Physiology & Behavior 142 (2015) 2027

Contents lists available at ScienceDirect

Physiology & Behavior

journal homepage: www.elsevier.com/locate/phb

Binge eating disorder and obesity: Preliminary evidence for distinct

cardiovascular and psychological phenotypes
Rebecca R. Klatzkin a,, Sierra Gaffney a, Kathryn Cyrus a, Elizabeth Bigus a, Kimberly A. Brownley b
a
b

Department of Psychology, Rhodes College, TN, USA

Department of Psychiatry, The University of North Carolina at Chapel Hill, NC, USA

H I G H L I G H T S

Obese women with binge eating disorder (BED) were compared to obese and normal weight non-BED women.
Obese BED group reported greater depression, perceived stress, and eating psychopathology.
Obese BED showed greater blood pressure, negative affect, and anxiety irrespective of stress task.
Stress-induced change in hunger was associated with cardiovascular measures in obese BED only.
Results indicate that BED and obesity are distinct in terms of psychological and physiological stress-related factors

a r t i c l e

i n f o

Article history:
Received 19 August 2014
Received in revised form 13 January 2015
Accepted 15 January 2015
Available online 16 January 2015
Keywords:
Binge eating disorder
Obesity
Stress
Cardiovascular
Hunger

a b s t r a c t
This study investigated cardiovascular functioning, mood, and eating-related psychological factors at rest and in
response to mental stress in three groups of women: 1) Obese women with binge eating disorder (BED; n = 9);
2) obese non-BED women (n = 15); and 3) normal weight (NW) non-BED women (n = 15). Compared to both
obese and NW non-BED women, obese women with BED showed heightened overall blood pressure and reported greater depression symptoms, perceived stress, and eating-related psychopathology. Additionally, obese
women with BED reported greater overall negative affect and state anxiety compared to obese non-BED
women. The heart rate response to stress was blunted in the obese BED group compared to the other groups,
but this effect was no longer signicant after controlling for baseline differences in depression. Correlational analyses revealed a positive association between stress-induced changes in hunger and cardiovascular measures only
in obese women with BED. Longitudinal studies are needed to determine if stress dysregulation and stressinduced increases in hunger contribute to the onset and/or maintenance of BED. In particular, studies utilizing
an additional NW BED control group are warranted in order to further examine the impact of BED above and beyond the impact of obesity on psychophysiological functioning and to inform the growing literature regarding
stress-related factors that distinguish the BED and obesity phenotypes.
2015 Elsevier Inc. All rights reserved.

1. Introduction
Over one-third of adults in the United States are obese [34]. Obesity
and obesity-related health conditions such as heart disease, stroke, type
2 diabetes, and certain cancers [33] constitute a signicant public health
problem costing the United States an estimated $147 billion annually
[10]. Recent ndings project that cumulative lifetime exposure to excess
weight and related comorbid conditions will increase due to earlier
onset of obesity [52]. Thus, there is a clear need for a greater understanding of the etiology of obesity and its correlates in order to inform
prevention and treatment efforts.
Corresponding author at: Rhodes College, 2000 North Parkway, Memphis, TN 38112,
USA.
E-mail address: klatzkinr@rhodes.edu (R.R. Klatzkin).

http://dx.doi.org/10.1016/j.physbeh.2015.01.018
0031-9384/ 2015 Elsevier Inc. All rights reserved.

One such correlate of obesity is binge eating. Binge eating involves

the consumption of an amount of food that is denitely larger than
most people would consume under like circumstances over a relatively
brief (e.g., within any 2-hour) discrete period of time. When binge eating occurs with sufcient regularity and is accompanied by various hallmark behavioral and psychological symptoms, an individual may be
diagnosed with binge-eating disorder (BED). BED is characterized by recurrent (at least 1 day per week for 3 months) binge-eating episodes
that occur in the absence of regular compensatory behaviors such as
purging. These binge episodes often involve eating more rapidly than
normal and until uncomfortably full and they are associated with feeling
depressed, disgusted, or guilty after overeating [1]. In the U.S., approximately 3.5% of women and 2.0% of men suffer from BED in their lifetimes
[24]. BED and obesity are highly comorbid, as individuals with BED are
more likely to be obese [37] and the prevalence of BED is nearly 2-fold

R.R. Klatzkin et al. / Physiology & Behavior 142 (2015) 2027

greater in obese compared to non-obese adults. Moreover, BED becomes more prevalent with greater obesity severity [7,47] and the prevalence of BED is higher among individuals who are seeking treatment
for obesity (2030%) compared to those in the general population [24,
49,50].
BED is associated with considerable psychological and physiological
dysfunction that distinguishes it from obesity [4,20,35,40,50,55,56]; it
aggregates in families independently of obesity and is caused in part
by familial factors distinct from those for obesity [23]. Yet, additional
studies are needed to further differentiate the BED phenotype from
the obesity phenotype in order to inform treatment development [50,
55]. The present study addressed this need by examining cardiovascular
and psychological stress reactivity in individuals with and without BED
across the weight spectrum.
Stress has been implicated in the etiology of BED [31,39,45,46] as
well as in the onset and maintenance of obesity (for review, see [48]).
The release of glucocorticoids following stress increases appetite as
well as the preference for comfort foods, a combination of factors that
nurture the development of binge eating and obesity (for reviews, see
[29,48]). Binge eating is associated with elevated levels of perceived
stress [39,54], and perceived stress is a precursor to binge eating in
non-clinical populations [5,13,21,38]. Furthermore, following a laboratory stressor, obese women with BED show increased hunger, desire
to binge eat, and rates of consumption of highly palatable foods compared to obese non-BED women [17,42].
Studies comparing the physiological stress response in obese BED
and non-BED individuals have been scarce and results have been
mixed, including greater reductions in parasympathetic activity [14],
blunted autonomic responses to stress and impaired stress recovery
[30], as well as heightened [17], blunted [41], or no differences [43] in
hypothalamicpituitaryadrenal (HPA) axis responses in obese BED
groups. One potential reason for the discrepancy in the literature may
be the lack of consistency in the comparison group(s). The vast majority
of prior studies have compared obese BED to obese non-BED control
groups, reporting signicant differences in cardiovascular, HPA-axis,
and psychological factors and thus evidence that it is the disorder, and
not obesity, contributing to the dysregulation seen in obese BED individuals [4,14,17,30,40,43,56]. In the absence of a normal weight (NW) control group, however, the relative importance of these differences cannot
be determined. That is to say, the impact of BED above and beyond the
impact of obesity on physiological and psychological dysfunction remains unclear.
Lo Sauro and colleagues [27] conducted an extensive review of the
literature on stress in eating disorders; based on their qualitative analysis, HPA-axis dysregulation observed in BED and obese individuals was
attributed mainly to excess weight. This conclusion was based on data
from studies assessing either BED participants only, obese participants
only, or comparing BED groups to obese non-BED groups. More recently,
however, Rosenberg et al. [41] found that obese BED individuals showed
blunted cortisol responses to stress as well as a positive association between the cortisol stress response and stress-induced increases in the
desire to binge eat and sweet cravings compared to both obese and
NW non-BED groups, suggesting that stress dysregulation in BED may
be a function of the disorder itself and not strictly obesity. Given that
these ndings pertain only to HPA-axis functioning, the current study
investigated the second major component of the stress axis, the sympathetic nervous system. The goal of the present study, therefore, was to
expand upon these recent ndings by investigating cardiovascular and
psychological stress responses in three groups of women: obese BED,
obese non-BED, and NW non-BED. The primary hypotheses were that
obese women with BED, as a group, would show greater cardiovascular and psychological stress dysregulation and eating-related psychopathology as well as greater overall perceived stress and depressive
symptoms compared to both groups of obese and NW non-BED
women. Furthermore, given the association between stress, hunger, and
food consumption in BED [17,42], our secondary hypothesis was that

21

obese women with BED would report greater increases in hunger following stress than both obese and NW non-BED women. For both our primary and secondary hypotheses, we expected that obese and NW non-BED
women would not differ signicantly from each other.
2. Materials & methods
2.1. Participants
The 39 women (1950 years of age) who comprise this report were
recruited via newspaper and posted advertisements online and in local
businesses targeting women who were overweight and not taking
blood pressure, stimulant, or psychoactive medications. These medications were exclusionary due to their inuence on cardiovascular
functioning and other variables of interest to the current study (e.g.
hunger, negative affect, and anxiety). Importantly, no advertisements
specically targeted women with BED or any eating disorder. Our recruitment strategies ensured that participants remained blind to the
study's main variable of interest, BED diagnostic status, in order to diminish demand characteristics. Participants were told that the purpose
of the study was to investigate the inuence of the menstrual cycle on
responses to mental stress in overweight and normal weight women.
A small percentage of advertisements eliminated the term overweight
in order to obtain our normal weight (NW) sample.
The nal sample of participants was composed of three groups:
1) Obese women with BED (n = 9); 2) obese non-BED women (n =
15); and 3) NW non-BED women (n = 15). All women in the BED
group met full DSM-V criteria for BED and women in the non-BED
groups had no history of any eating disorders. Participants in the two
obese groups had a body mass index (BMI) between 29 and 47 and
the NW group had a BMI between 19 and 24. The protocol was approved by the Institutional Review Board of Rhodes College and all participants provided informed, written consent. Participants received $45
compensation.
2.2. Preliminary screening protocol
Women responding to our advertisements received a link via email
directing them to a set of online screening questions aimed at excluding
prospective participants who were pregnant or breastfeeding, postmenopausal, taking prescription medication (excluding oral contraceptives,
see Table 1), had a cardiovascular disorder, or were regular smokers.
Women were also excluded if they reported seeking treatment for
weight or eating issues. This exclusionary criterion was intended to

Table 1
Mean ( SEM) demographic and baseline measures as a function of BED and obesity
status.

Body mass index a

Current major depressive or
anxiety disorder (%) b
Age
Minority race (%)
Oral contraceptive use (%)c
Beck depression inventory b
Perceived stress scale d
Restraint b
Eating concern b
Shape concern b
Weight concern b,e
Binge eating scale b
a
b
c
d
e

NW non-BED
n = 15

Obese non-BED
n = 15

Obese BED
n=9

21.5 (0.5)
2 (13%)

35.3 (1.3)
1 (7%)

37.9 (1.6)
8 (89%)

28.8 (1.7)
8 (53%)
5 (33%)
11.3 (2.6)
17.8 (2.5)
0.6 (0.2)
0.1 (0.03)
1.0 (0.2)
0.4 (0.1)
3.9 (0.6)

26.8 (1.2)
9 (60%)
1 (2%)
5.3 (1.2)
12.7 (1.1)
0.3 (0.1)
0.1 (0.04)
1.5 (0.2)
1.2 (0.2)
4.6 (1.3)

33.3 (3.1)
7 (78%)
0 (0%)
29.8 (3.9)
24.9 (2.4)
2.1 (0.3)
3.6 (0.5)
4.8 (0.5)
4.4 (0.4)
29.5 (3.9)

NW non-BED b obese BED and obese non-BED, p b .001.

Obese BED N obese non-BED and NW non-BED, p b .001.
NW non-BED N obese BED and obese non-BED, p b .05.
Obese BED N obese non-BED, p .01.
Obese non-BED N NW non-BED, p b .05.

22

R.R. Klatzkin et al. / Physiology & Behavior 142 (2015) 2027

prevent the potentially confounding inuence of treatment-related

coping strategies or awareness regarding the relationship between
stress, mood, and eating. A preliminary indication of BED was also
assessed via completion of the Eating Disorders Examination Questionnaire (see below) and later conrmed at study Visit #1.
2.3. Determination of eligibility
Of the 340 women who completed the preliminary screening protocol, 80 eligible participants proceeded to the laboratory for Visit #1.
During this session, participants underwent the Structured Clinical
Interview for DSM-IV Axis I disorders (SCID-I/NP; [11]) to determine
BED diagnostic status and to assess current Axis I mood and anxiety disorders. Height (cm) and weight (kg) were also assessed to calculate BMI
(kg/m2) and blood pressure measurements were taken with the
Oscar 2 oscillometric ambulatory blood pressure monitor (SunTech
Medical Instruments, Inc., Raleigh, NC). Women were excluded
from the study if they had a resting blood pressure N 159/99, were underweight (BMI b 19) or overweight (BMI between 25 and 28), or had a current Bipolar Disorder, Substance Abuse Disorder, Panic Disorder, or an
Eating Disorder other than BED. Because mood (26%) and anxiety
(24.5%) disorders are the most common co-morbidities with BED [58],
current Major Depressive Disorder and Anxiety Disorders (other than
Panic Disorder) were not considered exclusionary criteria unless psychotropic medications were being taken (see Table 1 below). If inclusionary
criteria were met, participants were asked to call the laboratory on day
1 of their next menstrual cycle to schedule laboratory Visit #2.
2.4. Procedure
Visit #2, the experimental protocol, took place during the follicular
phase (days 17) of the menstrual cycle and began between the hours
of 2:00 pm and 5:00 pm. The participants were asked to refrain from
eating and drinking anything other than water for at least one hour
prior to testing. Compliance was conrmed upon arrival.
2.4.1. Baseline rest
Participants completed questionnaires assessing perceived stress, depression symptoms, negative affect, anxiety, and hunger (see below). Immediately following, participants rested quietly for 10 min in order to
establish a baseline for stress testing.
2.4.2. The Trier Social Stress Test (TSST)
The TSST [26] is a stress test which reliably induces large and consistent cardiovascular responses and involves four components: 1) PreTask Instructions (5 min): The researcher informed the participants
that they will be giving a speech serving as an interview for their ideal
job. Researchers also explained that the speech will be audio- and
video-recorded for later analysis and will be followed by a serial subtraction task. Participants were then introduced to the selection committee who they were told would later listen to their job talk. This
committee was composed of three well-trained undergraduate research
assistants wearing white laboratory coats; 2) Speech Preparation Period
(5 min): The experimenter asked participants to imagine that they were
applying for their ideal job and to take 5 min to prepare their speech describing why they would be the ideal candidate for the position;
3) Speech (5 min): Immediately following the preparation period, the
selection committee returned to the testing room and asked the participants to deliver their speech. If the participant nished before 5 min,
the committee responded in a standardized way, with prepared questions to ensure that participants spoke for the entire period; and 4) Serial
Subtraction (5 min): The experimenter asked the participants to perform mental arithmetic by serially subtracting 13 from 2000 aloud as
quickly and accurately as possible. Their progress was monitored, and
when an error was made, the experimenter told the participants to
start over from the beginning. Finally, the participants completed

questionnaires measuring negative affect, anxiety, and hunger to obtain

subjective measures immediately followings stress.
2.5. Self-report questionnaires
Participants completed the Eating Disorders Examination Questionnaire (EDE-Q; [59]), adapted from the Eating Disorders Examination Interview, during the preliminary screening protocol to assess overall
eating-related psychopathology. The EDE-Q is a 36-item self-report
questionnaire of which 22 items yield four subscales' scores pertaining
to restraint, eating concern, shape concern, and weight concern in addition to a global score (range = 04). The questionnaire is scored using a
06 forced-choice, rating scale with variable anchors depending on the
question. Greater scores indicate more severe eating-related
psychopathology.
During baseline rest of Visit #2, binge eating was assessed using the
Binge Eating Scale [18] which consists of 16 forced-choice questions,
each with a set of three to four answer choices. Higher scores indicate
greater binge eating severity. The overall level of perceived life stress
was also measured during this time using the Perceived Stress Scale
(PSS; [60]). Items assess how unpredictable, uncontrollable, and
overloaded respondents view their lives, and directly inquire about
levels of experienced stress in the past month with answer choices
ranging from 0 (Never) to 4 (Very Often). Higher scores indicate greater
perceived stress. Self-reported depression symptoms were also measured during baseline rest using the 21-item Beck Depression Inventory
(BDI; [61]). This scale comprehensively assesses dysphoric symptoms,
including affective, cognitive, somatic, overt behavior, and interpersonal
symptoms of depression. Each forced-choice question has a set of at
least four possible answer choices, with increasing severity of depressive symptoms from 0 to 3.
Questionnaires assessing state anxiety, negative affect, and hunger
were administered at baseline rest and immediately post-stress. The
state anxiety portion of the Spielberger State-Trait Anxiety Questionnaire (STAI state; [62]) was used to assess self-reported situational anxiety levels and contains 21 statements describing how an individual
may feel at the present moment. Participants rate how they currently
feel on a scale from 1 (Not at all) to 4 (Very much so) and higher scores
indicate greater levels of state anxiety. Negative affect was assessed
using the Prole of Mood States (POMS-BI; [63]) which consists of 72
items related to mood and assesses both positive and negative affective
dimensions on a scale from 0 (Much unlike this) to 2 (Much like this).
Higher scores indicate greater negative affect. Finally, participants
rated their current level of hunger on a Hunger Visual Analog Scale
(VAS) from 0 (Not hungry) to 6 (Very hungry).
2.6. Cardiovascular measurements
The Oscar 2 oscillometric ambulatory blood pressure monitor
(SunTech Medical Instruments, Inc., Raleigh, NC) with an appropriately
sized arm cuff provided automated measurement of systolic blood pressure (SBP), diastolic blood pressure (DBP) and HR during the testing
session. All measurements took place while participants were in a comfortable seated position. Blood pressure and heart rate measures were
taken at minutes 1, 5, and 10 of baseline rest and minutes 0, 2, and 4
of both the speech and serial subtraction periods; values were averaged
to compute task levels.
3. Data analysis
3.1. Demographic and baseline measurements
Group differences in demographic factors were examined using a
Multivariate ANOVA for continuous variables and chi square analyses
for dichotomous variables as appropriate. A Multivariate ANOVA was
also used to assess group differences in eating-related psychopathology

R.R. Klatzkin et al. / Physiology & Behavior 142 (2015) 2027

using the four subscales of the EDE-Q (eating concern, shape concern,
weight concern, and restraint) and the score on the Binge Eating Scale.
Where signicant results emerged, post-hoc analyses with Bonferroni
corrections were conducted. Group differences in baseline depression
symptoms, perceived stress, state anxiety, negative affect, and hunger
were investigated using a Multivariate ANCOVA, with oral contraceptive
use as the covariate. Sidak corrected post-hoc comparisons were performed to determine specic group differences.
3.2. Cardiovascular and subjective psychological measurements
Separate repeated measures ANCOVAs were used to analyze cardiovascular factors, with Group (Obese BED, Obese non-BED, NW-nonBED) as the between-subject factor, and Time (Baseline, Speech Stress,
Math Stress) as the within-subject factor, with oral contraceptive use
as the covariate. Separate repeated measures ANCOVAs were also used
to analyze negative affect, state anxiety, and hunger, with Group
(Obese BED, Obese non-BED, NW-non-BED) as the between-subject factor, and Time (Baseline, Stress) as the within-subject factor, with oral
contraceptive use as the covariate. When group differences emerged,
Sidak corrected post-hoc comparisons were performed. When signicant interactions emerged, subsequent univariate ANCOVAs and repeated measures ANCOVAs performed separately by Group were used to
explore the nature of the interaction.
Given that depressive symptoms are associated with dysregulations
in cardiovascular stress responses in controls [3,36] and in women with
disordered eating [16], follow-up ANCOVAs were used to determine if
group differences in cardiovascular factors remained after adjusting
for differences in baseline depressive symptoms.
3.3. Relationship between cardiovascular stress responses, hunger, and
eating-related psychopathology
In order to determine if eating-related psychopathology (EDE-Q
subscale scores) and stress-induced hunger were associated with
cardiovascular responses to stress, Pearson productmoment
(Pearson's r) correlations were performed in each diagnostic group separately as well as the entire sample as a whole. Changes in cardiovascular
factors were calculated by subtracting baseline from speech stress values.
Speech stress values were chosen because this task was more effective at
increasing cardiovascular measures from baseline compared to the math
task (main effect of stress task [speech vs. math] for SBP, DBP, and HR:
Fs(1,35) = 8.830.2, ps b .01).
Reliability analysis for hunger and eating-related psychopathology
measures revealed a high internal consistency (Cronbach's alpha =
0.70). Consequently, only dietary restraint, eating concern, and stressinduced change in hunger were used in the correlational analyses
(Cronbach's alpha = 0.10) along with stress-induced changes in SBP,
DBP, and HR.

covariate in all stress-related analyses. Furthermore, the obese BED

group endorsed greater depression symptomatology than women in
both obese and NW non-BED groups (ps b .001), and higher perceived
stress than the obese non-BED group (p b .01).
4.2. Eating-related psychopathology
Group differences emerged in the EDE-Q subscales (Fs (2,36) =
22.892.6, ps b .001), and the BES, F(2,36) = 91.9, p b .001 (see
Table 1). Specically, women in the obese BED group had higher
scores on EDE-Q subscales of restraint, eating concern, shape concern, and weight concern as well as on the BES compared to both
obese and NW non-BED groups (ps b .001). The obese non-BED
group also reported greater weight concern than the NW non-BED
group (p b .05).
4.3. Subjective psychological ratings
Groups differed in negative affect, F(2,35) = 5.9, p b .01, state anxiety, F(2,35) = 6.1, p b .01, and hunger, F(2,35) = 3.4, p b .05, irrespective of Time (Figs. 13). Women in the obese BED group endorsed
greater overall negative affect and state anxiety ratings than the obese
non-BED group (ps b .01), while hunger ratings were numerically, but
not signicantly higher in NW non-BED women compared to obese
non-BED women (p = .08).
4.4. Cardiovascular measurements
Both the speech and math tasks induced signicant increases in SBP,
DBP, and HR from baseline, Fs(1,36) = 27.75148.8, ps b .001. Groups
differed in SBP, F(2,35) = 3.7, p b .05, and DBP, F(2,35) = 3.3, p =
.05, irrespective of Time. Women in the obese BED group had signicantly higher overall SBP than the NW non-BED group (p b .05)
(Fig. 4), and numerically, although not signicantly, higher overall
DBP compared to obese (p = .07) and NW non-BED groups (p = .10)
(Fig. 5). Stronger effects of Group on SBP and DBP emerged following
adjustments for depression symptoms, as the obese BED group showed
higher overall SBP, F(2,34) = 5.3, p b .05, and DBP, F(2,34) = 4.2, p b .05,
compared to both obese and NW non-BED groups (ps b .05).
Mauchly's test indicated that the assumption of sphericity had been
violated during the analysis of HR, 2 (2) = 61.5, p b .001, and therefore
degrees of freedom were corrected by using the GreenhouseGeisser estimates of sphericity ( = 0.69). With this correction, a Group Time interaction for HR emerged, F(3,48) = 3.1, p b .05. Simple effect analyses
were unable to explain the interaction, as no signicant Group differences
emerged at any time point and each Group showed signicant main

155

4. Results

NW non-BED

135

Negave Aect

4.1. Demographics and baseline measures

As summarized in Table 1, group differences emerged for BMI,
F(2,36) = 65.6, p b .001, current MDD or anxiety disorder, 2 (2) =
21.4, p b .001, oral contraceptive use, 2 (2) = 6.22, p b .05, baseline
measures of depression symptoms, F(2,35) = 20.6, p b .001, and perceived stress, F(2,35) = 7.6, p b .01, while groups did not differ on
mean age or proportion minority race (ps N .05). Specically, BMI was
lower in the NW non-BED group compared to both the obese nonBED and obese BED groups (ps b .001), and a greater percentage of
obese women with BED had a current MDD or anxiety disorder compared to both obese and NW non-BED groups. Oral contraceptive use
was greater in the NW non-BED group than the obese non-BED and
obese BED groups and, consequently, this variable was used as a

23

Obese non-BED
Obese BED

115
95
75
55
35
Baseline

Stress

Fig. 1. Mean (SEM) negative affect ratings at baseline and post-stress as a function of
BED and obesity status. Main effect of group, F(2,35) = 5.9, p b .01. BED N obese (p b .01).

24

R.R. Klatzkin et al. / Physiology & Behavior 142 (2015) 2027

65

170
NW non-BED
Obese non-BED

State Anxiety

55

Obese BED

50
45
40
35
30

NW non-BED
Systolic Blood Pressure (mmHg)

60

160

Obese non-BED
Obese BED

150
140
130
120

25
Baseline

Stress

110
Baseline

Fig. 2. Mean (SEM) state anxiety ratings at baseline and post-stress as a function of BED
and obesity status. Main effect of group, F(2, 35) = 6.1, p b .01. BED N obese (p b .01).
BED N NW (p = .08).

effects of Time (ps b .05). However, the effect of Time in the obese BED
group (p = .03) was less robust than both non-BED groups (ps = .002
and .0001 in obese and NW, respectively), suggesting blunted HR stress
responsiveness in obese BED women (Fig. 6). Following adjustments for
depression symptoms, this Group Time interaction for HR was no longer signicant (p N .05).

4.5. Relationship between cardiovascular stress responses, hunger, and

eating-related psychopathology
Overall, stress-induced changes in cardiovascular measures were
not related to dietary restraint, eating concern, or stress-induced changes in hunger ratings. Outliers for delta hunger were present, with one
participant in the NW non-BED group reporting a hunger decrease of
3, and one participant in the obese non-BED group reporting a hunger
decrease of 4, values that were much greater than the average for that
particular group (i.e. less than the rst quartile minus three times the interquartile range). When these outliers were removed, the results of the
correlational analyses in the sample as a whole did not change.
Within the obese BED group, more positive stress-induced changes
in hunger were associated with greater stress-induced changes in SBP
(r = 0.76, p b .01) and DBP (r = 0.78, p b .01) (Figs. 7 and 8,
respectively).

Speech

Math

Fig. 4. Mean (SEM) systolic blood pressure across baseline, speech stress, and math
stress as a function of BED and obesity status, adjusting for depression symptoms. Main effect of group, F(2,34) = 5.3, p b .05. Obese BED N obese non-BED and NW non-BED
(ps b .05).

Within the obese non-BED group, high dietary restraint was associated with greater stress-induced changes in HR, r = 0.55, p b .05. These
results did not change following the removal of the hunger outlier that
occurred within this group.
Within the NW non-BED group, no signicant associations emerged
initially. Following the removal of the hunger outlier that occurred
within this group, stress-induced changes in hunger scores were negatively correlated with stress-induced changes in DBP, r = 0.53, p =
.05, and HR, r = 0.66, p b .05.
5. Discussion
The goal of the present study was to investigate the distinct versus
shared phenotypes between BED and obesity with respect to cardiovascular functioning, mood- and stress-related psychological measures,
and eating-related psychopathology. The results supported our primary
hypotheses: compared to both obese and NW non-BED women, obese
women with BED showed heightened overall blood pressure and

4
NW non-BED
Obese non-BED

Hunger

Obese BED

Diastolic Blood Pressure (mmHg)

105

NW non-BED

100

Obese non-BED
Obese BED

95
90
85
80
75
70
65
Baseline

0
Baseline

Speech

Math

Stress

Fig. 3. Mean (SEM) hunger ratings at baseline and post-stress as a function of BED and
obesity status. Main effect of group, F(2,35) = 3.4, p b .05. NW non-BED N obese non-BED
(p = .08).

Fig. 5. Mean (SEM) diastolic blood pressure across baseline, speech stress, and math
stress as a function of BED and obesity status, adjusting for depression symptoms. Main effect of group, F(2,34) = 4.2, p b .05. Obese BED N obese non-BED and NW non-BED
(ps b .05).

R.R. Klatzkin et al. / Physiology & Behavior 142 (2015) 2027

96

Obese non-BED

86

Obese BED

81
76
71

Change in hunger rangs

NW non-BED

91
Heart Rate (bpm)

25

66

1
0
-1
-2
-3
-4
0

61
Speech

20

Math

Fig. 6. Mean (SEM) heart rate across baseline, speech stress, and math stress as a function of BED and obesity status, adjusting for depression symptoms.

reported greater depression symptoms; perceived stress; dietary restraint; and eating, shape, and weight concerns. Additionally, obese
women with BED reported greater overall negative affect and state anxiety compared to obese non-BED women. These results indicated
heightened physiological and psychological dysfunction in BED independent of obesity and irrespective of acute mental stress. Our secondary hypothesis predicting greater increases in hunger following stress
for obese women with BED was also supported, although indirectly.
While the change in hunger following stress did not differ as a function
of BED diagnostic status, correlational analyses revealed a positive association between stress-induced changes in hunger and cardiovascular
measures only in obese women with BED.
Although previous studies have assessed psychopathology and
stress-related mechanisms in obese BED versus obese non-BED controls,
this is the rst study to show distinctions in cardiovascular and psychological functioning between obese women with BED and both obese and
NW non-BED women. Inclusion of the NW non-BED control group
allowed for further differentiation between the effects of BED and the
effects of obesity, particularly with respect to the relationship between
cardiovascular and hunger responses to stress. Within the NW nonBED group, women who had greater cardiovascular responses to stress
showed no changes or decreases in hunger from baseline. In contrast,
women in the obese BED group who demonstrated greater cardiovascular reactivity showed more positive changes in hunger ratings poststress. No relationship between these factors existed for the obese
non-BED group. These results are in line with previous studies reporting
increased eating rates, hunger, and desire to binge eat following stress
in obese women with BED [17,42] and indicate that for these individuals, stress-induced binge eating may be a function of increased hunger
accompanying normal physiological responses to stress.
One explanation for the reported positive relationship between cardiovascular and hunger responses to stress in obese women with BED
may arise from the heightened negative affect, dietary restraint, and
anxiety reported by this group. Negative affect and dietary restraint
have been proposed as mechanisms underlying stress-induced eating
in healthy controls [9,57], whereas anxiety and negative affect have
been linked to binge eating and desire to binge eat in individuals with
BED [20,22,32,41]. It is possible that the stress-induced hunger and/or
eating may be contingent upon heightened levels of negative affect, dietary restraint, and anxiety, and that these factors may explain the increased stress-induced hunger and desire to binge eat in BED reported
in previous studies [17,42]. Future research is needed to explore how
these psychological factors may contribute to the relationship between
physiological stress reactivity, stress-induced hunger, and eatingrelated behaviors in BED and obesity.
Extending this line of evidence for the distinction between BED and
obesity were results showing heightened overall blood pressure in the

30

40

50

60

Change in speech SBP

Fig. 7. Changes in hunger ratings were positively correlated with changes in speech SBP
from baseline to stress in obese women with BED, r = 0.76, p b .01.

obese BED group versus obese and NW non-BED women. The tendency
for both non-BED control groups to cluster together on these measures
independent of the obese BED group gives further weight to the argument that it is the eating disorder, not obesity, which is responsible
for the cardiovascular dysregulation reported in the current investigation. Although groups did not differ in their cardiovascular stress reactivity, this nding for a generally unregulated stress system in BED is
similar to the ndings of Gluck et al. [17] who reported greater cortisol
concentrations in obese women with BED versus obese non-BED
women, irrespective of a cold pressor pain stressor. A clear delineation
between groups in the present study did not emerge, however, until
adjustments for depression symptoms were made. Given the link between depressive symptomatology and blunted cardiovascular stress
responses [3,16,36], greater symptoms of depression in the obese BED
group may have suppressed overall cardiovascular functioning. Thus,
controlling for depression symptoms may have allowed for the heightened blood pressure in this group to surface. Although Gluck et al. [17]
reported that depression symptoms did not explain the trend for a hyperactive HPA-axis in BED, our results indicate that prior studies
reporting no differences or attenuated responses in BED versus controls
[41,43] may be a result of greater depression in the BED group that went
unmeasured.
Adjusting for group differences in depressive symptoms also altered
the initial Group Time interaction for HR, suggesting that obese
women with BED showed blunted HR responses to stress compared to
obese and NW non-BED groups. These initial pre-adjustment results
are in line with prior research showing greater reductions in parasympathetic nervous system activity [14] and blunted HR responses to
stress [30] in obese women with BED. One factor that may explain
why these ndings did not withstand adjustment for depressive
2

Change in hunger rangs

Baseline

10

1
0
-1
-2
-3
-4
0

10

15

20

25

30

35

40

Change in speech DBP

Fig. 8. Changes in hunger ratings were positively correlated with changes in speech DBP
from baseline to stress in obese women with BED, r = 0.78, p b .01.

26

R.R. Klatzkin et al. / Physiology & Behavior 142 (2015) 2027

symptoms may be the greater abuse histories in BED [2]. Childhood trauma has been associated with blunted HR responses to speech and math
stressors [28], and although trauma was not assessed in the present report, trauma histories are closely associated with depression symptoms
[25,53]. Thus, attenuated stress-induced increases in HR in obese
women with BED may be a function of greater rates of abuse histories,
with depression potentially playing a mediating role. Further studies are
needed to assess the inuence of both histories of trauma and depression
on cardiovascular functioning in BED and obesity.
The unique characteristics of the population sample in the present
study strengthen the internal validity as well as the generalizability of
our ndings. First, participants were recruited exclusively from the
community in a metropolitan area. This strategy of recruiting from the
community allowed participants to be blind to the study's focus on
BED, eliminating potential group differences in demand characteristics
inherent to studies recruiting from treatment centers and other medical
settings, and also increased the generalizability of our ndings. Secondly, our participants were racially and ethnically diverse. Certain ethnic
and racial groups are more affected by obesity than others, particularly
non-Hispanic African Americans, who have the highest obesity rates
adjusting for age [12]. Thus, understanding obesity and related eating
disorders in this population is critical to inuencing prevalence rates
and treatment success in the community.
Despite its strengths, this study was not without its limitation. The
small sample sizes may have restricted our ability to detect group differences in addition to the ones reported. Replications utilizing a larger
sample, potentially including males in addition to females, are essential.
Furthermore, although ndings regarding the cortisol stress response in
obese women with BED are controversial and inconsistent [17,41,43],
including this measure of HPA-axis functioning may have strengthened
our ndings by adding evidence for dysregulation in both major stress
axes. Lastly, we did not assess food consumption post-stress, an important extension of our hunger data that would extend our understanding
of the relationship between psychophysiological stress measures and
eating-related behaviors in BED and obesity.
In conclusion, BED was associated with a dysregulation in psychophysiological functioning as evidenced by greater eating-related psychopathology, depressive symptoms, and perceived stress, as well as
heightened blood pressure, negative affect, and anxiety over time, irrespective of the stress manipulation. Moreover, the relationship between
stress-induced changes in cardiovascular measures and hunger differed
between obese women with BED and controls, particularly NW nonBED women. Given the vast array of evidence relating both psychological and physiological stress to eating-related behaviors [6,19,44,51], the
dysfunction in these areas reported in the present study may contribute
to the onset and maintenance of the BED.
As a whole, these ndings provide further evidence that BED and
obesity are distinct phenotypes with respect to measures of psychological and physiological stress. In order to substantiate this claim and further isolate the effects of BED from the effects of obesity, future studies
utilizing larger sample sizes as well as an additional NW BED control
group are warranted. In the few studies that have compared NW and
obese BED individuals, similar levels of restraint, eating and shape concerns, depression symptoms, and eating psychopathology have emerged
[8,15]. Prospective studies are needed, however, to determine whether
there is an additive effect of BED and obesity in terms of long term health
outcomes.
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