BRIEF REPORT

Stressful Life Events and Binge Eating Disorder Daniela Degortes, Paolo Santonastaso, Tatiana Zanetti, Elena Tenconi, Angela Veronese & Angela Favaro* Department of Neurosciences, University of Padova, Italy

Abstract Although there is evidence about the role played by stressful life events (SE) in the pathogenesis of eating disorders, few studies to date have explored this problem in binge eating disorder (BED). The aim of the present study was to examine SE preceding the onset of BED. A retrospective interview-based design was used to compare 107 patients with BED and 107 patients with bulimia nervosa (BN), matched for duration of illness. Compared with patients with BN, those with BED reported a greater number of traumatic events in the 6 months preceding onset, revealing more often three types of events: bereavement, separation from a family member and accidents. The presence of SE before onset showed a dose–response relationship with the severity of psychopathology at the time of referral for treatment. Study of SE in patients with BED may be important for better understanding of the pathogenetic pathway to this disorder and to provide adequate treatment. Copyright © 2014 John Wiley & Sons, Ltd and Eating Disorders Association. Keywords binge eating disorder; stressful life events; onset; pathogenesis *Correspondence Angela Favaro, MD, PhD, Clinica Psichiatrica, Dipartimento di Neuroscienze Via Giustiniani 3, 35128 Padua, Italy. Email: [email protected] Published online 18 July 2014 in Wiley Online Library (wileyonlinelibrary.com) DOI: 10.1002/erv.2308

Introduction Binge eating disorder (BED) has recently been added to the DSM5 ‘Feeding and eating disorders’ section (American Psychiatric Association, 2013). Although there was a great deal of research on this diagnosis in the last 20 years, research on genetic, environmental and psychosocial factors involved in its development and maintenance is warranted. In particular, the specific role of stressful life events (SE) in the pathogenesis of BED has received little attention in the literature to date. The relationship between stress and eating behaviour is of particular interest, because there is much evidence that the effects of stress on appetite are gender specific (Iwasaki-Sekino, ManoOtagiri, Ohata, Yamauchi, & Shibasaki, 2009). Alterations in appetite regulation due to stress may increase body-related worries and influence the ability to cope with such difficulties (Cattanach, Malley, & Rodin, 1988). However, prospective studies have also demonstrated that symptoms of eating disorders may affect the perception of stress expos ure and even increase exposure to psychological stress in the short term (Rosen, Compas, & Tacy, 1993). Adverse life events were commonly assessed retrospectively and, thus, represent non-specific retrospective correlates of eating disorders (Jacobi, Hayward, de Zwaan, Kraemer, & Agras, 2004), which may play a role as precipitating factors in anorexia nervosa (Rastam & Gillberg, 1992; Horesh et al., 1995; Gowers, North, Byram, & Weaver, 1996; Machado, Goncalves, Martins, Hoek, & Machado, 2014) and bulimia nervosa (BN) (Raffi, Rondini, Grandi, & Fava, 2000; Rojo, Conesa, Bermudez, & Livianos, 2006). Research evidence suggests that specific types of SE appear to precede the onset of various types of eating disorders. The onset of anorexia nervosa is often related to events of both loss such as 378

bereavement and separations from family or significant others (Kalucy, Crisp, & Harding, 1977; Beaumont, Abraham, Argall, George, & Glaun, 1978), problems with sexuality (Schmidt, Tiller, Blanchard, Andrews, & Treasure, 1997) and receiving critical comments about weight, shape or eating (Machado et al., 2014). On the contrary, events more frequently associated with the onset of BN involve social difficulties, such as disruption of family or social relationships or threats to physical safety (Welch, Doll, & Fairburn, 1997), losses and separation from significant others (Lacey, Coker, & Birtchnell, 1986) and health problems (Schmidt, Tiller, & Treasure, 1993). Studies specifically addressing risk factors for BED have found that certain adverse childhood experiences, psychiatric morbidity of parents, childhood obesity and adverse criticism about shape, weight and eating significantly increase the risk of developing BED (Fairburn et al., 1998; Grilo & Masheb, 2001; Striegel-Moore et al., 2005). To our knowledge, only one study has retrospectively examined the role of life events before the onset of BED (Pike et al., 2006). In that study, patients with BED reported a greater number of life events during the year preceding the onset of BED than either the non-psychiatric or psychiatric control groups. In addition, compared with non-psychiatric controls, patients with BED reported a greater number of specific events, such as relocation, bereavement, change in family structure, end of relationships, work-related stress, school or other sources, physical abuse and critical comments about weight, shape or eating. Instead, the differences between patients with BED and the psychiatric controls were less evident. It is of note that, in the field of eating disorders, no study to date has examined the role of SE within a pathoplastic framework. The distinction between a predisposition model and a pathoplastic

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model is important, and both models are of particular interest in describing the mechanisms of onset and severity of psychopathology in psychiatric patients. The predisposition model hypothesises that the role of SE as a risk factor is linked to the presence of other liability factors, such as genetic polymorphisms (e.g. 5HTTLPR) and/or problems in modulation of mood and emotion regulation (Akkermann et al., 2012; Munsch, Meyer, Quartier, & Wilhelm, 2011). In contrast, but not in contradiction with the predisposition model, the pathoplastic model hypothesises a direct role of SE in dysfunctional emotional reactivity and modulation of illness symptomatology and severity (Cromer, Schmidt, & Murphy, 2007). The aim of the present study was to assess retrospectively the frequency and types of SE preceding the onset of the eating disorder in a group of patients with BED compared with a group of patients with BN and to examine the relationship between these events and psychopathological features. Given the high stress reactivity demonstrated by patients with BED (Hilbert, Vögele, Tuschen-Caffier, & Hartmann, 2011), we hypothesised that the importance of SE as precipitating factors in this group of patients is greater than in patients with BN. In addition, we hypothesise a role of SE in increasing the reported psychopathology of patients in both patients with BED and BN.

Methods The subjects of the study were 107 patients with BED, consecutively referred to our Outpatient Eating Disorder Unit in Padova. The frequency and types of SE of patients with BED were

compared with those of a sample of 107 patients diagnosed with BN, matched for duration of illness, in order to avoid bias due to retrospective recall. All the study subjects were assessed with the Eating Disorders section of the Structured Clinical Interview for DSM-IV (American Psychiatric Association, 2000), a semi-structured interview to gather socio-demographic and clinical data, and two self-report questionnaires: the Hopkins Symptom Check List (Derogatis, Lipman, Rickels, Uhlenhuth, & Covi, 1974) to measure psychiatric symptoms and the Eating Disorder Inventory (Garner, Olmstead, & Polivy, 1983) to assess eating psychopathology. The semi-structured interview administered to all patients included a checklist describing 27 SE. Patients were asked to specify if the event occurred within the 6 months preceding the onset of the eating disorder and to score the subjective severity of each event [from 1 (slight) to 5 (catastrophic)]. Investigated life events were subdivided into three main categories: loss events (such as separations, bereavement, miscarriages and changes of home and work), social problems (disagreement with the partner, social problems, family conflicts, beginning of a romantic relationship, and occupational or legal problems) and traumatic events (accidents, physical illness and sexual abuse). Experiences of sexual and physical abuse were assessed both within the 6 months preceding the onset of the eating disorder (precipitating factor, Table 1) and in the lifetime. This assessment was performed using specific items contained in the semi-structured interview, as previously described (Favaro, Dalle Grave, & Santonastaso, 1998; Favaro, Ferrara, & Santonastaso, 2007).

Table 1 Stressful life events occurring within 6 months of onset of BED and BN

End of a romantic relationship Beginning of a romantic relationship Bereavement of a close relative/friend Disagreement with partner Separation of family members Financial difficulties Physical illnesses Accidents Illnesses/injuries of relatives Change of home Family conflicts Change of employment Problems at school High school qualification Occupational problems Social problems Miscarriages/abortion Sexual abuse Pregnancy Marriage Having children Legal problems

BED (n = 107) n (%)

BN (n = 107) n (%)

χ2

p

OR (95% CI)

28 (26.2) 16 (15.0) 28 (26.2) 28 (26.2) 22 (20.6) 28 (26.2) 14 (13.1) 12 (11.2) 13 (12.1) 14 (13.1) 49 (45.8) 12 (11.2) 26 (24.3) 8 (7.5) 8 (7.5) 22 (20.6) 4 (3.7) 5 (4.7) 3 (2.8) 3 (2.8) 1 (0.9) 1 (0.9)

38 (35.5) 12 (11.2) 15 (14.0) 28 (26.2) 8 (7.5) 20 (18.7) 7 (6.5) 2 (1.9) 8 (7.5) 10 (9.3) 60 (56.1) 9 (8.4) 28 (26.2) 13 (12.1) 7 (6.5) 21 (19.6) 3 (2.8) 4 (3.7) 2 (1.9) 1 (0.9) 2 (1.9) 1 (0.9)

2.20 0.66 4.98 0.00 7.86* 1.72 2.63 8.42* 1.33 0.75 2.27 0.48 0.10 1.33 0.07 0.03 0.15 0.12 0.21 1.07 0.34 0.00

0.138 0.417 0.026 1.00 0.005 0.189 0.105 0.004 0.249 0.385 0.132 0.490 0.753 0.249 0.789 0.865 0.700 0.733 0.650 0.302 0.557 1.00

0.6 (0.4–1.2) 1.4 (0.6–3.1) 2.2 (1.1–4.4) 1.0 (0.5–1.8) 3.2 (1.4–7.6) 1.5 (0.8–3.0) 2.2 (0.8–5.6) 6.6 (1.4–30.4) 1.7 (0.7–4.3) 1.5 (0.6–3.4) 0.7 (0.4–1.1) 1.4 (0.6–3.4) 0.9 (0.5–1.7) 0.6 (0.2–1.5) 1.2 (0.4–3.3) 1.1 (0.5–2.1) 1.3 (0.3–6.2) 1.3 (0.3–4.8) 1.5 (0.3–9.2) 3.1 (0.3–29.8) 0.5 (0.04–5.5) 1.0 (0.1–16.2)

Note: BED, binge eating disorder; BN, bulimia nervosa; OR, odds ratio; CI, confirdence interval. *p < 0.02 (threshold of significance according to false discovery rate method).

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Statistical Package for Social Sciences (PASW Statistics 18.0) software was used for statistical analyses. Student’s t-test, one-way analysis of variance and Pearson’s chi-squared test were used to compare independent groups. Cohen’s d and odds ratios were used to measure effect’s size. For Cohen’s d, an effect size of 0.2–0.3 was considered ‘small’, around 0.5 ‘medium’ and more than 0.8 ‘large’. The significance threshold was adjusted to p < 0.02 to control for multiple comparisons, according to the false discovery rate method (Benjamini & Hochberg, 1995).

Results At assessment, patients with BED had higher mean age than patients with BN (31.1 ± 11.1 vs. 25.4 ± 5.6; t = 4.78; p < 0.001), higher age at onset (23.3 ± 10.4 vs. 18.3 ± 4.4; t = 4.54; p < 0.001) and higher body mass index (31.6 ± 6.5 vs. 21.3 ± 3.2; t = 14.67; p < 0.001). As previously noted, the two groups of patients were paired according to duration of illness (70.1 ± 62.6 months in patients with BED and 70.0 ± 62.4 months in patients with BN). Table 1 lists the frequency of SE before onset in the two samples. Patients with BED reported two types of events significantly more often than patients with BN: separation from family members and accidents. Patients with BED also tended more often than patients with BN to report bereavement in the 6 months before onset. No significant differences were found in the average number of total SE (3.7 ± 3.8 vs. 3.2 ± 3.1; t = 1.13; n.s.; Cohen’s d = 0.14). Patients with BED tended to report a greater number of traumatic events than those with BN (0.4 ± 1.0 vs. 0.2 ± 0.6; t = 1.99; p = 0.047; Cohen’s d = 0.24), whereas no differences were found for loss events (1.1 ± 1.3 vs. 0.9 ± 1.1; t = 1.49; Cohen’s d = 0.17)

or social difficulties (2.0 ± 2.1 vs. 2.0 ± 1.9; t = 0.14; Cohen’s d = 0.00). No significant differences between the two groups of patients were found on the overall perceived severity of SE. In order to explore the relationship between SE and psychopathology in the BED group, the sample was subdivided according to number of SE. Table 2 lists the differences between patients with BED without SE before onset, patients with one to three SE and patients with more than three SE. Statistical analysis showed that SE before onset had a dose–response relationship with the severity of eating and general psychopathology. The group with the greatest number of SE before disorder onset also reported a higher frequency of binge eating episodes, although the difference was not statistically significant. No dose–response relationship between number of SE and psychopathology was found in the BN group, with the exception of the Eating Disorder Inventory bulimia subscale (F = 6.40; p = 0.002). No significant differences between BED and BN were found in lifetime experiences of sexual abuse or sexual/physical abuse during childhood. As a secondary analysis, we tested the role of obesity in our samples. A significantly higher rate of patients with BED were obese (body mass index ≥ 30 kg/m2) compared with patients with BN (53% vs. 3%; χ 2 = 52.02; p < 0.001). No differences between obese and non-obese patients with BED were found in the number of SE preceding the eating disorder onset. In comparison with non-obese patients with BED, obese patients with BED reported higher rate of lifetime history of sexual abuse (28% vs. 8%; χ 2 = 6.58; p = 0.01; OR = 4.29, 95% CI 1.3–13.9) and a trend towards a higher rate of childhood abuse (24% vs. 8%; χ 2 = 3.89; p = 0.05; OR = 3.8, 95% CI 0.95–14.8).

Table 2 Differences between patients with BED without SE, with one to three SE and more than three SE

Age Duration of illness Age of onset Body mass index Binge frequency† EDI drive for thinness EDI interoceptive awareness EDI bulimia EDI body dissatisfaction EDI ineffectiveness EDI perfectionism SCL somatization SCL obsessive–compulsive SCL interpersonal sensitivity SCL depression SCL anxiety SCL hostility

BED without SE (n = 10) Mean (SD)

BED with 1–3 SE (n = 54) Mean (SD)

BED with more than 3 SE (n = 43) Mean (SD)

F(2, 93)

30.9 (15.3) 52.3 (45.2) 23.1 (10.1) 27.6 (4.9) 5.9 (4.8) 15.0 (4.7) 9.0 (4.6) 13.0 (4.7) 22.5 (3.4) 6.9 (4.9) 3.6 (3.0) 0.7 (0.6) 1.3 (0.9) 0.9 (0.8) 0.9 (0.8) 0.9 (0.6) 0.5 (0.4)

31.9 (10.2) 67.5 (61.1) 24.6 (10.4) 32.2 (7.2) 6.1 (4.8) 11.2 (5.0) 9.9 (6.2) 11.9 (4.2) 21.5 (5.6) 10.3 (7.3) 4.9 (3.8) 1.3 (0.8) 1.6 (0.8) 1.8 (1.0) 1.7 (0.9) 1.5 (0.9) 1.2 (0.8)

30.2 (11.3) 77.4 (67.9) 21.7 (10.4) 31.9 (5.7) 6.5 (4.7) 12.5 (5.1) 13.3 (5.8) 12.4 (4.3) 22.8 (4.3) 14.4 (8.6) 6.9 (4.2) 1.5 (0.9) 2.0 (0.9) 2.3(1.0) 2.3 (1.0) 1.9 (1.0) 1.5 (0.9)

0.29 0.74 0.94 2.18 2 (χ ) 0.45 2.53 4.26* 0.32 0.73 5.30* 5.44* 4.34* 4.62* 7.87** 11.98** 4.92* 6.03**

Note: BED, binge eating disorder; SE, stressful life events; EDI, Eating Disorder Inventory; SCL, Symptom Check List. † Ordinal variable (Kruskal–Wallis test was used). *p < 0.02; **p < 0.005.

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Discussion

relationship may exist between stress-related events preceding the onset of the disorder and factors implicated in maintaining it and its psychopathological manifestations. No significant difference between the two groups of patients emerged regarding the frequency of childhood abuse or lifetime sexual abuse, whereas these types of events appear to differentiate obese and non-obese BED. Previous studies (Yanovski, Nelson, Dubbert, & Spitzer, 1993; Grilo & Masheb, 2001) did not observe differences in frequency of sexual abuse or childhood maltreatment in patients with BED according to obesity status. Although explanations of this relationship are yet to be understood, preliminary evidence suggests that, for some victims of abuse, binge eating may serve as a mediator between obesity and abuse, as well as an ‘adaptive function’ (Gustafson & Sarwes, 2004) to protect the person from negative emotional states related to the abuse. The present study has some methodological limitations, such as the retrospective collection of data on SE and the inclusion of subjects with long-term illness. In addition, the two samples (although similar in duration of illness) are different as regards age and age of onset. This represents a limitation because exposure to life events usually is correlated with age. At least partially, in our study, the inclusion of life events that only occurred in the year preceding the onset may reduce the impact of this limitation. In addition, the severity of psychopathology and the occurrence of personality disorders often associated with eating disorders may have influenced subjects’ memory of the events and their severity. One significant strength of the study is the large sample of patients, matched for duration of illness to reduce the risk of biases associated with inaccuracy of retrospective recall. Our sample of patients with BED is also representative of the relationship between BED and obesity as reported by previous research (Villarejo et al., 2012). In conclusion, the findings of the present study indicate that, in the 6 months preceding the onset of the eating disorder, patients with BED—like those with BN—report a high frequency of SE. Consistent with a pathoplastic model, multiple SE seem to influence the expression and perhaps also the course of BED, with amplified clinical severity. Further studies are necessary for better understanding of the role of SE in the onset of BED and the positive/negative contributions of factors, which can moderate the effects of stress in determining the risk and the course of this disorder. Personality traits, coping strategies and social support may be particularly important and can be targeted by preventive interventions in high-risk subjects or specific treatments after the onset of BED. Specific treatment tools (both psychotherapeutic and pharmacologic) should also be considered, if the importance of previous SE will be confirmed by future studies. Study of the impact of SE is important, not only to understand the complex aetiology of BED but also to examine the possibility of carrying out early interventions and specific therapeutic strategies.

In line with previous findings in the literature about eating disorders, the present study provides new evidence about the role of SE as risk-precipitating factors in BED. In this particular group of patients, SE also might have a role on the clinical and psychopathological manifestations after the onset of the disorder. Our hypothesis of higher reports of SE in patients with BED in comparison with patients with BN was only partially met. In comparison with BN, BED subjects tended to report a greater number of traumatic experiences, although no differences emerged in relation to the total number of SE. Previous findings suggested a close relationship between SE in the interpersonal domain and the onset of BED, supporting the idea that low social support triggers the onset of binge eating in these patients (Pike et al., 2006). Our study confirmed that patients with BED tend to report a high rate of SE related to interpersonal problems (family conflicts, social problems and disagreement with partner) but found no significant differences in this regard between the two groups of patients. These findings endorse the importance of social support and interpersonal functioning in the onset of binge eating in the wholespectrum patients with eating disorders. Our study highlights an association between number of SE and the severity of psychopathology, in particular as regards psychiatric symptoms. Previous studies provided data supporting the hypothesis of an accumulation of life events preceding the onset of such disorders (Rastam & Gillberg, 1992; Welch et al., 1997; Pike et al., 2006). Pike et al. (2006) also noted that patients with comorbid affective disorders reported a significantly greater number of SE than those without. These findings are in line with recent literature, which shows a dose–response model between cumulative adverse life events and mental health (Suliman et al., 2009; Keinan, Shrira, & Shmotkin, 2012). However, no study to date has examined the relationship between SE and eating disorders within a pathoplastic framework. Our data provide evidence of both phenomena in BED, because SE often precede the onset of the disorder (at least as much as in BN), and also might affect the severity of psychopathology several years after onset. Conversely, our findings did not support the pathoplastic relationship between SE and BN. This difference between the two groups of patients may be due to the different factors implicated in maintaining the two disorders. BN is hypothesised to be maintained principally by factors such as dietary restrictions and purging behaviours (Fairburn, Cooper, & Shafran, 2003), which are unrelated to previous stressful experiences and which are—by definition—absent in patients with BED. Instead, BED appears to be a disorder characterised by greater reactivity to everyday stress (Hilbert et al., 2011) and reduced effectiveness in interpersonal problem solving (Svaldi, Dorn, & Trentowska, 2011). In patients with BED, a stronger

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