Abstract
Background:
The DSM-5 introduced purging disorder as an other specified feeding or eating disorder characterized by recurrent purging in the absence of binge eating. The current study sought to describe the long-term outcome of purging disorder and to examine predictors of outcome.
Methods:
Women (N = 84) who met research criteria for purging disorder completed a comprehensive battery of baseline interview and questionnaire assessments. At an average of 10.24 (3.81) years follow-up, available records indicated all women were living, and over 95% were successfully located (n = 80) while over two-thirds (n = 58) completed follow-up assessments. Eating disorder status, full recovery status, and level of eating pathology were examined as outcomes. Severity and comorbidity indicators were tested as predictors of outcome.
Results:
Although women experienced a clinically significant reduction in global eating pathology, 58% continued to meet criteria for a DSM-5 eating disorder at follow-up. Only 30% met established criteria for full recovery. Women reported significant decreases in purging frequency, weight and shape concerns, and cognitive restraint, but did not report significant decreases in depressive and anxiety symptoms. Quality of life was impaired in the physical, psychological, and social domains. More severe weight and shape concerns at baseline predicted meeting criteria for an eating disorder at follow-up. Other baseline severity indicators and comorbidity did not predict outcome.
Conclusions:
Results highlight the severity and chronicity of purging disorder as a clinically significant eating disorder. Future work should examine maintenance factors to better adapt treatments for purging disorder.
Keywords: Purging disorder, eating disorder, outcome, follow-up, other specified feeding or eating disorder
Purging disorder (PD) is an other specified feeding or eating disorder characterized by recurrent purging behaviors (e.g., self-induced vomiting, laxative misuse, diuretic misuse) in the absence of recurrent binge-eating episodes (Keel and Striegel-Moore, 2009; American Psychiatric Association, 2013). Individuals with PD do not meet criteria for anorexia nervosa because their weight is not “significantly low,” and they do not meet criteria for bulimia nervosa because they do not consume “definitely large” amounts of food. PD is associated with clinically significant impairment and distress (Smith, Crowther, & Lavender, 2017), including increased risk for medical complications (Forney, Buchman-Schmitt, Keel, & Frank, 2016), suicidality (Smith et al., 2017), and mortality (Koch, Quadflieg, & Fichter, 2013). In cross-sectional comparisons, PD is distinct from bulimia nervosa on biological and psychological factors linked to binge-eating episodes (Dossat, Bodell, Williams, Eckel, & Keel, 2015; Keel, Haedt, & Edler, 2005; Keel, Wolfe, Liddle, Young, & Jimerson, 2007) while differences from anorexia nervosa have been studied less (Smith et al., 2017). PD has a prevalence comparable to other eating disorders, affecting up to 6% of girls and women in their lifetime (Stice et al., 2013; Glazer et al., 2019). Given its relatively recent introduction to the literature (Keel et al., 2005), little is known about the outcome of PD.
Literature has begun to describe the natural outcome of PD (Keel et al., 2005; Allen et al., 2013; Knoph et al., 2013; Stice et al., 2013; Watson et al., 2013; Allen et al., 2013). Remission rates have ranged from less than 10% at 6-month follow-up (Keel et al., 2005) to almost two-thirds at 5-year follow-up (Allen et al., 2013), with one study reporting 100% remission over a two-year period (Stice et al., 2013). This literature has been limited by small samples (n=17–37) (Keel et al., 2005; Allen et al., 2013; Stice et al., 2013), short duration of follow-up (Keel et al., 2005), inclusion of only pregnant women (Knoph et al., 2013; Watson et al., 2013), and a limited age range (Allen et al., 2013; Stice et al., 2013). These latter two limitations are particularly problematic, as parenthood is associated with decreased symptomatology (von Soest & Wichstrøm, 2008) and the peak age of onset is around 20 (Allen et al., 2013; Stice et al., 2013). The longest duration of follow-up in the literature comes from adults in a tertiary care sample and found that over 40% were remitted at 5-year follow-up (Koch et al., 2013). Despite a growing literature examining the outcome of PD, the long-term outcome associated with PD remains unknown.
The current study sought to describe the long-term outcome of PD in a well-characterized, community-based sample of women. Analyses examined three outcomes: presence of a DSM-5 eating disorder, presence of full recovery (Bardone-Cone et al., 2010), and change on a well-established continuous measure of eating pathology severity. Analyses also described changes in psychopathology and comorbidity. Indicators of severity (i.e., illness duration, purging frequency, weight and shape concerns, loss of control eating frequency) and indicators of comorbidity (i.e., depressive and anxiety symptoms, comorbid mood, anxiety, and substance use disorders) were tested as predictors of outcome.
Methods
Procedure
Women (n=84) from three previous community-based studies (Keel et al., 2018, 2005, 2007) were invited to participate in a follow-up study. Although the aims and specific recruitment criteria of the three parent studies varied, all studies utilized a standard set of diagnostic interviews and questionnaires. Women were invited to participate at follow-up if they met research criteria for PD (Keel and Striegel-Moore, 2009) at baseline. All participants were required to have a BMI ≥ 18.5 kg/m2 and purge at least once per week, on average, in the twelve weeks prior to the baseline interview. At baseline, participants identified as White (84.3%; n=70), Asian or Pacific Islander (7.2%; n=6), African-American/Black (4.8%; n=4), and Hispanic (3.6%; n=3). A minority reported a lifetime history of anorexia nervosa (14.3%; n=12) and binge-eating disorder (1.2%; n=1) at baseline; none reported a lifetime history of bulimia nervosa due to parent study eligibility requirements.
TLO Online Investigative Systems was used to locate participants and confirm that participants were living. Participants were invited to participate by letter, which described the study and included information on how to participate. Participants received up to four additional letters, and women who did not respond were contacted by another means (i.e., telephone, text, or e-mail). Participants were contacted in five waves beginning in October 2014 to increase mean duration of follow-up and minimize differences in duration of follow-up across study cohorts. Data collection ended in December 2017. Initially, participants were offered $25 for the interview and $10 for questionnaires. To increase participation, compensation was increased to $35 for the interview and $15 for questionnaires in August 2015. As another strategy to increase participation, a brief 20-minute version of the interview was offered for $15 compensation to establish eating disorder status at follow-up. All interviews were completed by doctoral students and supervised by the senior author (PKK). All participants provided informed consent prior to participation in follow-up assessments, following procedures approved by the local IRB. The authors assert that all procedures contributing to this work comply with the ethical standards of the relevant national and institutional committees on human experimentation and with the Helsinki Declaration of 1975, as revised in 2008.
Assessments
Eating Disorder Examination (EDE)
The EDE version 12.0 (Cooper & Fairburn, 1987) was administered at baseline to confirm PD diagnosis and at follow-up to determine eating disorder outcomes. The EDE produces a Global score and assesses eating disorder behaviors. The EDE distinguishes between “objective” bulimic episodes, which correspond to DSM-5 binge eating, and “subjective” bulimic episodes, characterized by a sense of loss of control while eating an amount of food that is not large. Baseline frequency of purging, frequency of loss of control eating episodes, and Global EDE score were used as measures of eating severity. At follow-up, the EDE was used to assess behavioral episodes (e.g., purging) over the prior 12 weeks and overall severity. Only diagnostic items were administered to participants who completed the short interview (n=6). Internal consistency for the Global score was good (alpha = .79 at baseline; alpha = .89 at follow-up) and interrater reliability for diagnosis was excellent (Kappa range: .91 to 1.0 at baseline; Kappa = 1.00 at follow-up).
Eating Disorder Examination Questionnaire (EDE-Q)
The EDE-Q is a questionnaire version of the EDE and was administered at follow-up as another means for assessing eating disorder status and severity (Fairburn & Beglin, 1994). The scale produces a Global score (alpha = .94) and four subscales: Restraint (alpha = .90), Eating Concerns (alpha = .86), Shape Concerns (alpha = .94), and Weight Concerns (alpha = .87). EDE-Q subscale scores were used in determining recovery status.
Outcome Definitions
Three outcome definitions were tested: presence of a DSM-5 eating disorder, the presence of full recovery (Bardone-Cone et al., 2010), and the EDE Global score. An eating disorder was rated as present if a participant met DSM-5 criteria for an eating disorder (i.e., anorexia nervosa, bulimia nervosa, binge-eating disorder, purging disorder, or other specified feeding or eating disorder (OSFED)) on the EDE. The minimum behavioral frequency criterion for DSM-5 OSFED was engaging in at least 12 behavioral episodes (e.g., objective or subjective binge-eating, self-induced vomiting, laxative misuse, diuretic misuse, fasting, excessive exercise) over the previous 12 weeks. The definition of full recovery was derived using the definition of Bardone-Cone and colleagues (Bardone-Cone et al., 2010). To be categorized as recovered, participants had to be free of objective binge-eating, self-induced vomiting, laxative misuse, diuretic misuse, and fasting over the prior 12 weeks on the EDE and report EDE-Q scores within one standard deviation of age-based norms (Mond, Hay, Rodgers, & Owen, 2006). The EDE Global score served as the continuous measure of eating pathology severity at follow-up.
Structured Clinical Interview for DSM-IV (SCID)
The SCID-IV (First, Spitzer, Gibbon, & Williams, 1995) assessed lifetime mood, anxiety, and substance use disorders at baseline. Illness duration was calculated using the baseline eating disorders module. At follow-up, the SCID overview assessed demographic and lifetime treatment history information. The SCID was modified for DSM-5 and used to assess current mood and substance use disorders at follow-up. Interrater reliability for diagnosis was excellent for mood and substance use disorders (Kappa = 1) and good for anxiety disorders (Kappa Range = .76 to 1).
Body Mass Index (BMI)
At baseline, participant height and weight were objectively measured with a wall-mounted ruler and digital scale without shoes in light, indoor clothing. At follow-up, participant height and weight were measured through self-report. Self-reported height and weight have acceptable agreement with objective measurement when objective measurement is not feasible (Bowman & DeLucia, 1992). BMI was calculated in kg/m2.
Body Shape Questionnaire (BSQ)
The BSQ (Cooper, Taylor, Cooper, & Fairburn, 1987) assessed the severity of weight and shape concerns. Previous work supports its test-retest reliability and associations with body image assessments (Rosen, Jones, Ramirez, & Waxman, 1996). Internal consistency was excellent at baseline (alpha = .95) and follow-up (alpha = .98).
Three Factor Eating Questionnaire (TFEQ)
The TFEQ’s three subscales (Cognitive Restraint, Disinhibition around Food, and Hunger) (Stunkard & Messick, 1985) were administered to characterize eating pathology. Internal consistencies at baseline and follow-up were good (Restraint alpha = .86 and .89; Disinhibition alpha = .79 and .86; Hunger alpha = .84 and .80).
Beck Depression Inventory (BDI)
The BDI (Beck, Ward, Mendelson, Mock, & Erbaugh, 1961) assessed depressive symptoms. Previous work supports the test-retest reliability and concurrent validity with other depression assessments (Beck, Steer, & Carbin, 1988). Internal consistency was good at baseline (alpha = .89). The Beck Depression Inventory-II (Beck, Steer, & Brown, 1996) was used in place of the original BDI at follow-up. The internal consistency was excellent (alpha = .93).
State Trait Anxiety Inventory (STAI)
The State and Trait subscales from the STAI (Speilberger, Gorusch, Lushene, Vagg, & Jacobs, 1983) assessed current anxiety symptoms. Previous work supports the STAI’s test-retest reliability (Keel et al., 2007). Internal consistency was excellent at baseline and follow-up for State (alpha = .93 and .96) and Trait (alpha = .91 and .94) subscales.
World Health Organization Quality of Life-BREF (WHOQoL-BREF)
The WHOQoL-BREF is a 26-item version of the WHOQoL (The WHOQoL Group, 1998) that assesses quality of life in four domains. It was administered only at follow-up. Internal consistency was good (alpha range = .82 to .85).
Clinical Impairment Assessment (CIA)
The CIA was administered at follow-up to assess impairment due to eating pathology over the past 28 days (Bohn et al., 2008). The scale has good test-retest reliability and is associated with clinician impairment ratings (Bohn et al., 2008). Internal consistency was excellent (alpha = .96).
Analytic Strategy
To understand if attrition was biased, those who participated were compared to those who did not participate for any reason (e.g., declined, unable to locate).
Posited predictors of outcome, baseline EDE Global scores, and duration of follow-up were standardized for analyses. Missing data needed for inferential statistics were multiply imputed 40 times using the package ‘mice’ in R (van Buuren, 2019). Data were imputed for the following baseline variables: STAI (State (n=1/84) and Trait (n=2/84)), duration of illness (n=5/84), and lifetime substance use disorders (n=2/84). Data were imputed for the following variables at follow-up: WHOQoL-BREF (n=30/84), EDE (n=35/84) and EDE-Q (n=30/84) Global scores, EDE (n=28/84) and EDE-Q (n=31/84) eating disorder status, full recovery status (n=28/84), purging frequency (n=28/84), current mood (n=37/84) or substance use disorder (n=34/84), CIA (n=31/84), BSQ (n= 30/84), TFEQ (n=31/84), BDI (n=31/84), and STAI (n=31/84). In addition to study variables, baseline age, duration of follow-up, follow-up WHOQol-BREF scores, and follow-up EDE-Q eating disorder status and Global scores were used as covariates in multiple imputation procedures. Baseline lifetime history of anorexia nervosa and lifetime history of treatment at follow-up were used in the imputation of outcome. Because 52% (n=29/56) denied any purging behaviors in the three months prior to follow-up interview, purging frequency was imputed using a zero-inflated negative binominal distribution using the package ‘countimp’ (Kleinke, 2019). Due to problems with model convergence, only baseline purging frequency, BDI, state anxiety, lifetime substance use, and duration of follow-up were used to impute follow-up purging frequency. The pattern of results was largely the same using listwise deletion.1 Missing data were not imputed for demographic information that was not used in inferential statistics including DSM-5 eating disorder diagnosis, parental status, and marital status at follow-up.
Paired t-tests were used to evaluate change in study variables over time using the ‘mi.t.test’ procedure in R (Kohl, 2019). Pooled chi-square tests were used to evaluate if DSM-5 eating disorder or recovery status was associated with comorbidity at follow-up using the ‘micombine.chisquare’ procedure in R (Robitzsch, Grund, & Henke, 2019). Logistic regression tested predictors of follow-up eating disorder and recovery status (van Buuren, 2019), adjusting for duration of follow-up (Keel & Mitchell, 1997). Multiple linear regression analyses tested predictors of follow-up EDE Global scores (van Buuren, 2019), adjusting for baseline EDE Global scores and duration of follow-up. All statistical tests were two-tailed. The alpha level was set at .05 given the descriptive nature of this study.
Results
Participation and Demographics
No deaths were found at follow-up. Over 95% of participants responded to recruitment materials (n=80); of these women, 73% (n=58) participated, reflecting 69% of the total target sample. Fifty-three women completed both an interview and questionnaire assessments, three women completed an interview only, and two women completed questionnaire assessments only. Women participated at a mean (SD) of 10.24 (3.81) years (range = 2.51 – 15.47 years; median = 11.26 years) after baseline.
Participation rates did not vary by parent study (p=.57), baseline recruitment site (p=.18), or race/ethnicity (p=.40). Women who were older at baseline were significantly more likely to participate at follow-up (t(72.59)=3.42, p=.001, d =.66). Participation rates were not associated with baseline EDE Global scores (p=.68) or posited predictors of outcome (p’s≥.09).
Among those who completed a follow-up interview (n=56), participants had a mean (SD) age of 34.05 (8.22) years (range: 22 – 54 years). Their mean self-reported BMI was in the normal range (M(SD)=23.27(3.47)), with none in the underweight range, 21.4% in the overweight range (n=12/56), and 3.6% in the obese range (n=2/56). Participants were 85.7% White (n=48/56), 7.1% Asian or Pacific Islander (n=4/56), 5.4% African American/Black (n=3/56), and 1.8% identified as more than one race (n=1/56). Additionally, 3.6% identified as Hispanic (n=2/56). Approximately half were married or living with a partner (53.6%; n=30/56) and approximately half had children (47.3%; n=26/55). The majority had a post-secondary degree (85.2%; n=46/54). One woman reported being unable to work and receiving government assistance (1.9%). Three-quarters (74.5%; n=41/55) reported a lifetime history of mental health treatment, and 36.0% (n=18/50) were receiving mental health treatment at follow-up.
Outcome
At follow-up, 57.6% (pooled n=48.4/84) met DSM-5 criteria for an eating disorder and 29.5% (pooled n=24.8/84) were fully recovered. Women with a DSM-5 eating disorder at follow-up reported significantly greater eating disorder-related impairment compared to women without an eating disorder (t(51.15)=3.16¸ p=.003, d =.64) and those fully recovered reported less impairment at the level of significance (t(23.8)=−2.06, p=.05, d =.51). Lifetime mental health treatment was not associated with outcome (DSM-5 eating disorder OR=0.99, p=.98; Recovery OR=1.55, p=.60; Global EDE t(31.04)=0.37, p=.72, d =.08). Similarly, a baseline history of anorexia nervosa was not associated with outcome (DSM-5 eating disorder OR=1.09, p=.92; Recovery OR=4.83, p=.10; Global EDE estimate=−.34, p=.56). For those with DSM-5 diagnoses at follow-up (n=35/56 who completed interviews), diagnoses were PD (28.6%; n=10/35), bulimia nervosa (11.4%; n=4/35), and OSFED (60.0%; n=21/35). None of the women met criteria for anorexia nervosa or binge-eating disorder at follow-up. Among those with OSFED, the modal presentation was recurrent non-purging compensatory behaviors with or without subjective binge-eating episodes (52.4%; n=11/21). Other presentations were as follows: subthreshold bulimia nervosa (19.0%; n=4/21), recurrent subjective binge-eating episodes (14.3%; n=3/21), subthreshold purging disorder (9.5%; n=2/21), and binge-eating disorder without associated features (4.8%; n=1/21). Almost half (43.9%; pooled n=36.9/84) reported purging over the twelve weeks prior to interview.
Approximately a quarter of women met criteria for a current mood disorder (Pooled Estimate=26.5%; n=22.3/84) and approximately a quarter met criteria for a substance use disorder (Pooled Estimate=28.0%; n=23.5/84) at follow-up. Meeting criteria for a mood disorder at follow-up was not associated with eating disorder status (F(1,177.41)=1.19, p=.28) or recovery status (F(1,226.2)=0.47, p=.49), nor was meeting criteria for a mood disorder associated with EDE Global scores (t(12.96)=1.27, p=.23). The pattern of results was the same for current substance use disorders (F(1,239.62)=1.81, p=.18; F(1,1036.32)=.16, p=.69; t(16.58)=0.90, p=.38).
Table 1 displays descriptive variables at baseline and follow-up. Women reported significant decreases in eating pathology, purging frequency, severity of weight and shape concerns, and cognitive restraint from baseline to follow-up (p’s≤.001). They did not report statistically significant decreases in disinhibition, hunger, depressive symptoms, state anxiety, or trait anxiety (p’s≥.06). BMI demonstrated a small increase over follow-up that did not reach statistical significance (p=.09). Relative to norms for women aged 30–39 (Hawthorne, Herrman, & Murphy, 2006), women with a history of PD had significantly impaired quality of life in the physical (M(SD)=75.30(18.26), t(55.45)=−2.51, p=.02, d=−.31), psychological (M(SD) = 62.20(19.18), t(53.58)=−5.45, p<.001, d=−.71), and social (M(SD) = 66.82(28.98), t(50.24)=−2.52, p=.01, d=−.32) domains at follow-up. Quality of life was not significantly impaired in the environmental domain (M(SD) = 76.69(19.59), t(55.58)=1.54, p=.13, d=.20).
Table 1.
Changes in eating disorder and psychopathology variables across naturalistic follow-up women with purging disorder
Baseline (n=84) | Follow-Up | t | Cohen’s d | |
---|---|---|---|---|
EDE Global | 3.44(0.89) | 2.08(1.41) | −6.24* | −0.90 |
Purging Frequency | 5.61(4.14) | 1.44(3.72) | −6.73* | −0.78 |
Body Shape Questionnaire | 133.46(27.00) | 109.14(46.60) | −3.71* | −0.52 |
TFEQ Restraint | 16.52(4.19) | 13.20(5.32) | −4.59* | −0.61 |
TFEQ Disinhibition | 8.10(3.76) | 7.24(4.20) | −1.51 | −0.19 |
TFEQ Hunger | 6.31(3.80) | 5.26(3.50) | −1.95 | −0.27 |
Body Mass Index | 22.49(1.82) | 23.22(3.51) | 1.75 | 0.24 |
Beck Depression Inventory | 11.28(8.28) | 12.34(9.50) | 0.75 | 0.10 |
State Anxiety | 39.99(11.45) | 38.75(13.12) | −0.59 | −0.08 |
Trait Anxiety | 44.56(10.66) | 43.71(12.09) | −0.48 | −0.06 |
Note: Values represent pooled estimates from multiple imputation analyses; EDE = Eating Disorder Examination; TFEQ = Three Factor Eating Questionnaire.
p< .001;
Table 2 displays parameter estimates from models testing predictors of outcome. More severe weight and shape concerns at baseline predicted a greater likelihood of a DSM-5 eating disorder diagnosis at follow-up, adjusting for duration of follow-up (p=.03). Other baseline severity indicators including illness duration (p=.60), purging frequency (p=.84), and loss of control eating frequency (p=.51) did not predict the presence of an eating disorder, adjusting for duration of follow-up. None of the severity indicators predicted recovery (p’s ≥ .07). Similarly, none of the severity indicators predicted EDE Global scores at follow-up (p’s≥.44).
Table 2.
Pooled logistic and multiple regression models testing predictors of eating disorder outcome and level of eating pathology at long-term follow-up in purging disorder
Predicting DSM-5 Eating Disorder Presence | Predicting Full Recovery | Predicting Level of Eating Pathology | ||||||||
---|---|---|---|---|---|---|---|---|---|---|
Intercept | Duration of Follow-up OR | Predictor OR |
Intercept | Duration of Follow-up OR | Predictor OR |
Intercept | Duration of Follow-up Beta | Baseline EDE Global Score Beta | Predictor Beta |
|
Severity Indicators (n=84) | ||||||||||
Illness Duration | 1.42 | 0.55 | 0.87 | 0.38** | 2.02 | 0.95 | 2.08*** | −0.25 | 0.31 | 0.04 |
Purging Frequency | 1.42 | 0.52* | 1.06 | 0.37** | 2.00 | 1.01 | 2.08*** | −0.24 | 0.31 | 0.15 |
Body Shape Questionnaire | 1.46 | 0.50* | 2.23* | 0.35** | 2.04 | .53 | 2.08*** | −0.23 | 0.27 | 0.06 |
Loss of control eating frequency | 1.42 | 0.47* | 1.26 | 0.37** | 2.14 | 0.87 | 2.08*** | −0.27 | 0.31 | 0.07 |
Comorbidity Measures (n=84) | ||||||||||
Beck Depression Inventory | 1.42 | 0.52* | 1.38 | 0.37** | 1.98 | 0.76 | 2.08*** | −0.27 | 0.41 | −0.25 |
State Anxiety | 1.43 | 0.52* | 1.30 | 0.36** | 2.02 | 0.74 | 2.08*** | −0.27 | 0.39 | −0.27 |
Lifetime Mood Disorder | 0.84 | 0.47* | 2.34 | 0.56 | 2.16* | 0.51 | 2.16*** | −0.23 | 0.34 | −0.14 |
Lifetime Anxiety Disorder | 1.44 | 0.53* | .96 | 0.38* | 2.00 | 1.00 | 2.06*** | −0.25 | 0.31 | 0.04 |
Lifetime Substance Use Disorder | 1.49 | 0.52* | 0.92 | 0.62 | 2.08 | 0.38 | 2.10*** | −0.24 | 0.32 | −0.04 |
Note: OR = Odds Ratio; EDE = Eating Disorder Examination;
p<.05;
p<.01;
p< .001;
Baseline measures of comorbidity, including depressive symptoms (p=.28), state anxiety (p=.36), lifetime mood disorders (p=.16), lifetime anxiety disorders (p=.94), and lifetime substance use disorders (p=.88), were not significantly associated with the presence of an eating disorder at follow-up. Similarly, these variables did not predict recovery (p’s≥.17), nor did these variables predict EDE Global scores at follow-up (p’s≥.20).
Discussion
The current study represents the first long-term, prospective follow-up of the natural outcome of PD. Available records indicated that all participants were living at follow-up, and over 95% were successfully located. A majority of those sought participated, and there was minimal evidence of biased participation. Results suggest PD exhibits a chronic course, with most women meeting criteria for a DSM-5 eating disorder at follow-up. More severe weight and shape concerns predicted a greater likelihood of having an eating disorder at follow-up. Approximately 30% of women were fully recovered from their eating disorder. However, no variables predicted recovery status or the continuous measure of outcome.
No deaths were observed in this study, in contrast to findings suggesting elevated mortality in PD (Koch et al., 2013). This may reflect severity differences in study populations, as the current study drew from the community whereas Koch and colleagues studied individuals receiving specialized inpatient eating disorder treatment. In addition, participants recruited for two of the studies were required to be free of medical conditions or treatment that might influence weight or appetite, which may have resulted in a somewhat healthier sample. More follow-up studies of PD are needed to understand if the disorder is associated with elevated mortality, as evidence for elevated mortality for other eating disorders, such as bulimia nervosa, did not emerge until larger studies and meta-analysis were undertaken (Arcelus, Mitchell, Wales, & Nielsen, 2011; Crow et al., 2009). Given the negative consequences associated with purging behaviors (Forney et al., 2016) and poor physical quality of life reported in this sample, medical monitoring of this population is recommended.
Although women reported a clinically meaningful decrease in eating pathology, less than half were free from an eating disorder at follow-up and less than 30% were fully recovered. Over twice as many women with baseline PD met criteria for PD than for bulimia nervosa at follow-up, consistent with epidemiological data (Glazer et al., 2019), and none met criteria for anorexia nervosa or binge-eating disorder. Most women met criteria for OSFED, transitioning from purging behaviors to non-purging compensatory behaviors that may be more socially acceptable (i.e., excessive exercise, fasting). These results provide evidence that some women with PD exhibit diagnostic stability, while others exhibit changes in symptom presentation, consistent with findings from a 5-year follow-up of a tertiary care sample of PD (Koch et al., 2013) and other eating disorder diagnoses (Eddy et al., 2010). More frequent follow-ups with comparisons to other eating disorders are needed to better understand if PD represents a unique illness presentation or is a stage of binge/purge-related eating disorders more broadly. Taken together, results reinforce the clinical significance of PD. Indeed, women reported diminished quality of life in the physical, psychological, and social domains, and three-quarters of participants had sought mental health treatment in their lifetime.
Significant improvements in eating pathology were observed for purging frequency, weight and shape concerns, and cognitive restraint. In contrast, women did not report statistically significant decreases in disinhibition and hunger. At baseline, disinhibition and hunger in PD fell between that of non-eating disordered controls and women with bulimia nervosa (Keel et al., 2018, 2005, 2007). If loss of control eating is less elevated for PD than other features of eating pathology, the lack of improvement may reflect a somewhat restricted range on this feature. Indeed, effect sizes compared to non-eating disordered controls at baseline were larger for weight and shape concerns (d = 4.17) and restraint (d = 3.90) relative to disinhibition around food (d = 1.71) and hunger (d = 0.94) (Keel et al., 2018, 2005, 2007).
Lifetime mental health treatment was not associated with any outcome measure. This may reflect limited sensitivity in the assessment of lifetime mental health treatment. In particular, the current study did not systematically assess for eating disorder treatment. It is possible that some participants sought mental health treatment for comorbid conditions and did not disclose their eating disorder to their providers. Alternately, existing treatments may not have been effective in addressing their symptoms, given some evidence from that cognitive-behavioral therapy may be more successful for those who experience binge-eating episodes (Waller et al., 2014). More systematic work is needed to evaluate appropriate treatments for PD.
There were no meaningful changes in depressive and anxiety symptoms over follow-up, and rates of current mood and substance use disorders were not associated with follow-up eating pathology. This contrasts with findings that comorbidity is associated with poor outcome in other eating disorders (Löwe et al., 2001; Bardone-Cone et al., 2010). Although a subset of the current sample comes from a study that excluded participants based on the presence of a current mood or substance use disorder (Keel et al., 2018), the pattern of results remained the same when those participants were excluded from analyses. This lack of association requires additional investigation, as meeting criteria for a current mood disorder was associated with worse outcome using listwise deletion in the full sample.
Greater weight and shape concerns predicted a greater likelihood of continuing to have a DSM-5 eating disorder at follow-up. This finding reinforces transdiagnostic eating disorder conceptualizations that emphasize weight and shape concerns as the central feature (Fairburn et al., 2009). No other baseline variables significantly predicted outcome in PD. The current study failed to replicate findings that depressive symptoms predict outcome (Koch et al., 2013), perhaps due to differences in sample severity. Contrary to prior work (Eddy et al., 2007), a history of anorexia nervosa was not associated with outcome. This likely reflects changes in recruitment criteria across parent studies. In the most recent parent study, participants were excluded based on a history of anorexia nervosa (Keel et al., 2018). Thus, a history of lifetime anorexia nervosa was confounded with duration of follow-up in this sample (OR = 3.27, p = .02). Null findings also may reflect the length of follow-up, as duration of follow-up is a potent predictor of outcome (Keel & Mitchell, 1997) and explained significant variance in eating disorder status (OR = 0.84, p = .04). Posited predictors of outcome were drawn from work on other eating disorders (Fichter, Quadflieg, & Hedlund, 2006; Helverskov et al., 2010; Keel, Mitchell, Miller, Davis, & Crow, 1999; Keski-Rahkonen et al., 2014; Koch et al., 2013) that may not extend to PD. The original studies in which women participated provided some evidence of unique disruptions in satiety in PD (Keel et al., 2018); however, the number of participants was too small to permit adequately powered analyses of whether these disruptions predicted outcome. Future work using machine learning approaches in larger samples may be valuable in generating hypotheses about additional predictors of outcome.
This study benefited from a high ascertainment rate, assessments with strong psychometric properties, a well-characterized sample, and high interrater reliability. Comparisons of baseline data do not suggest biased responding, and multiple imputation attenuated effects of missing data. The two-wave design prohibits an examination of course, short-term predictors of course, and the description of more frequent or fluid changes in course such as patterns of remission, cross-over, and relapse. Given the female sample, results may not generalize to males with PD. Variability in duration of follow-up and differences in recruitment criteria of the baseline studies may have limited power to find significant predictors of outcome. Finally, this study did not assess for eating disorder-focused treatment, and its naturalistic design precludes evaluation of possible treatment effects.
The current study represents the first to prospectively assess the long-term outcome of PD in a community-based sample. The low recovery rates and continued evidence of impairment reinforce the clinical significance of the syndrome even among those drawn from the community. More work is needed to answer questions about mortality, medical morbidity, and the role of comorbidity in predicting prognosis given findings from patients drawn from an inpatient treatment setting (Koch et al., 2013). Evidence that weight and shape concerns predicted likelihood of a DSM-5 eating disorder suggest that transdiagnostic cognitive-behavioral therapy for eating disorders may be well-suited for treating PD, consistent with findings from its application in samples that have included patients with PD (Fairburn et al., 2009). However, studies with multiple, short duration follow-ups are needed to better identify eating-disorder specific and transdiagnostic maintenance factors in order to adapt or develop empirically supported treatments for this population.
Acknowledgements:
This research was supported by National Institute of Mental Health (K.J.F. F31-MH105082), (P.K.K. R01-MH61836), (P.K.K. R01-MH111263) (P.K.K. R03-MH61320). Additional financial support came from the American Psychological Association Dissertation Research Award (K.J.F.), the Florida State University Dissertation Research Award (K.J.F.), the American Psychological Foundation/COGDOP Graduate Research Scholarship (K.J.F.), and Experiment.com crowdfunding (K.J.F.; doi: 10.18258/3354)
Footnotes
Previous presentation: Portions of this work were presented at the annual meeting of the Eating Disorders Research Society in New York, NY, October 27–29, 2016, at the International Conference on Eating Disorders in San Francisco, May 5–7, 2016, the International Conference on Eating Disorders, Prague, Czech Republic, June 8–10, 2017, and the International Conference on Eating Disorders, New York, NY, March 14 –16, 2019.
Disclosures: Pamela Keel receives royalties from Oxford University Press. Ross Crosby is a paid statistical consultant for Health Outcomes Solutions, Winter Park, Florida.
Using listwise deletion, the fully recovered group reported significantly lower CIA scores (t(50.79)=−6.87, p<.001). Having a mood disorder at follow-up was associated with a greater likelihood of having a DSM-5 eating disorder (Likelihood Ratio=5.19, p=.02) and higher EDE Global scores (t(41)=−2.71, p=.01).
References
- Allen KL, Byrne SM, Oddy WH, & Crosby RD (2013). Early onset binge eating and purging eating disorders: Course and outcome in a population-based study of adolescents. Journal of Abnormal Child Psychology, 41(7), 1083–1096. 10.1007/s10802-013-9747-7 [DOI] [PubMed] [Google Scholar]
- American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing. [Google Scholar]
- Arcelus J, Mitchell AJ, Wales J, & Nielsen S (2011). Mortality rates in patients with anorexia nervosa and other eating disorders: A meta-analysis of 36 studies. Archives of General Psychiatry, 68(7), 724–731. 10.1001/archgenpsychiatry.2011.74 [DOI] [PubMed] [Google Scholar]
- Bardone-Cone AM, Harney MB, Maldonado CR, Lawson MA, Robinson DP, Smith R, & Tosh A (2010). Defining recovery from an eating disorder: Conceptualization, validation, and examination of psychosocial functioning and psychiatric comorbidity. Behaviour Research and Therapy, 48(3), 194–202. 10.1016/j.brat.2009.11.001 [DOI] [PMC free article] [PubMed] [Google Scholar]
- Beck AT, Steer RA, & Brown GK (1996). Manual for the Beck Depression Inevntory-II. Retrieved from https://blog.naver.com/mistyeyed73/220427762670
- Beck AT, Steer RA, & Carbin MG (1988). Psychometric properties of the Beck Depression Inventory: Twenty-five years of evaluation. Clinical Psychology Review, 8(1), 77–100. 10.1016/0272-7358(88)90050-5 [DOI] [Google Scholar]
- Beck AT, Ward CH, Mendelson M, Mock J, & Erbaugh J (1961). An inventory for measuring depression. Archives of General Psychiatry, 4(6), 561–571. 10.1001/archpsyc.1961.01710120031004 [DOI] [PubMed] [Google Scholar]
- Bohn K, Doll HA, Cooper Z, O’Connor M, Palmer RL, & Fairburn CG (2008). The measurement of impairment due to eating disorder psychopathology. Behaviour Research and Therapy, 46(10), 1105–1110. 10.1016/j.brat.2008.06.012 [DOI] [PMC free article] [PubMed] [Google Scholar]
- Bowman RL, & DeLucia JL (1992). Accuracy of self-reported weight: A meta-analysis. Behavior Therapy, 23(4), 637–655. 10.1016/S0005-7894(05)80226-6 [DOI] [Google Scholar]
- Cooper PJ, Taylor MJ, Cooper Z, & Fairburn CG (1987). The development and validation of the Body Shape Questionnaire. International Journal of Eating Disorders, 6(4), 485–494. [DOI] [Google Scholar]
- Cooper Z, & Fairburn C (1987). The Eating Disorder Examination: A semi‐structured interview for the assessment of the specific psychopathology of eating disorders. International Journal of Eating Disorders, 6(1), 1–8. [DOI] [Google Scholar]
- Crow SJ, Peterson CB, Swanson SA, Raymond NC, Specker S, Eckert ED, & Mitchell JE (2009). Increased mortality in bulimia nervosa and other eating disorders. American Journal of Psychiatry, 166(12), 1342–1346. 10.1176/appi.ajp.2009.09020247 [DOI] [PubMed] [Google Scholar]
- Dossat AM, Bodell LP, Williams DL, Eckel LA, & Keel PK (2015). Preliminary examination of glucagon-like peptide-1 levels in women with purging disorder and bulimia nervosa. International Journal of Eating Disorders, 48(2), 199–205. 10.1002/eat.22264 [DOI] [PMC free article] [PubMed] [Google Scholar]
- Eddy KT, Dorer DJ, Franko DL, Tahilani K, Thompson‐Brenner H, & Herzog DB (2007). Should bulimia nervosa be subtyped by history of anorexia nervosa? A longitudinal validation. International Journal of Eating Disorders, 40(S3), S67–S71. 10.1002/eat.20422 [DOI] [PubMed] [Google Scholar]
- Eddy KT, Swanson SA, Crosby RD, Franko DL, Engel S, & Herzog DB (2010). How should DSM-V classify eating disorder not otherwise specified (EDNOS) presentations in women with lifetime anorexia or bulimia nervosa? Psychological Medicine, 40(10), 1735–1744. 10.1017/S0033291709992200 [DOI] [PMC free article] [PubMed] [Google Scholar]
- Fairburn CG, & Beglin SJ (1994). Assessment of eating disorders: Interview or self-report questionnaire? International Journal of Eating Disorders, 16(4), 363–370. [DOI] [PubMed] [Google Scholar]
- Fairburn CG, Cooper Z, Doll HA, O’Connor ME, Bohn K, Hawker DM, … Palmer RL (2009). Transdiagnostic cognitive-behavioral therapy for patients with eating disorders: A two-site trial with 60-week follow-up. American Journal of Psychiatry, 166(3), 311–319. 10.1176/appi.ajp.2008.08040608 [DOI] [PMC free article] [PubMed] [Google Scholar]
- Fichter MM, Quadflieg N, & Hedlund S (2006). Twelve-year course and outcome predictors of anorexia nervosa. International Journal of Eating Disorders, 39(2), 87–100. 10.1002/eat.20215 [DOI] [PubMed] [Google Scholar]
- First M, Spitzer RL, Gibbon M, & Williams JBW (1995). Structured Clinical Interview for DSM-IV Axis I Disorders. New York: New York State Psychiatric Institute. [Google Scholar]
- Forney KJ, Buchman-Schmitt JM, Keel PK, & Frank GKW (2016). The medical complications associated with purging. International Journal of Eating Disorders, 49(3), 249–259. 10.1002/eat.22504 [DOI] [PMC free article] [PubMed] [Google Scholar]
- Glazer KB, Sonneville KR, Micali N, Swanson SA, Crosby R, Horton NJ, … Field AE (2019). The course of eating disorders involving bingeing and purging among adolescent girls: Prevalence, stability, and transitions. Journal of Adolescent Health, 64(2), 165–171. 10.1016/j.jadohealth.2018.09.023 [DOI] [PMC free article] [PubMed] [Google Scholar]
- Hawthorne G, Herrman H, & Murphy B (2006). Interpreting the WHOQOL-Bref: Preliminary population norms and effect sizes. Social Indicators Research, 77(1), 37–59. [Google Scholar]
- Helverskov JL, Clausen L, Mors O, Frydenberg M, Thomsen PH, & Rokkedal K (2010). Trans-diagnostic outcome of eating disorders: A 30-month follow-up study of 629 patients. European Eating Disorders Review, 18(6), 453–463. 10.1002/erv.1025 [DOI] [PubMed] [Google Scholar]
- Keel PK, Eckel LA, Hildebrandt BA, Haedt‐Matt AA, Appelbaum J, & Jimerson DC (2018). Disturbance of gut satiety peptide in purging disorder. International Journal of Eating Disorders, 51(1), 53–61. 10.1002/eat.22806 [DOI] [PubMed] [Google Scholar]
- Keel PK, Haedt A, & Edler C (2005). Purging disorder: An ominous variant of bulimia nervosa? International Journal of Eating Disorders, 38(3), 191–199. 10.1002/eat.20179 [DOI] [PubMed] [Google Scholar]
- Keel PK, & Mitchell JE (1997). Outcome in bulimia nervosa. American Journal of Psychiatry, 154(3), 313–321. 10.1176/ajp.154.3.313 [DOI] [PubMed] [Google Scholar]
- Keel PK, Mitchell JE, Miller KB, Davis TL, & Crow SJ (1999). Long-term outcome of bulimia nervosa. Archives of General Psychiatry, 56(1), 63–69. 10.1001/archpsyc.56.1.63 [DOI] [PubMed] [Google Scholar]
- Keel PK, & Striegel‐Moore RH (2009). The validity and clinical utility of purging disorder. International Journal of Eating Disorders, 42(8), 706–719. 10.1002/eat.20718 [DOI] [PubMed] [Google Scholar]
- Keel PK, Wolfe BE, Liddle RA, Young KPD, & Jimerson DC (2007). Clinical features and physiological response to a test meal in purging disorder and bulimia nervosa. Archives of General Psychiatry, 64(9), 1058–1066. 10.1001/archpsyc.64.9.1058 [DOI] [PubMed] [Google Scholar]
- Keski-Rahkonen A, Raevuori A, Bulik CM, Hoek HW, Rissanen A, & Kaprio J (2014). Factors associated with recovery from anorexia nervosa: A population-based study. International Journal of Eating Disorders, 47(2), 117–123. 10.1002/eat.22168 [DOI] [PubMed] [Google Scholar]
- Kleinke K (2019). Package “countimp” (Version 2.0.7) Retrieved from https://github.com/kkleinke/countimp
- Knoph C, Von Holle A, Zerwas S, Torgersen L, Tambs K, Stoltenberg C, … Reichborn-Kjennerud T (2013). Course and predictors of maternal eating disorders in the postpartum period. International Journal of Eating Disorders, 46(4), 355–368. 10.1002/eat.22088 [DOI] [PMC free article] [PubMed] [Google Scholar]
- Koch S, Quadflieg N, & Fichter M (2013). Purging disorder: A comparison to established eating disorders with purging behaviour. European Eating Disorders Review, 21(4), 265–275. 10.1002/erv.2231 [DOI] [PubMed] [Google Scholar]
- Kohl M (2019). Package “MKmisc” (Version 1.6) Retrieved from https://cran.r-project.org/web/packages/MKmisc/MKmisc.pdf
- Löwe B, Zipfel S, Buchholz C, Dupont Y, Reas DL, & Herzog W (2001). Long-term outcome of anorexia nervosa in a prospective 21-year follow-up study. Psychological Medicine, 31(5), 881–890. 10.1017/S003329170100407X [DOI] [PubMed] [Google Scholar]
- Mond JM, Hay PJ, Rodgers B, & Owen C (2006). Eating Disorder Examination Questionnaire (EDE-Q): Norms for young adult women. Behaviour Research and Therapy, 44(1), 53–62. 10.1016/j.brat.2004.12.003 [DOI] [PubMed] [Google Scholar]
- Robitzsch A, Grund S, & Henke T (2019). Package “miceadds” (Version 3.5–14) Retrieved from https://cran.r-project.org/web/packages/miceadds/miceadds.pdf
- Rosen JC, Jones A, Ramirez E, & Waxman S (1996). Body Shape Questionnaire: Studies of validity and reliability. International Journal of Eating Disorders, 20(3), 315–319. [DOI] [PubMed] [Google Scholar]
- Smith KE, Crowther JH, & Lavender JM (2017). A review of purging disorder through meta-analysis. Journal of Abnormal Psychology, 126(5), 565–592. 10.1037/abn0000243 [DOI] [PMC free article] [PubMed] [Google Scholar]
- Speilberger CD, Gorusch RL, Lushene R, Vagg PR, & Jacobs GA (1983). The State-Trait Anxiety Inventory. Palo Alto, CA: Consulting Psychologists Press. [Google Scholar]
- Stice E, Marti CN, & Rhode P (2013). Prevalence, incidence, impairment, and course of the proposed DSM-5 eating disorder diagnoses in an 8-year prospective community study of young women. Journal of Abnormal Psychology, 122(2), 445–457. 10.1037/a0030679 [DOI] [PMC free article] [PubMed] [Google Scholar]
- Stunkard AJ, & Messick S (1985). The Three-Factor Eating Questionnaire to measure dietary restraint, disinhibition and hunger. Journal of Psychosomatic Research, 29(1), 71–83. 10.1016/0022-3999(85)90010-8 [DOI] [PubMed] [Google Scholar]
- The WHOQoL Group, T. W. (1998). Development of the World Health Organization WHOQOL-BREF Quality of Life Assessment. Psychological Medicine, 28(3), 551–558. [DOI] [PubMed] [Google Scholar]
- van Buuren S (2019). Package “mice” (Version 3.6.0) Retrieved from https://cran.r-project.org/web/packages/mice/mice.pdf
- von Soest T, & Wichstrøm L (2008). The impact of becoming a mother on eating problems. International Journal of Eating Disorders, 41(3), 215–223. 10.1002/eat.20493 [DOI] [PubMed] [Google Scholar]
- Waller G, Gray E, Hinrichsen H, Mountford V, Lawson R, & Patient E (2014). Cognitive-behavioral therapy for bulimia nervosa and atypical bulimic nervosa: Effectiveness in clinical settings. International Journal of Eating Disorders, 47(1), 13–17. 10.1002/eat.22181 [DOI] [PubMed] [Google Scholar]
- Watson HJ, Holle AV, Hamer RM, Berg CK, Torgersen L, Magnus P, … Bulik CM (2013). Remission, continuation and incidence of eating disorders during early pregnancy: A validation study in a population-based birth cohort. Psychological Medicine, 43(8), 1723–1734. 10.1017/S0033291712002516 [DOI] [PMC free article] [PubMed] [Google Scholar]