Recent research supports the idea that genes play a role in the development of many complex psychiatric and behavioral disorders, including eating disorders. Although no genes have been linked to anorexia or bulimia nervosa, heritability estimates from twin studies have been described in scientific and popular literature. Genetic causation may compete with other causal narratives that implicate individual choice, family problems, and cultural norms. In this dissertation, I treat genetic ideas as newly available "cultural tools" for individuals to use as they manage identities, organize action, and conceptualize their own behavior and condition. Through semi-structured interviews with fifty women who have a history of anorexia or bulimia nervosa, I describe their understandings of genetic causality for this complex disorder and its implications. Half the sample was currently receiving treatment (recruited from a hospital-based clinic); the other half had recovered (self-reported and recruited through a mass email).
Chapters 3 and 4 illuminate respondents' understandings of eating disorders and their causes before the idea of genetic influence is brought up as a topic of discussion. In Chapter 3, I present the complex, dynamic causal models put forth by respondents and their perceptions of their own ambiguous, ambivalent agency in carrying out eating disorder behavior. Respondents spoke of eating disorder causation in ways that were not reducible to biological, "environmental" (e.g., social, cultural, familial factors), nor "individual" (e.g., psychological, agentic) factors and frequently involved elements of all three in interaction with each other over time. I illustrate this dynamic interactive causation by highlighting three complex causal factors frequently cited by respondents: valorization of thinness, coping responses, and repetition over time. The language respondents used to describe eating disorder behavior suggested that they held complex notions of agency; the disorder and its constitutive behaviors were not simply "chosen" but there was nevertheless some role for agency or quasi-agency.
In Chapter 4, I focus on respondents' understandings of eating disorders and responses to specific terms describing eating disorders. There was consensus that eating disorders were problems, but disagreement about whether they were psychological problems, mental illnesses, brain diseases, physical illnesses, or choices. As respondents discussed whether and why a given term was appropriate (or not) for eating disorders, they revealed not only how they thought about eating disorders but also how they defined the terms presented. I summarized their reactions to all five terms with an index of medicalized term endorsement and found that respondents who were currently in treatment and those who had received more extensive treatment endorsed more medicalized terms.
In Chapter 5, I examined respondents' initial reactions to the idea that "some say there are genetic causes" followed by their more considered speculations about how genes could play a role. Most respondents had already mentioned genetics in relation to eating disorders before I brought it up. There were negative and positive initial statements and reactions about genetics. Some respondents found the idea implausible and characterized genetic explanations as simplistic and deterministic, with an inadequate role for environmental causes. Others thought it made sense and expected that it would remove blame and stigma from people with eating disorders and offer hope for new genetically-based treatments. People who had earlier endorsed medicalized views of eating disorders were more likely to hold "positive" initial views about genetics, as were people with more or current experience of treatment. Respondents' genetic theories allowed a great deal of room for agency and environmental influence. Most respondents found genes specifically "for" AN or BN less plausible than genes "for" something more general, such as personality type or addictive tendencies. I identified four ways that respondents combined genetic and non-genetic influence and rank-ordered theories according to how much conceptual "room" they allowed for non-genetic forces to shape an outcome, arguing that genes "for" AN or BN offered the least room and genes "for" body type the most.
Chapter 6 addresses the perceived implications of genetic causal ideas for people with eating disorders. In response to hypothetical scenarios involving genetics, most respondents perceived genetics to medicalize eating disorders by increasing their resemblance to other less contested diseases, by making treatment by healthcare professionals seem more necessary, or by raising expectations for biologically based treatments. In general, respondents interpreted genetic influence to imply less personal responsibility for the eating disorder, which in turn had a number of implications for their agency and future action vis-à-vis eating disorders.