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Psychiatry Research 215 (2014) 711717

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Psychiatry Research
journal homepage: www.elsevier.com/locate/psychres

On the role of sadness in the psychopathology of anorexia nervosa


Eva Naumann a,n, Brunna Tuschen-Cafer a, Ulrich Voderholzer b, Jennifer Svaldi a
a
b

University of Freiburg, Department of Clinical Psychology and Psychotherapy, Engelbergerstrasse 41, 79106 Freiburg, Germany
Schoen Clinic Roseneck, Prien, Germany

art ic l e i nf o

a b s t r a c t

Article history:
Received 5 July 2013
Received in revised form
14 December 2013
Accepted 27 December 2013
Available online 4 January 2014

Recent models on the development and maintenance of eating disorders propose negative emotions to
be important precursors for the occurrence of eating disorder symptomatology. In fact, previous research
on bulimia nervosa (BN) and binge eating disorder provides evidence that negative emotions are an
antecedent condition for binge eating. However, there is a lack of research examining the inuence of
negative emotions on restrictive eating and exercising in individuals with anorexia nervosa (AN). In an
experimental study, women with AN (n 39) and BN (n 34) as well as a non-eating disordered control
group (CG; n 34) watched a sadness-inducing lm clip. Before and after the lm clip participants rated
their current desire to engage in dietary restriction (DTR) and desire to exercise (DTE). Main results
reveal that DTR signicantly increased after the lm clip in women with AN only, while DTE decreased
over time in all groups. Results are in line with the notion that negative emotions have a prominent
inuence on the core eating pathology in AN.
& 2014 Elsevier Ireland Ltd. All rights reserved.

Keywords:
Eating disorders
Anorexia nervosa
Negative emotion
Sadness
Dietary restriction
Desire to exercise

1. Introduction
According to the Diagnostic and Statistical Manual of Mental
Disorders (DSM-5; American Psychiatric Association (APA), 2013)
anorexia nervosa (AN) is an eating disorder characterized by a
phobic fear of gaining weight along with an unwillingness to
maintain the minimal healthy body weight. Typical behaviors to
achieve or maintain underweight include caloric restriction which
sometimes even culminates in chronic self-imposed starvation.
The severe self-starvation is one reason for the increased morbidity and mortality associated with AN (Fichter et al., 2006; Mitchell
and Crow, 2006; Berkman et al., 2007). With a lifetime prevalence
of up to 80% extreme physical activity is another common weightreducing behavior in individuals suffering from AN (Davis et al.,
1997). While a regular amount of exercise has a benecial effect on
mood and physical health (Blumenthal et al., 2007; Deslandes
et al., 2009; Archer, 2012; Morris et al., 2012), research shows that
excessive exercise in AN is positively associated with eating
psychopathology, hospitalization periods and rates of relaps
(Strober et al., 1997; Solenberger, 2001; Peas-Lled et al., 2002;
Carter et al., 2004; Bewell-Weiss and Carter, 2010). As such, there
is a need for research identifying factors that trigger restriction of
food intake and excessive exercise in AN.
Models on the maintenance of eating disorders highlight the
importance of negative emotions in the occurrence of eating

Corresponding author. Tel.: 49 761 2033016; fax: 49 761 2033022.


E-mail address: eva.naumann@psychologie.uni-freiburg.de (E. Naumann).

0165-1781/$ - see front matter & 2014 Elsevier Ireland Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.psychres.2013.12.043

disorder symptomatology (Stice, 2001; Fairburn et al., 2003). As


such, a great body of research exists showing that negative
feelings trigger binge eating and purging behavior in bulimia
nervosa (BN) as well as binge attacks in binge eating disorder
(BED) (Alpers and Tuschen-Cafer, 2001; Hilbert and TuschenCafer, 2007; Smyth et al., 2007). For example, after an insecurity
and sadness-inducing guided imagery task ratings of hunger and
desire to binge increased in bulimic patients, whereas no changes
were found in healthy controls (Tuschen-Cafer and Voegele,
1999).
In contrast to BN and BED, research on the role of negative
emotions in the maintenance of anorectic behavior is still sparse.
Besides, on a theoretical level it remains controversial whether
eating pathology in AN can be inuenced by intense mood states.
Some theoretical accounts suggest that mood intolerance and
maladaptive emotion regulation behavior is rather atypical in
individuals with AN compared to other eating disorders (Fairburn
et al., 2003). On the other hand, there are recent models on the
onset and maintenance of AN that emphasize the emotion regulation functioning of anorectic behavior (Haynos and Fruzzetti, 2011).
That is, maladaptive behaviors as dietary restriction and excessive
exercise may be triggered by adverse emotional states and might
therefore serve as a dysfunctional form of emotion regulation.
Empirical evidence supports this notion showing that individuals
with AN have more difculties tolerating and regulating negative
emotions compared to healthy controls (Harrison et al., 2009;
Wildes et al., 2010; Svaldi et al., 2012). Moreover, one study
(Merwin et al., 2010) reports signicant positive correlations of
non-acceptance of emotional responses with dietary restriction in

712

E. Naumann et al. / Psychiatry Research 215 (2014) 711717

women with AN. In qualitative studies AN patients report that main


reasons for restriction of food intake include the inability to tolerate
adverse emotions, attempts to control negative emotions and efforts
to provide positive feelings like pride and security (Serpell et al.,
1999; Dignon et al., 2006; Nordb et al., 2006; Federici and Kaplan,
2008). Additionally, an ecological momentary assessment (EMA)
study (Engel et al., 2005) revealed a prominent correlation between
stressful events and affect lability with restrictive behavior and
rituals in AN. Further evidence for the reinforcing inuence of
negative mood on anorectic eating behavior stems from biopsychological studies showing that dietary restraint can have a decreasing
effect on the plasma tryptophan availability (Kaye, 2008). The
plasma tryptophan modulates brain 5-HT functional activity, which
in turn, is thought to have a positive inuence on mood (Frank et al.,
2001).
Regarding excessive exercise, there is indirect evidence of a
close linkage between negative emotions and extreme physical
activity in individuals with AN. For example, Peas-Lled et al.
(2002) found that subjects with AN subtyped as high excessive
exercisers were characterized by high levels of depression and
anxiety compared to those subtyped as low excessive exercisers.
Likewise, an EMA study on patients with AN and BN showed that
individuals with an increased desire to be physically active are
disposed to suffer from a chronically negative affect (Vansteelandt
et al., 2007).
Notwithstanding, the previously mentioned studies do not allow
to draw conclusions about cause and effect. In a very recent study
though Wildes et al. (2012) experimentally tested the effects of
negative mood on eating disorder symptoms in patients with AN.
Specically, AN participants either watched a negative emotioninducing lm clip or a neutral lm clip. Prior to and after the lm
clip, participants had to rate several self-constructed items on Likert
scales ranging from one (agree not at all) to ve (completely agree).
The items focused on maladaptive thoughts about eating, shape and
weight (e.g., I feel fat), as well as urges to engage in eating disorder
behaviors typically associated with AN (e.g., I want to restrict).
While no changes were found in AN participants allocated to the
neutral condition, those allocated to the negative mood condition
self-reported a signicant increase in eating disorder symptoms
following the negative emotion induction. However, as this study
summed up different kinds of eating disorder pathology (e.g., urge
to restrict, state body image disturbance) it remains unclear which
of the specic anorectic symptoms were actually triggered by the
induced adverse emotions. This is especially important as previous
studies were able to show that negative mood leads to an overestimation of the own body size as well as higher levels of body
dissatisfaction (Plies and Florin, 1992; Baker et al., 1995). Therefore,
it is possible that only changes in the items measuring body image
disturbances were responsible for the results of Wildes et al. (2012).
In light of the research just mentioned, the aim of the present
study was to experimentally test the inuence of negative emotions
on the urge to engage in dietary restriction (DTR) and exercise (DTE)
in patients with AN. Based on former studies identifying sadness to
be a common pre-binge emotion in BN and BED (Cooper and
Bowskill, 1986; Chua et al., 2004), a sadness-inducing lm clip was
used as negative emotional stimulus. In addition to an AN group, we
included both a non-eating disordered control group and a group of
females with BN. The former was included to test for possible effects
of mood on eating pathology. The latter was included in order to
provide information about differential effects between the two eating
disorders, as previous studies reported high rates of syndrome shift
(Agras et al., 2000) and similarities (Norman and Herzog, 1983)
between AN and BN. With regard to the extensive overlap in the
diagnostic criteria particularly between AN of bulimic subtype and BN
(American Psychiatric Association (APA), 2013), analyses comparing
AN restrictive and bulimic subtypes were also included to further

explore whether the affect regulation model ts both AN subtypes.


In line with current models on the onset and maintenance of
AN (Haynos and Fruzzetti, 2011), we predicted that an induction of
sadness would lead to an increase of DTR and DTE only in individuals
with AN.
2. Method
2.1. Participants
The sample consisted of women with a DSM-IV-TR (American Psychiatric
Association (APA), 2000) diagnosis of AN (n 39) and BN (n34) recruited from
an inpatient clinic and via advertisements and announcements in the local media.
The non-eating disordered control group (n34) was recruited via ads in the local
media. Twenty-nine (74.35%) AN subjects were classied as restrictive subtype and
10 (26.31%) as bulimic subtype.
Exclusion criteria for all participants included the presence of current substance abuse or addiction (except sustained full remission), bipolar disorder, past
psychosis, schizophrenia (currently symptomatic) and current suicidal ideation.
Eating disorders were diagnosed by means of the Eating Disorder Examination
Interview (EDE; Fairburn and Cooper, 1993; Hilbert et al., 2004). All other diagnoses
were established by means of the Structured Clinical Interview (SCID) for DSM-IV
Axis I and the borderline personality section of the Axis II interview (First et al.,
1997; Wittchen et al., 1997). Studies show that the prevalence of eating disorders
is high in adolescent females (e.g., Hudson et al., 2007; Le Grange et al., 2012).
Therefore, to increase the ecological validity of the study the lower age limit for
participants was 16 years.
2.2. Materials
2.2.1. Induction of sadness
In order to induce sadness a scene from the movie The Lion King (length:
2 min, 11 s) was selected in which a young lion nds his father dead. As part of a set
of standardized emotional lm stimuli, this movie scene from The Lion King has
been shown to reliably elicit sadness with little inuence on other negative
emotions (Rottenberg et al., 2007). The following instruction adapted from Gross
(1998) was presented prior to the clip: We will now be showing you a short lm
clip. It is important to us that you watch the lm clip carefully. However, if you nd
the lm to be too distressing, please call the experimenter. To intensify sadness,
a freeze image was presented after the lm clip for 15 s, in which the young lion
snuggles up to his dead father.
2.2.2. Manipulation check items
On the day of the experiment, participants were instructed to eat 12 h prior to
the experiment. However, during the hour before the experiment no food intake
was allowed to control for hunger.
To check whether participants really had comparable initial hunger levels,
participants rated how hungry they were on a 100 mm Visual Analog Scale (VAS)
anchored from not at all to very much at the beginning of the experiment.
To ensure that the lm clip induced sadness, emotional states were rated by the
participants before and after the lm-clip on 100 mm VASs anchored from not at
all to very much. State sadness was assessed by the item At the moment I feel
sad. Current positive emotion was assessed by the following item: At the moment
I feel happy.
2.2.3. Self-reported desire to engage in dietary restriction (DTR) and desire to exercise
(DTE)
Like the manipulation check items, items on DTR and DTE were presented via
computer on 100 mm VASs anchored from not at all to very much. Items were
presented prior to (baseline) and after watching the lm clip (post-lm).
Current DTR was assessed using the following self-constructed item: At
the moment I do not want to eat anything. The item At the moment I would like
to exercise was used to measure the current DTE.
2.2.4. Questionnaires
Internal consistencies of our study sample for the questionnaires were
calculated for the entire sample. The following questionnaires were administered:
(1) The Eating Disorder Examination Questionnaire (EDE-Q; Fairburn and Beglin,
1994) is a 36-item self-report measure that assesses the severity of eating
pathology with four subscales (restraint eating, eating concern, weight concern
and shape concern) and with a global score. The global score and the subscales
show high internal consistency, stability and validity (Fairburn and Beglin, 1994;
Hilbert et al., 2007). Internal consistencies in our study ranged from 0.91 (EDE-Q
weight concern) to 0.98 (EDE-Q global score). (2) The current version of
the Beck Depression Inventory-II (BDI Beck et al., 1996; Hautzinger et al., 2007) is
a self-report measure that assesses severity of depression over the last two weeks.

E. Naumann et al. / Psychiatry Research 215 (2014) 711717


It consists of 21 items with a scale ranging from 0 to 3 and shows high internal
consistency ( 0.84), test-retest reliability (rtt 0.75) and discriminant validity
(Kuehner et al., 2007). The internal consistency in our study was 0.96.
2.3. Procedure
Diagnostics and experimental sessions were conducted on separate days with
no more than one week in-between. Participants were informed that they will be
presented with a number of lm clips and pictures in the context of different
experiments revolving around their emotional reactions. All subjects gave their
informed consent before taking part in the experiment. In the case of under aged
individuals written informed consent of one parental unit was required in addition.
The study was approved by the local ethic committee.
Presentation software (Neurobs, Inc., Albany, California, USA) was used for the
presentation of the instructions, stimulus delivery and to record participants0
subjective ratings. On arrival at the experimental session, participants were lead to
a quiet laboratory room, seated in front of a 17-inch monitor and were given
headphones. After instructing participants on the experiment, the laboratory
assistant left the participant alone in the room and started the experiment. At
rst, participants rated their current emotional states, DTR, and DTE (baseline).
Then, the instruction to carefully watch the following lm clip was presented (see
Section 2.2.1). To ensure that participants had enough time to read and understand
this instruction, they had to press a button in order to continue with the
experiment. Then, the lm clip and the still image of the lm clip were presented.
Afterwards, subjective ratings (post-lm) were re-assessed. After this segment,
participants made a pause and then continued with other experimental assignments unrelated to this paper.
2.4. Statistical analyses
Socio-demographic characteristics and manipulation check on baseline hunger
were analyzed by means of univariate analyses of variance (ANOVAs). Manipulation
check on the sadness induction and hypotheses were tested by means of repeated
measures ANOVAs.1 If the assumption of sphericity was not met (Mauchlys
Sphericity Test: p o0.05), degrees of freedom for dependent variables were
corrected conservatively by Greenhouse-Geisser. Being exceedingly robust against
violation of normality (Tabachnick and Fidell, 2007), ANOVAs were also adopted for
variables deviating from normal distribution. Where indicated, Scheff post-hoc
tests were conducted to identify pairwise differences among the groups. Effect
sizes of the main effects and interactions are reported by partial eta squared (2),
whereby values larger than 0.01 refer to small, 0.06 to moderate, and 0.14 to large
effect sizes (Cohen, 1988). Effect sizes for post-hoc analyses are reported by Cohen0 s
d (Cohen, 1988), whereby values larger than 0.20 refer to small, 0.50 to moderate,
and 0.80 to large effect sizes. All tests of signicance were two tailed.

3. Results
3.1. Socio-demographics and questionnaires
Groups did not differ signicantly in age, marital status and
educational level. As expected, Body Mass Index (BMI weight/
height) in the AN group was signicantly lower compared to the
other two groups, which did not differ from one another in terms
of weight. Regarding eating pathology and depression, there were
no signicant differences between the two eating disorder samples, while both groups had signicantly higher scores on the
respective scales compared to the CG (see Table 1 for means (M),
standard deviations (S.D.), frequencies and statistics).
3.2. Manipulation check
With regard to the initial hunger, an ANOVA revealed that there
were no signicant differences in hunger levels at the baseline
measurement between the groups, F (2, 104) 0.17, p 0.84 (AN
group: M 10.20, S.D. 17.20; BN group: M 12.38, S.D. 21.45;
CG: M 10.00, S.D. 17.23).
A 3 (Group: AN, BN, CG)  2 (Time: baseline, post-lm) repeated
measures ANOVA on sadness revealed a signicant main effect of
time, F (1, 104) 196.92, po0.001, 2 0.65, whereby in all groups
1

The results of ANCOVAs with BDI as a covariate yielded comparable results.

713

subjective sadness signicantly increased after watching the lm


clip (baseline: M28.85, S.D.30.90; post-lm: M 71.79, S.
D. 27.41). In addition, the main effect of group was signicant, F
(2, 104)23.83, po0.001, 2 0.31. Scheffe0 s post-hoc analyses
showed that there were no signicant differences in subjective
sadness between AN (baseline: M34.65, S.D.32.77; post-lm:
M78.10, S.D.25.20) and BN (baseline: M44.20, S.D.29.91;
post-lm: M 81.38, S.D.18.41), p0.42, while both eating disorder groups reported signicantly higher state sadness at the
baseline and the post-lm measurement compared to the CG
(baseline: M6.85, S.D.12.40; post-lm: M54.97, S.D. 30.15),
pso0.001, ds41.33. There was no signicant group  time interaction, F (2, 104)1.03, p0.36.
A repeated measures group (AN, BN, CG)  time (baseline, postlm) ANOVA conducted on positive emotion yield a signicant main
effect of time, F (1, 104) 182.16, po0.001, 2 0.64, and group, F (2,
104)15.97, po0.001, 2 0.24, while there was no signicant
group  time interaction, F (2, 104)2.94, p0.06. Thereby, positive
emotion decreased signicantly in all groups (baseline: M43.84, S.
D. 25.15; post-lm: M16.15, S.D. 22.13). Scheffe0 s post-hoc tests
revealed no signicant differences between AN (baseline: M42.31,
S.D. 26.38; post-lm: M16.15, S.D. 22.13) and BN (baseline:
M 37.54, S.D.25.94; post-lm: M15.27, S.D. 18.08) in positive
emotions, p0.42, while both eating disorder groups had signicantly lower state positive emotion at the baseline and the post-lm
assessment in comparison to the CG, (baseline: M 69.22,
S.D. 17.30; post-lm: M37.80, S.D.18.64), pso0.001, ds41.00.
3.3. Desire to engage in dietary restriction (DTR)
A 3 (group: AN, BN, CG)  2 (time: baseline, post-lm) repeated
measures ANOVA conducted on DTR yield a signicant main effect
of group, F (2, 104)12.60, po0.001, 2 0.20, whereby the AN and
BN group did not signicantly differ in their DTR levels, p0.27,
while both eating disorder groups had signicantly higher DTR
scores compared to the CG, pso0.007, ds40.78. There also was a
signicant main effect of time, F (1, 104)11.38, p 0.001, 2 0.10,
and a signicant group  time interaction, F (2, 104)6.09, p0.003,
2 0.11. To further explore the signicant main effect of time and the
signicant group  time interaction, follow-up paired t-tests on the
DTR baseline and DTR post-lm scores were conducted separately
for group. Follow-up paired t-tests showed that only in the AN group
there was a signicant increase in the DTR after the sadness-inducing
lm clip, t  5.03, d.f. 38, po0.001, d 0.72. There was no
signicant change in the DTR from prior to after the lm clip in
the BN group, t  0.769, d.f.33, p0.45, and the CG, t  0.23, d.
f.33, p0.82 (see Fig. 1a for Ms and S.D.s).
In order to check for possible differences in DTR change
between the two AN subtypes, a 2 (subtype: restrictive AN, bulimic
AN)  2 (time: baseline, post-lm) repeated ANOVA was conducted on DTR. The results revealed no signicant main effect of
subtype, F (1, 37) 3.24, p 0.08, and no signicant subtype  time
interaction, F (1, 37) 0.14, p 0.71. There was a signicant main
effect of time, F (1, 37) 20.48, p o0.001, 2 0.36, showing that
both the restrictive AN group (baseline: M 46.62, S.D. 37.22;
post-lm: M 69.62, S.D. 31.78) and the bulimic AN group (baseline: M63.60, S.D. 31.22; post-lm: M 90.70, S.D. 16.47)
showed an increase in DTR in response to a sadness-inducing
lm clip.
3.4. Desire to exercise (DTE)
A group (AN, BN, CG)  time (baseline, post-lm) repeated
measures ANOVA conducted on DTE revealed a signicant main
effect of group, F (2, 104) 3.37, p0.03, 2 0.06, whereby women
with AN reported signicantly higher DTE scores than the CG

714

E. Naumann et al. / Psychiatry Research 215 (2014) 711717

Table 1
Socio-demographics and overall psychopathology presented separately for participants with anorexia nervosa (AN), bulimia nervosa (BN) and non-eating disordered
controls (CG).

Age (years)

AN n39

BN n 34

CG n 34

Statistics

M (S.D.)/Frequency

M (S.D.)/Frequency

M (S.D.)/Frequency

F or 2

25.54 (11.06)

25.94 (8.34)

25.88 (10.73)

0.02

0.98

2 (6) 11.07

0.09

2 (4) 1.26

0.87

69.60
83.74
84.74
99.76
144.14
132.00
89.24

o0.001
o0.001
o0.001
o0.001
o0.001
o0.001
o0.001

o 0.001
0.23
0.73
0.43
0.23
0.81
0.53

o 0.001
o 0.001
o 0.001
o 0.001
o 0.001
o 0.001
o 0.001

0.23
o 0.001
o 0.001
o 0.001
o 0.001
o 0.001
o 0.001

Marital status
Single
Partnership
Married
Divorced

23
12
3
1

17
15
2
0

10
17
3
4

Education level
Low education
Middle education
High education

2
16
21

2
11
21

1
11
22

BMI
EDE-QRE
EDE-QEC
EDE-QWC
EDE-QSC
EDE-QGS
BDI

15.05 (1.89)
5.27 (1.69)
4.47 (1.72)
4.87 (1.60)
5.38 (1.41)
5.07 (1.44)
28.23 (10.53)

22.44 (4.20)
4.71 (1.53)
4.71 (1.32)
5.25 (1.20)
5.82 (0.99)
5.24 (1.02)
25.94 (10.11)

21.23 (2.14)
1.33 (0.61)
1.11 (0.15)
1.44 (0.63)
1.78 (0.65)
1.48 (0.51)
3.20 (2.61)

Scheff post-hoc tests


p (AN vs. BN)

p (AN vs. CG)

p (BN vs. CG)

Note: BMI body mass index (weight/height2); EDE-Q eating disorder examination questionnaire; RE restraint subscale; EC eating concerns subscale; WC weight
concerns subscale; SC shape concerns subscale; GS global score; and BDI beck depression inventory.

80

100

60

60

AN
BN

40

CG

AN

40

BN
CG

20

20
0

Mean DTE

Mean DTR

80

baseline post-film

baseline

post-film

Fig. 1. Means on the desire to engage in dietary restriction (DTR; (a)) and desire to exercise (DTE; (b)) before and after a sadness-inducing lm clip. Results are presented
separately for women with anorexia nervosa (AN), bulimia nervosa (BN) and non-eating disordered controls (CG). Bars represent standard deviations.

throughout the experiment, p0.03, d0.62, while there were no


differences between the eating disorder groups or the CG and the
BN group, po0.34. In addition, there was a signicant main effect of
time, F (1, 104)8.59, p 0.004, 2 0.08. Thereby, all groups
showed a signicant decrease in DTE after watching the lm-clip.
There was no signicant group  time interaction, F (2, 104)0.98,
p0.34. (see Fig. 1b for Ms and S.D.s).

4. Discussion
Current models of AN propose that negative emotions play an
important role in the maintenance of anorectic behavior (Haynos
and Fruzzetti, 2011). While much efforts have been invested to
analyze the relation between negative emotions and binge eating
in BN and BED (Alpers and Tuschen-Cafer, 2001; Hilbert and
Tuschen-Cafer, 2007; Smyth et al., 2007), there is a lack of

research on the inuence of adverse feelings in the occurrence


of eating disorder symptoms in AN. Therefore, the present study
was designed to experimentally investigate the effects of sadness
on the DTR and DTE as two common weight-reducing behaviors in
AN. For this purpose, a sadness-inducing lm clip was presented to
women with AN, BN and a non-eating disordered control group.
Prior to and after the lm clip participants rated their current
emotions as well as their DTR and DTE on VASs. It was predicted
that only in females with AN the DTR and the DTE would increase
after inducing sadness.
With regard to the main hypothesis of the study, the results
reveal that compared to the BN and non-eating disordered CG, the
DTR signicantly increased after the sadness-inducing lm clip in
women with AN. In line with recent models on the development
and maintenance of anorectic behavior (Haynos and Fruzzetti,
2011) and previous studies (Engel et al., 2005; Wildes et al., 2012),
these results support the notion that caloric restriction in AN is

E. Naumann et al. / Psychiatry Research 215 (2014) 711717

triggered, and therefore possibly maintained by negative emotional states. Thus, similarly to BN and BED (Alpers and TuschenCafer, 2001; Hilbert and Tuschen-Cafer, 2007; Smyth et al.,
2007) results suggest that individuals with AN might engage in
dietary restriction in order to escape from or control negative
affect.
Noteworthy, the present study found no changes in DTR after
sadness induction in non-eating disordered controls and women
with BN. This is an interesting nding, given the fact that caloric
restriction is also highly prevalent in BN (Rossiter et al., 1989). It is
possible that the emotion regulation functioning of dietary restriction is rather specic for patients with AN. Interestingly, when
analyzing the two AN subtypes separately, we found that AN
patients of bulimic and restrictive subtype both reacted to the lm
clip with an increase in their DTR. Though AN females of the
bulimic subtype also suffer from binge eating and purging, our
results indicate that within the emotion regulation domain they
might have more in common with their restrictive counterparts.
Thus, these results provide further support for the validity and
relevance of the diagnostic system regarding the classication of
AN subtypes.
Contrary to our hypothesis, DTE signicantly decreased after
the sadness-eliciting lm clip in all participants. These ndings
stand in contrast to the notion that physical activity serves an
affect regulation functioning in AN (Haynos and Fruzzetti, 2011) as
well as studies showing that excessive exercise in AN is positively
connected to chronic negative emotions (Peas-Lled et al., 2002;
Vansteelandt et al., 2007). However, it is possible that our results
on the DTE are highly inuenced by the side effects of the sadness
induction. That is, previous research has shown that sadness is
associated with mental and physical passivity (Schwartz et al.,
1981; Rucken and Petty, 2004), which in short term might have
inhibited the DTE in all participants. However, participants of the
current study rated their DTE directly after they had watched the
lm clip, i.e., when a strong feeling of sadness was still present.
It therefore remains unclear whether individuals with AN use
physical activity to cope with their depressive mood at a later level
of the sadness generation process. It would be interesting in future
to also examine the long term effects of sadness on exercise in
eating disorders. Furthermore, it would be interesting for future
research to induce other negative emotions than sadness, for it is
possible that different emotions lead to different eating disorder
symptoms. For example, anger as a further highly prevalent
emotion in eating disorders (Waller et al., 2003) is suggested
to be associated with a high action readiness and heightened
physiological arousal (Schwartz et al., 1981; Frijda, 1987), and
therefore possibly is closer related to exercising in eating disorders
than sadness. Another possible explanation for our results on the
DTE is that the conceptualization of the corresponding item was
very broad, given the diversity of the concept (e.g., there is a
difference between an urge to move, a desire to engage in sports, a
feeling of restlessness). Therefore, future studies should consider
using more specic items to operationalize DTE. Nevertheless,
there also is literature emphasizing that the drive for activity in AN
rather results from biological consequences of the malnutrition
status of the patients, and thus is relative unrelated to emotional
states (Casper, 2006). In fact, animal research displays that
starvation in rats leads to hyperactivity and increased exercising
behavior (Pirke et al., 1993); a connection that is supposed to be
mediated by the low plasma leptin levels found in food-restricted
rats and patients with AN (Balligand et al., 1998; Hebebrand et al.,
2003; Holtkamp et al., 2003). However, correlational analyses
on the current samples showed that there were no signicant
associations of BMIs and the DTE ratings (all rso  0.326, all
ps40.060). This, along with research on the mood stabilizing
effect of physical activity (Blumenthal et al., 2007) as well as our

715

results on the signicant change in the DTE after the sadness


induction stand against the assumption that activity levels in AN
are solely determined by the hypoleptinemia associated with food
restriction. Hence, future studies are needed to further explore the
role of emotions in the occurrence of exercise in eating disorders
(e.g., by using EMA).
With regard to the limitations of the present study, it is
important to critically note that only self-report measures were
included. In the context of bulimic spectrum eating disorders
research has shown that binge eating is preceded by a strong desire
to binge (Steiger et al., 1999; Engelberg et al., 2005). On the other
hand results of a study by Waters et al., 2001 illustrate that not
every urge to binge automatically leads to an actual binge attack.
Similarly, in individuals diagnosed with AN the DTR or DTE
presumably is not always equivalent to real behavior, since external
factors like social circumstances also need to be taken into account.
Future studies that integrate more objective measures of restrictive
eating (e.g., real food intake in a laboratory task) and exercising
(e.g., monitoring movement via a kinesiometer) are clearly needed.
In this regard, it must be critically mentioned that our items also do
not directly assess the motivation for the eating disordered behavior. As such, a self-reported increase in the item At the moment
I do not want to eat anything may not necessarily be associated
with a desire to regulate weight. More specically, it is well possible
that increases in DTR are merely a consequence of decreases in
appetite following a negative emotional state rather than reecting
an increased desire to control or regulate weight. Therefore, future
studies should more thoroughly focus on the motivational aspects
underlying the desire to restrict food intake following a sadness
induction. Additionally, these studies should denitely include
multiple and validated items to assess DTR and DTE to ensure and
strengthen the reliability of the results found. Ultimately, bogus
taste tests implemented after sadness induction would improve the
ecological validity of the reported results. Likewise, EMA could be
used to test the impact of sadness on exercise in AN.
A further limitation of the current study is that we have not
collected information on the time of the last meal, the last binge
eating episode, or the last time the participants engaged in
exercise. Obviously, the engagement in such behavior could have
inuenced our results. On the other hand, all participants were
instructed to eat 12 h prior to the experiment and not to eat
anything within 1 h prior to the experimental session. More
important though, baseline levels of current hunger did not differ
within the two experimental conditions. Nevertheless, future
studies should not solely rely on self-report data and rather serve
a standardized meal prior to the experimental session.
Another issue concerns the fact that no neutral lm clip was
included in the experimental design. Thus, it is not clear whether the
emotional content of the lm stimulus was responsible for our results.
That is, DTR in participants with AN might have increased for reasons
other than negative emotions. Such factors may include naturally
occurring daily uctuations or time of day. This seems unlikely,
though, as participants were tested throughout the day. Also, against
this assumption we point out that Wildes et al. (2012) showed eating
disorder symptoms in AN not to change following a neutral lm clip.
Last but not least, the low sample size of the group with AN
bulimic subtype (n 10) compared to the group with AN restrictive
subtype (n 29) is a further limitation of the current study.
Though this is in line with research showing that the restrictive
subtype is more prevalent than the bulimic subtype (Garnkel
et al., 1996), future studies with more balanced and higher sample
sizes regarding the AN subtypes are needed to provide reliable
information on whether both AN subtypes differ in their reactions
to negative emotions.
In sum, our results suggest that similarly to BN and BED, negative
emotions are an antecedent condition in the core pathology of AN as

716

E. Naumann et al. / Psychiatry Research 215 (2014) 711717

well. However, further support from studies inducing different


emotions (e.g., anger, disgust, shame, anxiety) and using more
differentiated assessments of dietary restriction and exercising (e.
g., multiple specic items, including objective measures) is clearly
needed. Even though our data suggest an increase of DTR by
sadness, the underlying mechanisms remain yet unclear. In an
empirically well validated model, Gross (1998) dened emotion
regulation (ER) as the process by which we inuence what kinds of
emotions we have, when we have them, and how we perceive and
express them [Gross, 2002; p. 282]. Two frequently examined ER
strategies are expressive suppression and cognitive reappraisal.
Along a temporal continuum, reappraisal occurs early, and should
thus enable an individual to modify an emotional sequence before
emotion response tendencies have been fully generated. Suppression, on the other hand, occurs late in the emotion-generative
process and therefore requires an effortful management of emotion
response tendencies as they continually arise. Evidence suggests
that compared to individuals without AN, those with AN more often
suppress and less often reappraise their emotions (Svaldi et al.,
2012). As such, it can be assumed that patients with AN adopted
different emotion regulation strategies following the sadness induction. To address this issue, studies that analyze the differential
impact emotion regulation strategies have on DTR in women with
AN are needed.
Taken together with our ndings, this research could have
prominent implications for current clinical efforts to include
trainings of functional emotion regulation skills in the therapy of
AN. Future studies are needed to investigate whether the integration of such emotion focused interventions improve the effectiveness of existing AN treatment programs.

Acknowledgments
We want to thank the Scientic Society of Freiburg for their
generous grant, which enabled us to complete this study. We
gratefully acknowledge the excellent support of the staff of the
Schoen Clinic Roseneck in Germany. We thank all the participants
for their commitment and dedication.
References
Agras, W.S., Walsh, T., Fairburn, C.G., Wilson, G.T., Kraemer, H.C., 2000. A multicenter comparison of cognitive-behavioral therapy and interpersonal psychotherapy for bulimia nervosa. Archives of General Psychiatry 57, 459466.
Alpers, G.W., Tuschen-Cafer, B., 2001. Negative feelings and the desire to eat in
bulimia nervosa. Eating Behaviors 2, 339352.
American Psychiatric Association (APA), 2000. Diagnostic and Statistical Manual of
Mental Disorders, fourth ed. American Psychiatric Association, Washington, DC.
(Text revision).
American Psychiatric Association (APA), 2013. Diagnostic and Statistical Manual of
Mental Disorders, fth ed. American Psychiatric Publishing, Arlington, VA.
Archer, T., 2012. Inuence of physical exercise on traumatic brain injury decits:
scaffolding effect. Neurotoxicity Research 21, 418434.
Baker, J.D., Williamson, D.A., Sylve, C., 1995. Body image disturbance, memory bias, and
body dysphoria: effects of negative mood induction. Behavior Therapy 26, 747759.
Balligand, J.L., Brichard, S.M., Brichard, V., Desager, J.P., Lambert, M., 1998.
Hypoleptinemia in patients with anorexia nervosa: loss of circadian rhythm
and unresponsiveness to short-term refeeding. European Journal of Endocrinology/European Federation of Endocrine Societies 138, 415420.
Beck, A.T., Steer, R.A., Brown, G.K., 1996. Manual for the beck depression inventoryII. Psychological Corporation, San Antonio.
Berkman, N.D., Lohr, K.N., Bulik, C.M., 2007. Outcomes of eating disorders: a systematic
review of the literature. International Journal of Eating Disorders 40, 293309.
Bewell-Weiss, C.V., Carter, J.C., 2010. Predictors of excessive exercise in anorexia
nervosa. Comprehensive Psychiatry 51, 566571.
Blumenthal, J.A., Babyak, M.A., Doraiswamy, P.M., Watkins, L., Hoffman, B.M.,
Barbour, K.A, Herman, S., Craighead, W.E., Brosse, A.L., Waugh, R., Hinderliter,
A., Sherwood, A., 2007. Exercise and pharmacotherapy in the treatment of
major depressive disorder. Psychosomatic Medicine 69, 587596.
Carter, J.C., Blackmore, E., Sutandar-Pinnock, K., Woodside, D.B., 2004. Relapse in
anorexia nervosa: a survival analysis. Psychological Medicine 34, 671679.

Casper, R.C., 2006. The drive for activity and restlessness in anorexia nervosa:
potential pathways. Journal of Affective Disorders 92, 99107.
Chua, J.L., Touyz, S., Hill, A.J., 2004. Negative mood-induced overeating in obese
binge eaters: an experimental study. International Journal of Obesity and
Related Metabolic Disorders: Journal of the International Association for the
Study of Obesity 28, 606610.
Cohen, J., 1988. Statistical Power Analysis for the Behavioral Sciences. vol. 2.
Hillsdale, Lawrence Erlbaum, New Jersey.
Cooper, P.J., Bowskill, R., 1986. Dysphoric mood and overeating. British Journal of
Clinical Psychology/The British Psychological Society 25, 155156.
Davis, C., Katzman, D.K., Kaptein, S., Kirsh, C., Brewer, H., Kalmbach, K., Olmsted, M.P.,
Woodside, D.B., Kaplan, A.S., 1997. The prevalence of high-level exercise in the
eating disorders: etiological implications. Comprehensive Psychiatry 38, 321326.
Deslandes, A., Moraes, H., Ferreira, C., Veiga, H., Silveira, H., Mouta, R., Pompeu, F.A.,
Coutinho, E.S., Laks, J., 2009. Exercise and mental health: many reasons to
move. Neuropsychobiology 59, 191198.
Dignon, A., Beardsmore, A., Spain, S., Kuan, A., 2006. 0 Why I won0 t eat: patient
testimony from 15 anorexics concerning the causes of their disorder. Journal of
Health Psychology 11, 942956.
Engel, S.G., Wonderlich, S.A., Crosby, R.D., Wright, T.L., Mitchell, J.E., Crow, S.J.,
Venegoni, E.E., 2005. A study of patients with anorexia nervosa using ecologic
momentary assessment. International Journal of Eating Disorders 38, 335339.
Engelberg, M.J., Gauvin, L., Steiger, H., 2005. A naturalistic evaluation of the relation
between dietary restraint, the urge to binge, and actual binge eating: a
clarication. International Journal of Eating Disorders 38, 355360.
Fairburn, C.G., Beglin, S.J., 1994. Assessment of eating disorders: interview or selfreport questionnaire? International Journal of Eating Disorders 16, 363370.
Fairburn, C.G., Cooper, Z., 1993. The eating disorder examination. In: Fairburn, C.G.,
Wilson, G.T. (Eds.), Binge Eating: Nature, Assessment and Treatment, 12th ed.
Guilford Press, New York, pp. 317360.
Fairburn, C.G., Cooper, Z., Shafran, R., 2003. Cognitive behavior therapy for eating
disorders: a transdiagnostic theory and treatment. Behavior Research and
Therapy 41, 509528.
Federici, A., Kaplan, A.S., 2008. The patient0 s account of relapse and recovery in
anorexia nervosa: a qualitative study. European Eating Disorders Review: The
Journal of the Eating Disorders Association 16, 110.
Fichter, M.M., Quaieg, N., Hedlund, S., 2006. Twelve-year course and outcome
predictors of anorexia nervosa. International Journal of Eating Disorders 39, 87100.
First, M.B., Spitzer, R.L., Gibbon, M., Williams, T.W., 1997. Structured Clinical
Interview for DSM-IV Axis I and II Disorders. American Psychiatric Press,
Washington, DC.
Frank, G.K., Kaye, W.H., Weltzin, T.E., Perel, J., Moos, H., McConaha, C., Pollice, C.,
2001. Altered response to meta-chlorophenylpiperazine in anorexia nervosa:
support for a persistent alteration of serotonin activity after short-term weight
restoration. International Journal of Eating Disorders 30, 5768.
Frijda, N.H., 1987. Emotion, cognitive structure, and action tendency. Cognition and
Emotion 1, 115143.
Garnkel, P.E., Lin, E., Goering, P., Spegg, C., Goldbloom, D., Kennedy, S., Kaplan, A.S.,
Woodside, D.B., 1996. Should amenorrhoea be necessary for the diagnosis of
anorexia nervosa? Evidence from a Canadian community sample. British
Journal of Psychiatry: The Journal of Mental Science 168, 500506.
Gross, J.J., 1998. The emerging eld of emotion regulation: an integrative review.
Review of General Psychology 2, 271299.
Gross, J.J., 2002. Emotion regulation: Affective, cognitive, and social consequences.
Psychophysiology 39, 281291.
Harrison, A., Sullivan, S., Tchanturia, K., Treasure, J., 2009. Emotion recognition and
regulation in anorexia nervosa. Clinical Psychology and Psychotherapy 16,
348356.
Hautzinger, M., Keller, F., Kuehner, C., 2007. Deutsche Adaptation des Beck
Depressions-Inventars BDI-II. Harcourt Test Services, Frankfurt.
Haynos, A.F., Fruzzetti, A.E., 2011. Anorexia nervosa as a disorder of emotion
dysregulation: evidence and treatment implications. Clinical Psychology:
Sciene and Practice 18, 183202.
Hebebrand, J., Exner, C., Hebebrand, K., Holtkamp, C., Casper, R.C., Remschmidt, H.,
Herpertz-Dahlmann, B., Klingenspor, M., 2003. Hyperactivity in patients with
anorexia nervosa and in semistarved rats: evidence for a pivotal role of
hypoleptinemia. Physiology and Behavior 79, 2537.
Hilbert, A., Tuschen-Cafer, B., 2007. Maintenance of binge eating through negative
mood: a naturalistic comparison of binge eating disorder and bulimia nervosa.
International Journal of Eating Disorders 40, 521530.
Hilbert, A., Tuschen-Cafer, B., Karwautz, A., Niederhofer, H, Munsch, S., 2007.
Eating disorder examination-questionnaire. Evaluation der deutschsprachigen
Uebersetzung. Diagnostica 53, 144154.
Hilbert, A., Tuschen-Cafer, B., Ohm, M., 2004. Eating disorder examination: Eine
Deutschsprachige version des strukturierten Essstoerungsinterviews. Diagnostica 50, 98106.
Holtkamp, K., Herpertz-Dahlmann, B., Mika, C., Heer, M., Heussen, N., Fichter, M.,
Herpertz, S., Senf, W., Blum, W.F., Schweiger, U., Warnke, A., Ballauff, A., Remschmidt,
H., Hebebrand, J., 2003. Elevated physical activity and low leptin levels co-occur in
patients with anorexia nervosa. Journal of Clinical Endocrinology and Metabolism
88, 51695174.
Hudson, J.I., Hiripi, E., Harrison, G.P., Kessler, R.C., 2007. The prevalence and
correlates of eating disorders in the national comorbidity survey replication.
Biological Psychiatry 61, 348358.
Kaye, W., 2008. Neurobiology of anorexia and bulimia nervosa. Physiology and
Behavior 94, 121135.

E. Naumann et al. / Psychiatry Research 215 (2014) 711717

Kuehner, C., Buerger, C., Keller, F., Hautzinger, M., 2007. Reliabilitaet und Validitaet
des revidierten Beck-Depressionsinventars (BDI-II). Der Nervenarzt 78,
651656.
Le Grange, D., Swanson, S.A., Crow, S.J., Merikangas, K.R., 2012. Eating disorder not
otherwise specied presentation in the US population. International Journal of
Eating Disorders 45, 711718.
Merwin, R., Zucker, N., Lacy, J., Elliott, C., 2010. Interoceptive awareness in eating
disorders: distinguishing lack of clarity from nonacceptance of internal experience. Cognition and Emotion 24, 892902.
Mitchell, J.E., Crow, S., 2006. Medical complications of anorexia nervosa and
bulimia nervosa. Current Opinion in Psychiatry 19, 438443.
Morris, A., Do, D., Gottlieb-Smith, R., Ng, J., Jain, A., Wright, S., Shochet, R., 2012.
Impact of a tness intervention on medical students. Southern Medical Journal
105, 630634.
Nordb, R.H.S., Espeset, E.M.S., Gulliksen, K.S., Skrderud, F., Holte, A., 2006. The
meaning of self-starvation: qualitative study of patients0 perception of anorexia
nervosa. International Journal of Eating Disorders 39, 556564.
Norman, D.K., Herzog, D.B., 1983. Bulimia, anorexia nervosa, and anorexia nervosa
with bulimia: a comparative analysis of MMPI proles. International Journal of
Eating Disorders 2, 4352.
Peas-Lled, E., Vaz Leal, F.J., Waller, G., 2002. Excessive exercise in anorexia
nervosa and bulimia nervosa: relation to eating characteristics and general
psychopathology. International Journal of Eating Disorders 31, 370375.
Pirke, K.M., Broocks, A., Wilckens, T., Marquard, R., Schweiger, U., 1993. Starvationinduced hyperactivity in the rat: the role of endocrine and neurotransmitter
changes. Neuroscience and Biobehavioral Reviews 17, 287294.
Plies, A., Florin, I., 1992. Effects of negative mood induction effects of negative mood
induction on the body image of restrained eaters. Psychology and Health 7,
235242.
Rossiter, E.M., Wilson, G.T., Goldstein, L., 1989. Bulimia nervosa and dietary
restraint. Behavior Research and Therapy 27, 465468.
Rottenberg, J., Ray, R.D., Gross, J.J., 2007. Emotion elicitation using lms. In: Coan, J.
A., Allen, J.J.B. (Eds.), The Handbook of Emotion Elicitation and Assessment.
Oxford University Press, New York, pp. 924.
Rucken, D.D., Petty, R.E., 2004. Emotion specicity and consumer behavior: anger,
sadness, and preference for activity. Motivation and Emotion 28, 321.
Schwartz, G.E., Weinberger, D.A., Singer, J.A., 1981. Cardiovascular differentiation of
happiness, sadness, anger, and fear following imagery and exercise. Psychosomatic Medicine 43, 343364.
Serpell, L., Treasure, J., Teasdale, J., Sullivan, V., 1999. Anorexia nervosa: friend or
foe?. International Journal of Eating Disorders, 25; , pp. 177186.

717

Smyth, J.M., Wonderlich, S.A., Heron, K.E., Sliwinski, M.J., Crosby, R.D., Mitchell, J.E.,
Engel, S.G., 2007. Daily and momentary mood and stress are associated with
binge eating and vomiting in bulimia nervosa patients in the natural environment. Journal of Consulting and Clinical Psychology 75, 629638.
Solenberger, S.E., 2001. Exercise and eating disorders: a 3-year inpatient hospital
record analysis. Eating Behaviors 2, 151168.
Steiger, H., Lehoux, P.M., Gauvin, L., 1999. Impulsivity, dietary control and the urge
to binge in bulimic syndromes. International Journal of Eating Disorders 26,
261274.
Stice, E., 2001. A prospective test of the dual-pathway model of bulimic pathology:
mediating effects of dieting and negative affect. Journal of Abnormal Psychology 110, 124135.
Strober, M., Freeman, R., Morrell, W., 1997. The long-term course of severe anorexia
nervosa in adolescents: survival analysis of recovery, relapse, and outcome
predictors over 10-15 years in a prospective study. International Journal of
Eating Disorders 22, 339360.
Svaldi, J., Griepenstroh, J., Tuschen-Cafer, B., Ehring, T., 2012. Emotion regulation
decits in eating disorders: a marker of eating pathology or general psychopathology? Psychiatry Research 197, 103111.
Tabachnick, B.G., Fidell, L.S., 2007. Using Multivariate Statistics, 5th ed. Pearson
Education Inc, Boston.
Tuschen-Cafer, B., Voegele, C., 1999. Psychological and physiological reactivity to
stress: an experimental study on bulimic patients, restrained eaters and
controls. Psychotherapy and Psychosomatics 68, 333340.
Vansteelandt, K., Rijmen, F., Pieters, G., Probst, M., Vanderlinden, J., 2007. Drive for
thinness, affect regulation and physical activity in eating disorders: a daily life
study. Behavior Research and Therapy 45, 17171734.
Waller, G., Babbs, M., Milligan, R., Meyer, C., Ohanian, V., Leung, N., 2003. Anger and
core beliefs in the eating disorders. International Journal of Eating Disorders 34,
118124.
Waters, A., Hill, A., Waller, G., 2001. Internal and external antecedents of binge
eating episodes in a group of women with bulimia nervosa. International
Journal of Eating Disorders 29, 1722.
Wildes, J.E., Marcus, M.D., Bright, A.C., Dapelo, M.M., Psychol, M.C., 2012. Emotion
and eating disorder symptoms in patients with anorexia nervosa: An experimental study. International Journal of Eating Disorders 45, 876882.
Wildes, J.E., Ringham, R.M., Marcus, M.D., 2010. Emotion avoidance in patients with
anorexia nervosa: Initial test of a functional model. International Journal of
Eating Disorders 43, 398404.
Wittchen, H., Zaudig, M., Fydrich, T., 1997. Strukturiertes Klinisches Interview fuer
DSM-IV, Achse I und II. Hogrefe, Goettingen.

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