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Purpose: Because past research has investigated nonverbal behaviors in clusters, it is unclear what status value is ascribed to individual nonverbal behaviors. I test status cues theory to investigate whether response latency functions as a status cue. I explore whether it affects behavioral influence or if it only signals assertiveness and does not have status value. I also explore how one's interpretation of response latency impacts behavioral influence.

Methodology: In a two-condition laboratory experiment, I isolate response latency and test its strength independently, and then I measure behavioral influence, participants' response latency, and perceptions of assertiveness. I also conduct interviews to investigate how participants interpret their partner's response latency to understand how people ascribe different meanings to the same nonverbal behavior.

Findings: I find that response latency alone does not affect behavioral influence, in part because how people interpret it varies. However, response latency does significantly impact participants' own response latency and their perceptions of their partner's assertiveness.

Practical Implications: This research demonstrates the intricacies of nonverbal behavior and status. More specifically, this work underscores important conceptual differences between assertiveness and status, and demonstrates how the interpretation of nonverbal behavior can impact behavioral influence.

Since World War II, rates of type 2 diabetes (henceforth diabetes) have skyrocketed, leading to talk of an “epidemic,” believed to result from formerly “adaptive” genotypes colliding with “affluent” postindustrial societies – largely their food excesses and physically undemanding jobs. Hence, experts describe diabetes as a struggle between biology and behaviors – “genes-as-destiny” and “lifestyles-as-choice” – said to have spared no social group. However, racial and ethnic minorities and the poor are affected disproportionately.

In this paper I challenge the “genes–lifestyle” framework and argue that the epidemic, particularly its distribution, is produced not by affluence but by poverty. The cumulative effect of malnutrition or hyperglycemia during pregnancy, of stunting in young children, of structural constraints over healthy lifestyles, and of the lack of a right to adequate medical care, which are all the results of poverty, leads to diabetes and its complications, and to disparities in their distribution among social groups. Hence, diabetes disparities are not mere differences but differences that are avoidable, unnecessary, and unjust. I also highlight selected conceptual problems of the genes–lifestyle framework that mislead about the potential contributions of genetics to human health.

I conclude that because the roots of the diabetes epidemic lie in inequities in social power, the solutions required are not medical but political, and ought to concern a sociologically informed bioethics. I also conclude that insofar as dominant accounts of the diabetes epidemic ignore or downplay these roots, they will legitimize research and policies that reproduce or even increase diabetes disparities. The paper is part of a larger project on the political ecology of diabetes.