Qualitative methods can reveal unanticipated findings and investigate meanings and understandings of interview themes more fully than quantitative methods, but often must sacrifice uniformity of question wording and ordering in order to do so (Weiss 1994). To illustrate why qualitative methods are appropriate for this project, I explain why I considered and abandoned the idea of using the revised Illness Perception Questionnaire (IPQ-R) for this project. This questionnaire is based on Leventhal’s self-regulatory model (Leventhal et al. 1984) and includes standardized questions with a fixed set of response options to assess perceptions of illness and has been used to study perceptions of eating disorders. This questionnaire includes subsections that are relevant to this project: causality (including the item “hereditary – it runs in my family”), control over symptoms, and expectations about treatment (Moss-Morris 2002). However, this questionnaire was not created specifically for
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eating disorders and contains a number of inappropriate items. For example, the causal subscale asks respondents their level of agreement on a 5-point Likert scale with 18 causes, many of which make sense for disorders such as cardiovascular disease or cancer, but not for eating disorders. Some items are nonsensical for eating disorders (smoking, pollution in the environment), and others are indicators or outcomes of eating disorders: “diet or eating habits”, “my own behavior” and “my emotional state” (IPQ-R). Not surprisingly, this causal subscale was found to have low internal consistency in a study of eating disorders
perceptions (Stockford et al. 2007). To make the IPQ-R questionnaire more relevant to AN, Quiles (2007) added a subset of eight eating disorder specific causes, such as “media influence” and “need to be perfect.” However, even this improved version is still a standardized fixed response questionnaire and would not allow me to understand the meanings and consequences of these causes for respondents, much less discover
unanticipated themes. Standardization of questions would threaten validity at this exploratory stage (see Schaeffer and Maynard 2003 for a discussion of standardization).
The order of questions asked in the interview guides was flexible, with one exception (see Appendix for interview guide). If a respondent spontaneously brought up genetics before I asked about it, I asked general, non-directive probes, rather than following up with questions about genetics that appear later in the guide. These later questions would have introduced concepts of genetic causality that might have affected their answers about other, non-genetic topics. A few respondents knew ahead of time that there would be questions about genetics. At least one inpatient reported having heard about the interview from other inpatients who had already participated, and one recovered person did as well. For most interviews, I asked questions in the order of the interview guide (see Appendix).
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The guide was flexible in the wording of questions to adjust to what respondents told me. As Charmaz has written, “Questions must both explore the interviewer’s topic and fit the participant’s experience” (2003: 315). In interviews, I was sensitive to the respondent’s own view of her eating disorder and avoided imposing a different view through my vocabulary. Before the interviews, I was concerned that some respondents might object to the term “eating disorder”, but this did not happen. With all respondents, I tried to elicit their perspectives and avoid terminology that could influence their answers or reduce rapport.
My interviewing technique was not as flexible as some other qualitative approaches. If qualitative and quantitative methods are on a continuum, my approach was toward the structured, quantitative end. Because my analysis (described below) involved a direct comparison of respondents’ answers to specific questions, I was less inclined toward flexibility than some qualitative researchers. I wanted everyone to answer most of the questions, except for probes designed only to fill out an incomplete answer. In addition, because this project was primarily about the meanings of genetic explanations for behavior, I introduced these concepts in a later part of the interview even if they were not already part of the respondents’ consciousness.
The interview was in eight parts. The following description of the interview guide is based on the guide for currently diagnosed patients; the version for recovered people is in the past tense. (The interview guide submitted with the dissertation proposal was shortened to generate an average interview of about an hour and a half.)
(1) Background questions. To begin the interview, I asked respondents easy-to- answer questions about their age, education, etc. I confirmed with the respondent her
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were short-answer questions and ran the risk of “training” the respondent to give short answers to future open-ended questions, they were useful for establishing rapport at the start of the interview. In subsequent sections the wording of questions and the use of probes let the respondent know that longer answers were preferred.
(2) Personal experiences with eating disorders, with attention to causality. This section began with very general questions asking the respondent for her thoughts about what AN (or BN) is, and how it began for her.7 I was as non-directive as possible in eliciting this history in order to get at the respondent’s own narrative of illness.8 These general questions also helped the respondent start talking about her experience in general terms and provided jumping-off points for questions about causality. I asked respondents what they thought were causal factors, risk factors, or contributing factors, and why the eating disorder started
when it did.9 I asked if she thought she had been at risk for an eating disorder compared to other people she knew; previous research on genetic causality suggests that this framing of
7 I found this to be a better opening than two alternative strategies, one that was too broad – “tell me about your
eating disorder” – and the other that seemed at odds with most respondents’ experience – “how do you talk about your eating disorder to other people.” Many avoided talking about it with others, as might be expected with a psychiatric diagnosis. Because the reasons why a person might want to hide their disorder are relevant to the stigma and conceptualization of eating disorders, I worked this question in when it felt more comfortable to do so.
8 Narratives are “interpretive devices, through which people represent themselves, both to themselves and to
others” (Lawler 2002: 242). Many of my research questions implicitly involve narratives because they are about causes and how they influence outcomes. Eliciting a narrative early in the interview, before any specific questions about cause, enabled me to minimize my influence on the narrative created. Despite such efforts, patients being interviewed are giving accounts of their own behavior for particular audiences (including the interviewer) and may be motivated to talk about some things and hide others. Their sense of what is a socially desirable and convincing account was likely influenced by their impressions of me.
9 These two questions are adapted from Arthur Kleinman’s questions for uncovering explanatory models
(1980). Several of these questions assume that respondents would agree they have a problem, which may not be the case for people with AN. I do not claim that these questions necessarily uncover explanatory models because respondent answers are also a way of accounting for themselves in a particular interview situation (Scott and Lyman 1968, Estroff et al. 1991, Young 1982, Groleau et al. 2006), and/or “constitute an imaginative attempt to find a legitimate and meaningful place for [the disorder or disease] in their lives” (Lawton 2003, describing Williams 1984). I have adapted the original questions to make sense for eating disorders and to encourage respondents to think not only about cause but also risk factors, which are important in
conceptualizing genetic causality and may not be elicited with standard questions about cause (French et al. 2005).
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the question is more likely to elicit ideas about genetics than exclusively causal language (French et al. 2005). To get at causality in yet more ways, I asked whether the eating disorder could have been prevented, and whether there are things that make the eating disorder worse or reoccur. I did not introduce specific contributing factors (e.g., genetics, gender) until later in the interview. During this part of the interview, I elicited the broad outlines of the respondent’s experience with treatment, the number of times she had been hospitalized (if any), and information for calculating the lowest BMI for respondents with a history of AN.
(3) Perceptions of eating disorders In this section, I elicited the respondent’s
perceptions of eating disorders as well as her sense of others’ perceptions of eating disorders. Because the respondent may not have had a medicalized understanding of her condition, I asked how she felt about having had an eating disorder, and (later in the section) whether and how eating disorders had been a problem for her. A question on preferred terminology was included but yielded little because respondents were comfortable with the official
classifications (e.g., “anorexia”). To get at self-presentation, I asked how she tended to explain it to others when she had to, and if she preferred not to, why. I inquired about others’ reactions, including unwanted reactions, wrong ideas and stereotypes about eating disorders. I asked how she would ideally want people to understand eating disorders.
(4) Reactions to specific ideas about eating disorders Here I asked respondents to react to seven different ways of viewing eating disorders. The respondent was told that some options might seem obviously true or false and her honest reaction was requested. I asked, “How do you react to the idea of [AN/BN] as a...” and inserted the following terms one at a time: psychological problem, mental illness, brain disease, physical illness, choice, lifestyle,
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and problem with our society or culture. I probed their reactions to mental illness, brain disease, and choice in particular, to find out what aspects of the eating disorder made these terms appropriate or not. I then inquired about whether there were other ways of thinking about eating disorders that seemed accurate and followed up about models they had
mentioned that were not among the seven (such as addiction). I asked how they themselves preferred to think of eating disorders and whether their views had changed over time. Last, I asked those with a diagnosis of AN if they saw BN any differently, and vice versa.
(5) Specific causes. This set of questions focused on specific causally relevant areas that respondents may not have mentioned before: gender, biology, and genetics. I began by surfacing any remaining ideas about causality before introducing specific ideas, by asking if there were any other important causal factors, even if they were not personally relevant. I asked, “are some kinds of people more likely to develop eating disorders than others?” and, “are there some situations, settings, and environments that make people more likely to develop eating disorders?” Following this, I asked for more of their ideas about social and cultural causes, introduced already as one of the seven models of eating disorders, and asked specifically why more women and girls develop eating disorders compared to men and boys.
Before asking about genetics directly, I told the respondent, “Some say there are biological causes, where something in your body or brain could make you more likely to have [AN/BN],” and asked what they had heard. This question was designed to bring to the surface any thoughts about genetics before asking the same question again, this time
specifying “genetic causes, where something about your genes could make you more likely to have [AN/BN]”. I asked for their reaction to this idea, probing for negative or positive emotional reactions, and how plausible or relevant it seemed. I explained that I had several
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more questions about genetics and reassured them that I did not expect them to know correct answers but was interested in their best guesses about how genes might be involved in eating disorders. Would everyone with those genes develop [AN/BN]? Does everyone with the disorder have those genes? What makes more sense, genes for [AN/BN] specifically, or genes for something more general that influences it? What would the more general thing be? I also asked for their reactions to the idea that genes could affect one’s temperament or personality, making [AN/BN] more likely. All questions about genetics as a causal factor were framed as hypothetical and under investigation in order to minimize geneticization of eating disorders by my research (Brunger & Cox 2000, as cited by Cox & Starzomski 2004).
(6) Hypothetical scenario 1: Media campaign. To elicit ideas about the implications of genetic conceptions, I asked respondents to imagine there were a media campaign to promote the idea that genetics play some role in the development of eating disorders. I said that this might involve posters saying “Genes matter for eating disorders” and asked what the reaction might be. I probed about possible good or bad effects for people with AN or BN.
(7) Hypothetical scenario 2: Test for genetic predisposition. In this section I focused on the complex model of genetic causality, in which genes predispose a person to eating disorders. This section came last, after I had already explored fully the respondent’s ideas about genetic causation with minimal influence from me. This section enabled exploration of the meaning and implications of genetic susceptibility or genetic risk factors. In order to make the conversation less abstract, I asked respondents to imagine that there were a test to assess their genetic predisposition, and consider whether they would want it.10 In the
10
A flaw of this question is that it does not accommodate an important lay theory of genetic causality in eating disorders, namely that genetics may predispose them to a broad range of disorders, of which AN and BN are only one possibility. Asking them about a predictive test for AN or BN would suggest genes that are specifically linked to one of these disorders. Thus, while the question had been designed to get at complex
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preamble I provided explicit information to discourage a deterministic view: “Because both genes and environment play a role, it is not likely that a genetic test could ever predict whether a person will develop an eating disorder. There is no test at this time. But for a moment let’s say you could get a genetic to find out if your genes made you more likely to develop [AN/BN]. Would you want to know?” They were then asked if they would prefer to find out they did or did not have a genetic predisposition. I then asked them to imagine that they found out they had been at a high genetic risk for an eating disorder and how this would change their and others’ views on eating disorders, including causes, treatment, recovery, and genetic family members, and responsibility.
(8) Closing questions To conclude the interview with a general question that was still relevant to interview themes, I asked, “If you were giving advice to someone with [AN/BN] about how to think about it, what advice would you give?” I followed by asking what kind of research they would be interested in learning about and what advice they might have for treatment providers. I concluded with a few questions to assess the interview questions and how they felt about the interview.
After every interview, I administered the EDE-Q questionnaire to assess eating disorder symptoms.11 In sociology, the self-report of diagnosis by a healthcare provider would be sufficient to describe my sample, but to make my research potentially useful to psychologists and other clinicians, I provided objective information about eating disorder symptoms of both currently diagnosed and recovered people (Bulik 2008, personal communication). I chose the self-report paper version rather than the in-person interview
causality by focusing on the probabilistic nature of genetic influence, it inadvertently channeled genetic causality into a narrow “gene for” model, albeit probabilistic.
11 This questionnaire was originally included as an appendix but removed because making it publically available
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version (Cooper and Fairburn 1987) because stigmatized behavior tends to be more accurately reported when the mode of data collection distances the interviewer and respondent (Lyberg and Kasprzyk 2004 [1991]). The self-report also enabled me to avoid taking the role of clinician (Kleinman 1980). Because the questionnaire reflects a
medicalized view of eating disorders that could influence respondent answers, I administered it after the interview was over. Several respondents ran out of time at the interview,
completed it apart from me, and returned it to me later by mail. I informed respondents that they could skip any uncomfortable questions in the in-person interview and questionnaire. In a study comparing the EDE (Eating Disorder Examination) administered by a clinician with the self-administered EDE-Q questionnaire, the self-administered version had higher reports of binge eating and concerns about shape, though this may be because self-reporters had too expansive a definition of what constituted a binge and loss of control (Fairburn and Beglin 1994). A recent assessment of the EDE-Q found that it had satisfactory internal consistency (Peterson et al. 2007) The EDE-Q has 36 items and takes less than 15 minutes to assess frequency and severity of key eating disorder symptoms. (See Table 2.3 and discussion in the next section for more information.)