of reductionism and embodied difference within epidemiology where the “interconnectedness of group status, power and wellbeing” (p. 15), those factors poignantly part of lay knowledges of CVD), never enter the etiological frame. It is the etio-logics that are the objects of analysis here, and Shim takes the expert–lay knowledge divide head on. Knowledge production is “suffused with social and political concerns” (p. 17), she writes. This statement is not new. However in Shim’s Heartsick, we are shown yet again, and in perhaps the most compelling way to date, the gears and levers of the etio-logics of health inequity generally and those found in cardiovascular disease in particular—etio-logics that keep the sociohistorical context and accounts of heartsickness out of cardiovascular disease epidemiology.

Key to Shim’s analytic is her framing of etiological “usual suspects.” Usual suspects are the “go to” culprits for what causes disease patterns across sociological differences (e.g., racial categories, socioeconomic status, and sex). Shim writes, “This usual suspects approach encompasses both a kind of conceptual devolution—wherein complex, manifold social processes are flattened into individual-level characteristics—and methodological routinization as a standard operating procedure” (p. 18). This theory– method has three interrelated effects, explains Shim.

First, usual-suspects logic transforms sociological phenomena into individualistic phenomena. That is, stratified social ordering is black boxed into traits or attributes proper of individual bodies. As Shim so adroitly avers, this black boxing occludes important factors that explain risk of risks as well as the consequences of nonrandom experiences that correspond to race, SES, and gender/sex. Both variances in risk and different life experience are precisely what usual-suspects etio-logics erase and thus cannot account for as fundamental etiological concerns.

Second, the usual-suspects logic having individualized the social worlds in which people live maintains that these social factors must be controlled for so to get at the presumably more fundamental factors that explain variations in risk and incidence of disease attributable to these risks. It is as if scholars tried to explain depression variance without considering shared experiences widely recognized as appropriately depressive (e.g., survivors of war, dislocation, layoffs, or collective traumas). Most would consider ignoring contextual factors, social status, and their attendant experiences, while searching for causes of both risks for and variances in incidence of disease misguided, or less charitably, foolishness. Shim’s book demonstrates that explaining away race, SES, and gender/sex in the search for the causes or variances in disease rates by group misses the most powerful explanatory tools available.

Third, and finally, Shim notes, that even when epidemiologists were interested in race or the results of a study showed variances between racially categorized groups, epidemiologists caught in the usual-suspects logic often posit other differences as the putative risk factor. To wit, variances in disease incidence between racially labeled groups were explained away as differences in SES, culture, or troublingly, physiology.

After an analytically robust chapter on the history and construction of difference in cardiovascular epidemiology, Shim uses rich ethnographic data in three chapters that demonstrate the inter-articulations of race, class, and gender respectively. In Chapter 6, Shim details the institutionalized ways the usual-suspects logics endure. For example, researchers must account for the usual suspects to be credible, and the NIH practically requires the selection of the usual suspects (or a robust justification if researchers do not). Shim also notes the convenience of using the usual suspects as proxies for neighborhood effects or conditions that can change over the life course (parental status, exposures to toxins, SES) and that are thus too costly to track.

In several places in the book, Shim makes the case for a combined lay–expert approach as a corrective to the usual-suspects logics. She compellingly argues that lay expertise contains novel insight that can lead to a way out for the logics of difference. After all, the relationship between social inequalities and health inequalities are contained in lay accounts of life events and in different conditions of life. How could it be otherwise? However, on a more somber note, Shim realizes that the politics of knowledge will endure in ways that prevent new logics to fully emerge or the short comings of old ones to be easily seen. To wit, the social production of disease is but a manifestation of the social production of inequity. Epidemiology of CVD, like all knowledge-making enterprises, must be understood as part of these larger forces.

Shim’s work is a significant contribution to the debates about social difference writ large, not only those pertaining to heart disease. As an ethnographic analysis of technoscience and the etio-logics of epidemiology in particular, Shim’s attention to the ways race, SES, and gender/sex work similarly, in concert and alone, stands apart. Epidemiologists might find in Shim the requisite conceptual velocity to break free from the orbit of etio-logics that occlude rather than explain risk and disease variance between, and, as many social epidemiologists have argued, within sociohistorically important groups.

Heartsick is a very approachable book that could be assigned to undergraduates, graduates students, and cardiologists alike without losing either its erudition or pointed edge. Moreover, Shim’s careful analytical and ethnographic detail stands as both cautionary tale and sign of hope. For we cannot improve our knowledge of a problem like cardiovascular disease without understanding the problems of our knowledge itself. Shim’s Heartsick does both well.