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Biological Psychology 131 (2018) 96–106

Contents lists available at ScienceDirect

Biological Psychology
journal homepage: www.elsevier.com/locate/biopsycho

Stress-induced eating in women with binge-eating disorder and


obesity
Rebecca R. Klatzkin a,∗ , Sierra Gaffney a , Kathryn Cyrus a , Elizabeth Bigus a ,
Kimberly A. Brownley b
a
Department of Psychology, Rhodes College, TN, USA
b
Department of Psychiatry, The University of North Carolina at Chapel Hill, NC, USA

a r t i c l e i n f o a b s t r a c t

Article history: The purpose of the current study was to investigate stress-induced eating in women with binge-eating
Received 24 May 2016 disorder (BED) and obesity. Three groups of women [obese with BED (n = 9); obese non-BED (n = 11); and
Received in revised form normal weight (NW) non-BED (n = 12)], rated their levels of hunger and psychological distress before and
27 September 2016
after completing the Trier Social Stress Test, followed by food anticipation and then consumption of their
Accepted 3 November 2016
preferred snack food. We differentiated between the motivational and hedonic components of eating
Available online 9 November 2016
by measuring the amount of food participants poured into a serving bowl compared to the amount
consumed. Stress did not affect poured and consumed calories differently between groups. Across all
Keywords:
Binge eating
subjects, calories poured and consumed were positively correlated with post-stress hunger, but calories
Obesity poured was positively correlated with post-stress anxiety and negative affect. These results indicate that
Stress stress-related psychological factors may be more strongly associated with the motivational drive to eat
Hunger (i.e. amount poured) rather than the hedonic aspects of eating (i.e. amount consumed) for women in
general. Exploratory correlation analyses per subgroup suggest that post-stress hunger was positively
associated with calories poured and consumed in both non-BED groups. In the obese BED group, calories
consumed was negatively associated with dietary restraint and, although not significantly, positively
associated with stress-induced changes in anxiety.These findings suggest that stress-induced snacking
in obese BED women may be influenced by psychological factors more so than homeostatic hunger
mechanisms. After controlling for dietary restraint and negative affect, the NW non-BED women ate
a greater percentage of the food they poured than both obese groups, suggesting that obesity may be
associated with a heightened motivational drive to eat coupled with a reduction in hedonic pleasure
from eating post-stress. Further studies that incorporate novel approaches to measuring the motivational
versus hedonic aspects of stress-induced eating may expose nuanced eating behaviors that differentiate
BED and obesity. If confirmed, our findings would support prevention and treatment strategies that target
subsets of women based on obesity and BED status.
© 2016 Elsevier B.V. All rights reserved.

1. Introduction ogy of obesity and its comorbid conditions is imperative in order


to inform prevention and treatment efforts.
Obesity is a global health epidemic that directly affects 20% of Binge eating involves the consumption of an amount of food
the worldwide population and one-third of adults in the United that is larger than most people would consume under like circum-
States (World Heath Statistics, 2015). Obesity is also a leading stances over a relatively brief, discrete period of time (e.g., ≤2 h).
risk factor for mortality among noncommunicable diseases such When binge eating occurs with sufficient regularity and is accom-
as metabolic syndrome, cancer, and cardiovascular disease (World panied by various hallmark symptoms such as loss of control, an
Health Organization, 2009). A greater understanding of the etiol- 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 compen-
satory behaviors such as purging. These binge-eating episodes are
∗ Corresponding author at: Rhodes College, 2000 North Parkway, Memphis, TN likely to be associated with feeling depressed, disgusted, or guilty
38112, USA. after overeating and often involve eating more rapidly than nor-
E-mail address: klatzkinr@rhodes.edu (R.R. Klatzkin).

https://doi.org/10.1016/j.biopsycho.2016.11.002
0301-0511/© 2016 Elsevier B.V. All rights reserved.
R.R. Klatzkin et al. / Biological Psychology 131 (2018) 96–106 97

mal and until uncomfortably full (American Psychiatric Association, stress has only been assessed immediately following a stressor
2013). In the United States, approximately 3.5% of women and (Gluck et al., 2004; Rosenberg et al., 2013; Rutters, Nieuwenhuizen,
2.0% of men suffer from BED in their lifetimes (Hudson, Hiripi, Lemmens, Born, & Westerterp-Plantenga, 2009; Schulz & Laessle,
Pope, & Kessler, 2007). BED is more common than anorexia ner- 2012; van Strien, Roelofs, & de Weerth, 2013). The present study
vosa and bulimia nervosa and represents an equally substantial, if extends the current literature by examining eating behaviors
not greater, public health burden with respect to physical health- 45 min post-stress.
related quality of life, psychiatric comorbidity, and the stable and The current study also explores the possibility of distinct phys-
chronic nature of the disorder (Ágh et al., 2015; Hudson et al., iological and psychological moderators of stress and snacking as a
2007). BED is highly correlated with obesity (Hudson et al., 2007), function of BED and obesity status. The restraint model of binge eat-
and among obese individuals, BED is a marker for greater impair- ing posits that concerns about shape and weight lead to restrained
ment in health-related quality of life (Ágh et al., 2015; Rieger, eating, which promotes binge eating and, in turn, leads to a circular
Wilfley, Stein, Marino, & Crow, 2005) and greater medical and psy- pattern of further restriction and binge eating (Lowe, 1993; Polivy
chiatric morbidity (Bulik, Sullivan, & Kendler, 2002; Greeno, Wing, & Herman, 1985). Dietary restraint is correlated with obesity and
& Shiffman, 2000; Peterson, Latendresse, Bartholome, Warren, & binge-eating behaviors (Andrés & Saldaña, 2014) as well as labora-
Raymond, 2012; Ramacciotti et al., 2008; Striegel-Moore & Franko, tory stress-induced eating in non-clinical samples (for review, see
2008; Wonderlich, Gordon, Mitchell, Crosby, & Engel, 2009). Greeno & Wing, 1994). Obese individuals with BED report greater
Stress has been implicated in both the etiology of BED (Moore dietary restraint than obese non-BED individuals (Bas, Bozan, &
& Cunningham, 2012; Pinaquy, Chabrol, Simon, Louvet, & Barbe, Cigerim, 2008; Klatzkin et al., 2015), but less dietary restraint than
2003; Simon et al., 2006) as well as in the onset and mainte- individuals with bulimia nervosa (Elran-Barak et al., 2015). Fur-
nance of obesity (for review, see Sominsky & Spencer, 2014). thermore, dietary restraint is correlated with reduced activation
Perceived life stress correlates positively with binge eating fre- of brain regions associated with impulse control in obese indi-
quency (Pinaquy et al., 2003; Wolff, Crosby, Roberts, & Wittrock, viduals with BED, but not in their non-BED counterparts (Balodis
2000; Woods, Racine, & Klump, 2010) and is a precursor to binge et al., 2013). Similarly, negative affect is strongly associated with
eating in clinical (Goldschmidt et al., 2014) and non-clinical pop- palatable food intake (Epel, Lapidus, McEwen, & Brownell, 2001;
ulations (Crowther, Sanftner, Bonifazi, & Shepherd, 2001; Freeman Rutters et al., 2009; Telch & Agras, 1996) and binge eating (Haedt-
and Gil, 2004; Groesz et al., 2012; Pike et al., 2006). Labora- Matt & Keel, 2011; Hilbert & Tuschen-Caffier, 2007; Stickney,
tory studies of stress responses and stress-related eating in obese Miltenberger, & Wolff, 1999; Wolff et al., 2000), and has been shown
individuals with and without BED have yielded mixed results, how- to mediate the relationship between stress and binge eating in
ever. Observations include increased hunger, desire to binge eat, bulimia (Goldschmidt et al., 2014). The relationship between neg-
and consumption rates of highly palatable foods (Gluck, Geliebter, ative affect and binge eating has been shown to differ between
Hung, & Yahav, 2004; Rosenberg et al., 2013; Schulz & Laessle, clinical and non-clinical samples (Hilbert & Tuschen-Caffier, 2007;
2012) as well as no differences in stress-induced hunger or over- Wolff et al., 2000), underscoring the need to explore differences in
all food intake (Klatzkin, Gaffney, Cyrus, Bigus, & Brownley, 2015; the relative influence of negative affect on eating behaviors in both
Schulz and Laessle, 2012; Telch & Agras, 1996) in obese BED groups. obesity and BED. In this manner, a recent study reported that cop-
In addition, compared with obese individuals without BED, those ing motives (e.g. the need to cheer up when in a negative mood)
with BED have been shown to exhibit heightened (Gluck et al., were associated with binge-eating severity irrespective of obesity
2004), blunted (Rosenberg et al., 2013), or no differences (Schulz (Boggiano et al., 2014). Thus, moderators of stress and eating may
& Laessle, 2012) in hypothalamic–pituitary–adrenal (HPA) axis have differential effects based on obesity and binge-eating status. A
stress responses as well as greater reductions in parasympathetic greater understanding of the separate predictors of stress-induced
activity (Friederich et al., 2006), blunted autonomic responses eating for obesity and BED may inform the development of tailored
to stress (Messerli-Bürgy, Engesser, Lemmenmeier, Steptoe, & relapse prevention strategies.
Laederach-Hofmann, 2010), and no differences in cardiovascular Taken together, the evidence for distinct stress-related pheno-
stress responses (Klatzkin et al., 2015). types for obesity and BED (Klatzkin et al., 2015; Rosenberg et al.,
These studies differed methodologically and only two of them 2013) and for the strong association between stress and binge eat-
included a normal weight non-BED control group to facilitate ing (Crowther et al., 2001; Freeman & Gil, 2004; Goldschmidt et al.,
understanding of the unique and additive effects of obesity and BED 2014; Groesz et al., 2012; Pike et al., 2006; Pinaquy et al., 2003;
on physiological stress reactivity (Klatzkin et al., 2015; Rosenberg Wolff et al., 2000; Woods et al., 2010) suggests that additional stud-
et al., 2013). Using a 3-group design, we recently reported elevated ies to tease apart the underlying mechanisms of stress-induced
blood pressure and psychological distress throughout rest and eating between these populations are warranted. In order to
mental stress in obese women with BED compared with obese and gain a better understanding of the BED phenotype, we examine
normal weight women without BED, who did not differ from each stress-induced eating behaviors as well as the psychophysiologi-
other (Klatzkin et al., 2015). Thus, it appears that the stress-related cal moderators of the relationship between stress and snacking in
psychophysiological dysfunction in BED occurs independently of women with and without BED across the weight spectrum.
obesity, although further examination of the mechanisms by which Given that stress-induced cortisol activates brain reward path-
the stress-related dysfunction contributes to the eating disorder is ways (Adam & Epel, 2007) and that binge eating and obesity share
warranted. neurobiological and behavioral traits with food and other drug
Stress may have a long-lasting influence on eating behaviors, addictions (Kalon, Hong, Tobin, & Schulte, 2016; Smith & Robbins,
as individuals with BED tend to experience binge cravings and 2013), we sought to determine the impact of stress on the hedonic
binge eating in the evening in the privacy of their own homes and components of eating in BED and obesity. In order to differentiate
when alone (Abraham & Beumont, 1982; Masheb, Grilo, & White, between the motivational and pleasurable aspects of eating (’want-
2011; Pla-Sanjuanelo et al., 2015) long after the acute stressor has ing’ versus ‘liking’, respectively; Berridge, 2009; Dalton & Finlayson,
subsided. Furthermore, stress-induced hunger, desire to eat, and 2014; Robinson & Berridge, 1993), we measured the amount of
cortisol have been shown to continually rise up to 60 min following snack food that participants voluntarily poured into a serving
stress in both BED and non-BED obese women (Gluck et al., 2004). bowl as well as the amount consumed. In light of the inconsis-
To our knowledge, assessment of eating behaviors and eating- tencies in the literature, we anticipated that this nuanced analysis
related psychological factors following laboratory-induced mental of reward-based eating would lead to a greater understanding of
98 R.R. Klatzkin et al. / Biological Psychology 131 (2018) 96–106

stress-induced food consumption in obese women with BED com- participants underwent the Structured Clinical Interview for DSM-
pared to obese and normal weight non-BED women. Furthermore, IV Axis I disorders (SCID-I/NP; First, Spitzer, Gibbon, & Williams,
in our exploratory analysis, we hypothesized that psychophysio- 2002) to determine BED diagnostic status and to assess current
logical moderators of the relationship between stress and snacking Axis I mood and anxiety disorders. Height (cm) and weight (kg)
would differ in obese women with BED compared to their non-BED were also assessed to calculate BMI (kg/m2) and blood pressure
counterparts. measurements were taken with the Oscar 2 oscillometric ambu-
latory blood pressure monitor (SunTech Medical Instruments, Inc.,
2. Materials and methods Raleigh, NC). Women were excluded from the study if they had a
resting blood pressure > 159/99, were underweight (BMI < 19) or
2.1. Participants overweight (BMI between 26 and 28), or had a current Bipolar
Disorder, Substance Abuse Disorder, Panic Disorder, or an Eating
We recruited women (18–50 years of age) via newspaper Disorder other than BED. Because mood (26%) and anxiety (24.5%)
and posted advertisements (both online and in local businesses) disorders are the most common co-morbidities with BED (Grilo,
targeting women who were overweight and not taking blood pres- White, & Masheb, 2009), current Major Depressive Disorder and
sure, stimulant, or psychoactive medications. A small percentage Anxiety Disorders (other than Panic Disorder) were not considered
of advertisements eliminated the term “overweight” in order to exclusionary criteria unless individuals were using psychotropic
obtain our normal weight (NW) sample. Importantly, no advertise- medications. If inclusionary criteria were met, participants were
ments specifically targeted women with BED or any eating disorder. asked to call the laboratory on day 1 of the following menstrual
Both our recruitment strategies and the clinical assessment of DSM- cycle to schedule their first testing session.
IV Axis I eating, mood, and anxiety disorders (see Methods section)
ensured that participants remained blind to the study’s main vari- 2.4. Procedure
able of interest, BED diagnostic status, in order to diminish demand
characteristics. Participants were told that the purpose of the study In addition to the goals of the current report, the overarching
was to investigate the influence of the menstrual cycle on responses research study had additional aims that were addressed in the first
to mental stress in overweight and normal weight women. testing session and can be found in a recent report (Klatzkin et al.,
The final sample of participants in the current report was com- 2015). The results from the second testing session are presented in
prised of three groups of women: (1) Obese BED (n = 9); (2) Obese the current report.
non-BED (n = 11); and (3) NW non-BED (n = 12). All women in the Each testing session occurred during the follicular phase (days
BED group met full DSM-V criteria for BED while women in the non- 1–7) of the menstrual cycle, which was assessed via self-report.
BED groups had no history of any eating disorders. Participants in Participants called on day 1 of their menstrual cycles to schedule
the two obese groups had a body mass index (BMI) between 31 and each laboratory visit. The average time between testing sessions
47 and participants in the NW group had a BMI between 19 and was 37.75 days and did not significantly differ between groups. The
25. The protocol was approved by the Institutional Review Board experimental protocols began between the hours of 2:00 p.m. and
of Rhodes College and all participants provided informed, written 5:00 p.m. The participants were asked to refrain from eating and
consent. Participants received $30 compensation for completing drinking anything other than water for at least one hour prior to
the experimental protocol described in the current report and a testing. Compliance was confirmed upon arrival.
total of $75 for completing the full study (see below). The laboratory protocol for the second testing session described
in this report consisted of (1) a baseline rest period; (2) a mental
stress task; (3) a food anticipation period; and (4) and assessment of
2.2. Preliminary screening protocol eating behaviors. A blood pressure monitor with arm cuff provided
automated cardiovascular measurements throughout testing. Each
Women responding to our advertisements received a link portion of the protocol is described in detail below (see Fig. 1).
via email directing them to a set of online screening questions
aimed at excluding prospective participants who were pregnant 2.4.1. Baseline rest
or breastfeeding, postmenopausal, taking prescription medication Participants completed questionnaires assessing binge-eating
(excluding oral contraceptives, see Table 1), had a cardiovascular symptoms, dietary restraint, perceived stress, depression symp-
disorder, or were regular smokers. Women were also excluded toms, state anxiety, negative affect, and hunger (see below).
if they reported seeking treatment for weight or eating issues. Participants then rested quietly for 10 min in order to establish a
This exclusionary criterion was intended to prevent the potentially baseline for stress testing.
confounding influences of treatment-related coping strategies
regarding stress, mood, and eating. A preliminary indication of BED 2.4.2. The Trier Social Stress Test (TSST)
diagnostic status was also assessed via completion of the Eating The TSST (Kirschbaum, Pirke, & Hellhammer, 1993) is a mental
Disorders Examination Questionnaire (EDE-Q) and later confirmed stress test which reliably induces large and consistent cardiovascu-
via structured clinical interview (see below). lar and neuroendocrine responses and involves four components:

2.3. Determination of eligibility 1) Pre- Task Instructions (5 min): The researcher informed the par-
ticipants that they will be giving a speech serving as an interview
Of the 340 women who completed the preliminary screening for a job as a campaign manager for a local politician. Researchers
protocol, 80 eligible participants (23.5%) proceeded to the lab- also explained that the speech will be audio- and video-recorded
oratory to determine eligibility via clinical interview. The small for later analysis and will be followed by a serial subtraction task.
percentage can be explained by both the exclusionary criteria as Participants were then introduced to the ‘selection committee’
well as the fact that prospective participants must have endorsed who they were told would later listen to their job talk. This com-
substantial objective binge eating or lack thereof on the EDE-Q in mittee was composed of three well-trained research assistants
order to be eligible for the clinical interview portion of the study. If wearing white laboratory coats.
prospective participants endorsed mild to moderate binge-eating 2) Speech Preparation Period (5 min): The experimenter asked par-
behaviors, they were excluded at this stage. During this session, ticipants to imagine that they were applying for the job of a
R.R. Klatzkin et al. / Biological Psychology 131 (2018) 96–106 99

Table 1
Mean (±SD) baseline demographic factors as a function of BED and obesity status.

NW non-BED Obese non-BED Obese BED


n = 12 n = 11 n=9

Age 28.24 (±6.9) 26.39 (±3.6) 33.25 (±9.4)


Minority race (%) 7 (58%) 7 (64%) 7 (78%)
Body Mass Indexa 21.65 (±1.8) 33.06 (±5.1) 37.88 (±4.7)
Oral Contraceptive Use (%) 4 (33%) 1 (9%) 0 (0%)
Dietary Restraintb 0.22 (±0.29) 0.85 (±0.97) 1.42 (±1.16)
Perceived Stress Scaleb 12.0 (±8.8) 16.7 (±5.8) 20.1 (±6.3)
Binge Eating Scalec 2.33 (±1.5) 4.82 (±5.4) 24.11 (±10.6)
Beck Depression Inventoryd 8.42 (±9.3) 6.45 (±4.0) 20 (±14.4)
a
NW non-BED < Obese BED and Obese non-BED, p < 0.001.
b
Obese BED > NW non-BED, p < 0.05.
Obese BED > Obese non-BED and NW non-BED; c p < 0.001; d p < 0.05.

Fig. 1. Laboratory protocol.

campaign manager for a local politician and to take 5 min to and asked participants to rank their preference from #1-6. Instruc-
prepare their speech describing why they would be the ideal tions also informed participants that they would receive their snack
candidate for the position. towards the end of the stress recovery period. Participants then sat
3) Speech (5 min): Immediately following the preparation period, and rested quietly, with the option to read magazines that were
the selection committee returned to the testing room and asked unrelated to food, weight-related issues, etc.
the participants to deliver their speech. If the participant fin- Thirty minutes following the completion of stress testing,
ished before 5 min, the committee responded in a standardized participants completed questionnaires measuring negative affect,
way, with prepared questions to ensure that participants spoke anxiety, and hunger to obtain self-report measures during the food
for the entire period. anticipation period.
4) Serial Subtraction (5 min): The experimenter asked the partic-
ipants to perform mental math by serially subtracting 13 from
1022 aloud as quickly and accurately as possible. Their progress
was monitored, and when an error was made, the experimenter 2.4.4. Assessment of eating behaviors
told the participants to start over from the beginning. Imme- Forty-five minutes following the completion of stress test-
diately following the stress tasks, the participants completed ing, researchers provided participants with the snack food item
questionnaires measuring negative affect, anxiety, and hunger ranked #1 on their snack food preference survey. Researchers
to obtain post-stress self-report measures. told participants that they were providing them with the food
that they had previously chosen and to eat with their dominant
hand so that the arm with the blood pressure cuff remained still
2.4.3. Food anticipation period during ongoing readings. Researchers then presented a tray con-
Following stress testing and self-report measurements, partici- taining one plastic food storage container filled with a total of
pants were asked to rank their preferences for palatable food items 20 servings of their top ranked snack food item (peanut but-
they were to receive at a later time. In order to keep participants ter pretzels = 800 g, 2800 cal; chocolate covered raisins = 800 g,
blind to the nature of the study, written instructions explained 3800 cal; M&Ms = 840 g, 4200 cal; potato chips = 560 g, 3000 cal;
that due to the length of the experiment and the fact that par- baked cheese crackers = 600 g, 3000 cal; and jelly beans = 800 g,
ticipants were asked to refrain from eating one hour prior to the 2800 cal) as well as a bowl in which to pour the food. Participants
study, the Institutional Review Board mandated a snack be pro- were given either a large, medium, or small plastic food storage
vided. The snack food preference form included pictures of six container depending on the snack food chosen such that 20 serv-
palatable food items (peanut butter pretzels, chocolate covered ings filled the container. Participants were left alone in the testing
raisins, M&Ms, potato chips, baked cheese crackers, and jelly beans) room to portion and consume their chosen snacks.
100 R.R. Klatzkin et al. / Biological Psychology 131 (2018) 96–106

After fifteen minutes with the food items, the tray was removed statements describing how an individual may feel at the present
and participants were once again asked to complete questionnaires moment. Participants rate how they currently feel on a scale from
measuring negative affect, anxiety, and hunger to obtain self-report 1 (Not at all) to 4 (Very much so) and higher scores indicate
measures following food consumption. Participants were then pro- greater levels of state anxiety. Negative affect was assessed using
vided with $30 and debriefed. the Profile of Mood States (POMS-BI; Lorr & McNair, 1988) which
In order to assess reward-based eating behaviors, servings and consists of 72 items related to mood and assesses both positive
calories were measured in the following ways: (1) total poured (i.e. and negative affective dimensions on a scale from 0 (Much unlike
motivation for food or “wanting”; (2) total consumed (i.e. pleasure this) to 3 (Much like this). The POMS items are composed of
from food consumption or “liking”; and (3) percentage of the pour six empirically derived sub-scales: Elated-Depressed, Composed-
that was consumed. To assess the amount of snack food poured into Anxious, Agreeable-Hostile, Confident-Unsure, Energetic-Tired and
the bowl, the weight of the food left in the container (g) following Clearheaded-Confused. Higher scores indicate greater negative
food consumption was subtracted from the original weight of the affect. Finally, participants rated their current level of hunger on
food in the container. In order to calculate total food consumption, a numerical rating scale from 0 (Not hungry) to 6 (Very hungry).
the weight of the food left in the bowl was then subtracted from the
amount of food poured. Weight in grams was used to calculate the 2.6. Physiological measurements
number of servings poured and consumed and this was converted
to calories using the macronutrient content per serving provided The Oscar 2 oscillometric ambulatory blood pressure monitor
on the nutrition label of the chosen food item. (SunTechMedical Instruments, Inc., Raleigh, NC) with an appropri-
ately sized arm cuff provided automated measurement of systolic
2.5. Self-report questionnaires blood pressure (SBP), diastolic blood pressure (DBP) and heart rate
(HR) during the testing session. All measurements took place while
Participants completed the Eating Disorders Examination Ques- participants were in a comfortable seated position. Blood pressure
tionnaire (EDE-Q; Fairburn & Beglin, 1994), adapted from the Eating and heart rate measures were taken at minutes 0, 5, and 10 of
Disorders Examination Interview, during the preliminary screening baseline rest and minutes 0, 2, and 4 of both the speech and serial
protocol. The EDE-Q is a 36-item self-report, but for the purposes of subtraction periods; values were averaged to compute task levels.
the present study, only items 13–21 were used to provide a prelimi- Measurements taken at 0, 5, and 10 min of the food anticipation
nary indication of BED diagnostic status. These items ask how many period and also the food consumption period were each averaged to
times or how many days over the past four weeks participants have constitute cardiovascular functioning during the respective phases
engaged in binge-eating related thoughts and behaviors. of the study.
Questionnaires assessing dietary restraint, binge-eating symp- Saliva was collected in 1.5 mL Eppendorf tubes at the end of the
toms, perceived stress, and depression symptoms were admin- baseline rest period and 30 min following stress induction. Saliva
istered during the baseline rest period. Dietary restraint was samples were frozen within 30 min of collection at −20◦ C until
examined using the restraint subscale of the EDE-Q (Fairburn & assayed. On the day of testing, all samples were centrifuged at
Beglin, 1994). The restraint subscale is comprised of five questions 3000 rpm for 15 min to remove mucins and were analyzed in dupli-
assessing the number of days over the past 28 days that the par- cate by enzyme immunoassay (Salimetrics, State College, PA). The
ticipant has displayed restraint over eating, avoidance of eating, mean intra-assay coefficient of variation was 7.8% and the inter-
food avoidance, dietary rules, and empty stomach. The question- assay coefficient was 12.6%.
naire is scored using a 0–6 forced-choice rating scale from no
days to 28 days. Greater scores indicate greater dietary restraint. 2.7. Data analysis
Binge-eating symptoms were assessed using the Binge Eating Scale
(BES; Gormally, Black, Daston, & Rardin, 1982) which consists 2.7.1. Demographics and baseline measures
of 16 forced-choice questions, each with a set of three to four Group differences in demographic factors and oral contra-
answer choices. Higher scores indicate greater binge-eating sever- ceptive use were examined using a Multivariate ANOVA for
ity. The overall level of perceived life stress was measured using continuous variables and chi square analyses for dichotomous vari-
the Perceived Stress Scale (PSS; Cohen, Kamarck, & Mermelstein, ables as appropriate. Where significant results emerged, post-hoc
1983). Items assess how unpredictable, uncontrollable, and over- analyses with Bonferroni corrections were conducted. Group differ-
loaded respondents view their lives, and directly inquire about ences in baseline dietary restraint, perceived stress, binge-eating
levels of experienced stress in the past month with answer choices symptoms, and depression symptoms were investigated using a
ranging from 0 (Never) to 4 (Very Often). Higher scores indi- Multivariate ANCOVA, with oral contraceptive use as the covariate.
cate greater perceived stress. Self-reported depression symptoms Sidak corrected post-hoc comparisons were performed to deter-
were assessed using the 21-item Beck Depression Inventory (BDI; mine specific group differences.
Beck & Beamesderfer, 1974). This scale comprehensively assesses Oral contraceptive use was entered as a covariate in all subse-
dysphoric symptoms, including affective, cognitive, somatic, overt quent ANOVAs due to its influence on cardiovascular factors (Shen,
behavior, and interpersonal symptoms of depression. Each forced- Lin, Jiang, Li, & Zhang, 1994) and psychological variables (Shahnazi
choice question has a set of at least four possible answer choices, et al., 2014) as well as the association of fluctuating female sex hor-
with increasing severity of depressive symptoms from 0 to 3. Higher mones with eating behaviors (Edler, Lipson, & Keel, 2007; Klump,
scores indicate greater depressive symptoms. Keel, Culbert, & Edler, 2008).
Questionnaires assessing state anxiety, negative affect, and
hunger were administered at four time points throughout the 2.7.2. Self-reported psychological measures and physiological
study: (1) baseline rest, (2) the completion of stress testing, (3) measurements
following food anticipation (i.e. 30 min after the completion of Separate repeated measures ANCOVAs were used to analyze
stress testing), and (4) following food consumption (i.e. 60 min group differences in negative affect, state anxiety, hunger and
after the completion of stress testing). The state anxiety portion cardiovascular factors over time, with Group (Obese BED, Obese
of the Spielberger State-Trait Anxiety Questionnaire (STAI state; non-BED, NW-non-BED) as the between-subject factor, and Time
Spielberger, Gorsuch, Lushene, Vagg, & Jacobs, 1983) was used (Baseline, Stress, Food Anticipation, Food Consumption) as the
to assess self-reported situational anxiety levels and contains 21 within-subject factor, with oral contraceptive use as the covari-
R.R. Klatzkin et al. / Biological Psychology 131 (2018) 96–106 101

ate. Speech stress cardiovascular values were used because this 180

task was more effective at increasing cardiovascular measures NW non-BED


160
from baseline compared to the math task (main effect of stress Obese non-BED
140
task [speech vs. math] for SBP, DBP, and HR: Fs(1,28) = 18.1–31.0, Obese BED

ps < 0.001). When group differences emerged, Sidak corrected post- 120

Negave Affect
hoc comparisons were performed. 100
A repeated measures ANCOVA was also used to analyze group
80
differences in cortisol over time, with Group (Obese BED < Obese
non-BED, NW non-BED) as the between-subjects factor and Time 60

(Baseline, Stress) as the within-subject factor, with oral contracep- 40


tive use at the covariate. Cortisol data was not provided by one
20
participant in the NW non-BED and one participant from the Obese
BED group. 0
Baseline Stress Food Food
Ancipaon Consumpon
2.7.3. Eating behaviors
A Multivariate ANCOVA was used to assess group differences in Fig. 2. Mean (SD) negative affect ratings across baseline, stress, food anticipation,
the amount of calories and servings poured and consumed, as well and food consumption as a function of BED and obesity status. Main effect of Group:
F(2, 28) = 3.6, p < 0.05, Obese BED > NW non-BED, regardless of Time (p < 0.05).
as the percentage of the pour that was consumed, with oral contra-
ceptive use as a covariate. Given that negative affect and dietary
restraint are associated with stress-induced eating behaviors in p < 0.05, perceived stress, F(2,28) = 4.53, p < 0.05, binge-eating
women with disordered eating (Pike et al., 2006; Steiger et al., 2005) symptoms, F(2, 28) = 30.2, p < 0.001, and depression symptoms,
as well as healthy controls (Epel et al., 2001; Zellner et al., 2006), F(2,28) = 5.16, p < 0.05. As expected, BMI was lower in the NW non-
follow-up ANCOVAs were used to determine if group differences in BED group compared to both the obese non-BED and obese BED
eating behaviors following stress emerged after adjusting for group groups, who did not differ from each other (ps < 0.001). In addition,
differences in these self-reported psychological factors. Due to the the obese BED group endorsed greater binge eating and depres-
fact that negative affect was heightened in obese BED women across sion symptomatology than both obese and NW non-BED groups
multiple time points (see Results below), area under the curve with (p < 0.001 and p < 0.05, respectively) and higher dietary restraint
respect to ground (AUCg) for negative affect was used as the covari- and perceived stress than the NW non-BED group (ps < 0.05). No
ate. When group differences were present, Sidak corrected post-hoc main effects of Group were present for mean age, proportion minor-
comparisons were performed. Two obese non-BED participants did ity race, or oral contraceptive use (ps < 0.05).
not pour or consume any food and were thus eliminated from these
analyses. 3.2. Self-reported psychological measures
We examined for outliers in all eating variables and determined
that one participant in the obese BED group consumed significantly The stress task induced significant increases in negative affect,
more calories (350 more) and servings (2.5 more) than the average F(1, 28) = 7.2, p < 0.05, and anxiety, F(1, 28) = 5.2, p < 0.05, but not
for that group (i.e. greater than the third quartile plus 1.5 times hunger (p > 0.05) in the entire sample as a whole.
the interquartile range). Following the removal of this outlier, the There was a main effect of Group for negative affect, F(2,
results of the Multivariate ANCOVA for both calories and servings 28) = 3.6, p < 0.05, as obese BED women showed greater nega-
did not change. tive affect compared to NW non-BED women, regardless of Time
(p < 0.05; see Fig. 2). There was not a main effect of Time or
2.7.4. Relationship between eating behaviors and stress-related a Group × Time interaction for negative affect (ps > 0.05). No
psychological and cardiovascular factors main effects or interactions emerged for state anxiety or hunger
In order to determine if physiological factors and self-reported (ps > 0.05).
psychological measures following stress were associated with eat-
ing behaviors, Pearson product–moment (Pearson’s r) correlations 3.3. Physiological measurements
were performed in each diagnostic group separately as well as the
entire sample as a whole. In order to decrease Type I error rate, only Both the speech and math tasks induced significant increases
calories consumed and poured, as well as the percentage of poured in SBP, DBP, and HR, but not cortisol, from baseline to stress,
snack food consumed, were used as measures of food consumption. Fs(1,29) = 30.16–110.67, ps < 0.001.
Changes in cortisol, SBP, DBP, and HR from baseline to speech stress, There was a main effect of Group for SBP, F(2, 28) = 5.18, p < 0.05,
as well as stress-related psychological factors of dietary restraint as obese BED women showed heightened overall SBP compared to
and post-stress ratings of hunger, negative affect, and anxiety were NW non-BED women, irrespective of Time (p < 0.05; see Fig. 3).
used as predictors in the correlational analyses. There was not a main effect of Time or a Group × Time interaction
Following the removal of the outlier for caloric consumption, for SBP (ps > 0.05). No significant main effect or interactions were
results of the correlational analyses in the entire sample as a whole found for cortisol, DBP, or HR.
did not change. Significant results, however, did emerge following
outlier removal in the separate analysis of the obese BED group. 3.4. Eating behaviors
The results following outlier removal in this subgroup of women
are reported below. Neither the amount of food consumed, the amount of food
poured, nor the percentage of poured food consumed (calories or
3. Results servings) differed significantly by Group or Time (ps > 0.05; see
Table 2). However, significant group main effects for the percentage
3.1. Demographics and baseline measures of poured snack food consumed emerged when dietary restraint
and negative affect were included as covariates in the analysis
As summarized in Table 1, main effects of Group emerged (servings: F(2, 24) = 4.54, p < 0.05; calories: F(2, 24) = 4.58, p < 0.05).
for BMI, F(2,29) = 53.3, p < 0.001, dietary restraint, F(2, 28) = 4.0, The NW non-BED group consumed a larger percentage of the snack
102 R.R. Klatzkin et al. / Biological Psychology 131 (2018) 96–106

Table 2
Mean (±SD) eating behaviors as a function of BED and obesity status.

NW non-BED Obese non-BED Obese BED


n = 12 n=9 n=9

Calories poured 236.7 (±138.8) 360.6 (±176.8) 411.3 (±241.8)


Calories consumed 208.6 (±129.1) 282.1 (±192.6) 275.1 (±141.2)*
*
When outlier is removed (n = 8), Mean (±SD) = 231.4 (±55.8).

170 in HR from baseline to stress (r = −0.33, p = 0.07). Eating behav-


NW non-BED
iors were not associated with dietary restraint or stress-induced
160
Systolic Blood Pressure (mmHg)

Obese non-BED
changes in blood pressure or cortisol (ps > 0.05).
Obese BED
150
3.5.2. Sub-group analyses
140
Within the NW non-BED group, calories poured was nega-
130
tively associated with stress-induced changes in HR (r = −0.66,
p < 0.05) and cortisol (r = −0.60, p = 0.05) and positively associated
120 with post-stress hunger ratings (r = 0.76, p < 0.01). Calories poured
was also negatively associated with stress-induced changes in DBP
110
(r = −0.53, p = 0.08), although not significantly (Table 3). Calories
consumed was positively associated with post-stress hunger rat-
100
Baseline Stress Food Food ings (r = 0.66, p < 0.01), negatively associated with stress-induced
Ancipaon Consumpon changes in cortisol (r = −0.60, p = 0.05) and although not signifi-
cantly, negatively associated with stress-induced changes in HR
Fig. 3. Mean (SD) systolic blood pressure across baseline, stress, food anticipation,
(r = −0.55, p = 0.06). Eating behaviors were not associated with
and food consumption as a function of BED and obesity status. Main effect of Group:
F(2, 28) = 5.18, p < 0.05, Obese BED > NW non-BED, regardless of Time (p < 0.05). dietary restraint or post-stress negative affect and anxiety ratings
(ps > 0.05).
110
Within the Obese non-BED group, pouring more calories was
associated with greater post-stress hunger ratings (r = 0.73, p <
100
0.05; see Table 3). No eating behaviors were significantly associ-
Percentage of Poured Snack Food
Consumed (servings or calories)

90 ated with dietary restraint, post-stress hunger, anxiety, negative


80
affect, or stress-induced physiological measures (ps > 0.05).
Within the Obese BED group, lower caloric consumption was
70
associated with greater dietary restraint (r = −0.72, p < 0.05; see
60 Table 3). Nonsignificant trends were found for a positive association
between post-stress anxiety and caloric consumption and (r = 0.65,
50
p = 0.08), and for a negative association between stress-induced
40 change in cortisol and the percentage of poured food consumed
30 (r = −0.62, p = 0.099). Eating behaviors were not significantly asso-
ciated with post-stress hunger or negative affect ratings, or with
20
stress-induced changes in cardiovascular factors (ps > 0.05).
10
NW non-BED Obese non-BED Obese BED
4. Discussion
Fig. 4. Mean (SD) percentage of poured snack food consumed as a function of BED
and obesity status, with dietary restraint and AUCg negative affect as covariates. The current study examined stress-induced eating behav-
Main effect of Group for servings: F(2, 24) = 4.54, p < 0.05; calories: F(2, 24) = 4.58, iors and the psychophysiological moderators of the relationship
p < 0.05, NW non-BED > Obese non-BED and Obese BED (ps < 0.05).
between stress and snacking in three groups of women: normal
weight without BED, obese without BED, and obese with BED. Post-
food poured than both obese groups (ps < 0.05; see Fig. 4). Control- stress hunger was positively associated with both calories poured
ling for dietary restraint and negative affect did not change the lack and consumed, while post-stress anxiety and negative affect were
of group differences in the amount of food poured and consumed positively associated only with calories poured. Although prelimi-
(calories or servings). nary, these results indicate that psychological factors may be more
Groups did not differ in their chosen snack food or the percent- important predictors of the motivational aspects of snacking (i.e.
age of sweet versus salty snack foods chosen (ps > 0.05). All snacks calories poured) than the pleasurable aspects for women in general.
were ranked first at least once, while baked cheese crackers were When analyzed separately by group, post-stress hunger was posi-
the most popular, and jelly beans the least popular choice. tively associated with calories poured and calories consumed only
in the non-BED groups. Caloric consumption was negatively corre-
3.5. Relationship between eating behaviors and stress-related lated with dietary restraint and tended to correlate positively with
psychophysiological factors stress-induced changes in anxiety ratings in the obese BED group.
Results from these exploratory analyses suggest that psychological
3.5.1. Total group analyses factors rather than physiological hunger may be more salient pre-
Pouring more calories was associated with greater post-stress dictors of stress-induced snacking among obese women with BED
anxiety (r = 0.40, p < 0.05), negative affect (r = 0.41, p < 0.05), and than among women without BED. Finally, despite heightened blood
hunger ratings (r = 0.49, p < 0.01). Calorie consumption was posi- pressure in obese women with BED versus obese non-BED and nor-
tively associated with post-stress hunger ratings (r = 0.57, p < 0.01) mal weight non-BED women, total food intake 45 min following
and although not significantly, negatively associated with changes stress did not differ between groups. Yet, the normal weight non-
R.R. Klatzkin et al. / Biological Psychology 131 (2018) 96–106 103

% poured food
BED group consumed a larger percentage of the snack food they

(n = 31)

consumed
poured into their serving bowl than both groups of obese women

r = −0.22
r = −0.06
r = −0.10
r = −0.08
r = −0.05
r = 0.13
after controlling for negative affect and dietary restraint.
While previous studies have also reported no differences in total
food intake following stress in obese BED and non-BED individuals
Total Group
(Schulz & Laessle, 2012; Telch & Agras, 1996), our additional nor-

consumed
(n = 31)

r = −0.26
r = −0.20

r = −0.10
Calories

r = 0.48*
mal weight non-BED control group enabled the current study to

r = 0.24
r = 0.06
more effectively distinguish between the effects of BED and those
of obesity on stress-induced snack food consumption. The smaller
percentage of poured food that was consumed in the obese BED and
(n = 32)

r = −0.21
r = 0.49#

r = 0.41#
r = 0.40#
Calories

obese non-BED groups indicated that obesity may be associated


poured

r = 0.15
r = 0.08

with a heightened motivational drive to eat (i.e. ‘wanting’/amount


poured), coupled with a reduction in pleasure from eating (i.e.
‘liking’/amount consumed) following stress. In light of research
% poured food

showing sensitized ‘wanting’ without commensurate ‘liking’ in


(n = 8)

consumed

r = −0.62+
drug addictions (Berridge, 2009) and the amplification of palat-
r = −0.22
r = −0.25
r = −0.47
r = 0.21
r = 0.12

able food ‘wanting’ via injection of corticotropin-releasing factor


into brain reward centers (Peciña, Schulkin, & Berridge, 2006), our
results highlight the need to further investigate common underly-
Obese BED

ing mechanisms of stress-induced ‘wanting’ in drug addiction and


(n = 8)

consumed

r = −0.72#

obesity.
r = 0.65+
Calories

r = 0.54
r = 0.17

r = 0.52
r = 0.06

The incentive salience model proposes that the rewarding


nature of palatable food can be divided into two distinct com-
ponents, i.e. ‘liking’ and ‘wanting’ (Robinson & Berridge, 1993).
‘Wanting’ is operationalized as the reward-based desire for food,
(n = 9)

r = −0.31
Calories
poured

r = 0.21
r = 0.47
r = 0.42
r = 0.23

r = 0.39

while ‘liking’ has been defined as the pleasurable response to


receipt of palatable food (Berridge, 2009). Incentive salience mech-
anisms may be augmented by stress, thus playing a role in
stress-induced eating (Dallman et al., 2006). Schulz and Laessle
% poured food

(2012) reported heightened motivation for food in obese BED


consumed

r = −0.002

r = −0.14

versus obese non-BED subjects in their investigation of microstruc-


r = 0.48

r = 0.32

r = 0.13
r = 0.30

tural eating behaviors following stress. Although these group


differences were based on BED diagnosis rather than obesity sta-
Obese non-BED

tus as in the current study, the lack of a normal weight non-BED


Correlations between eating behaviors and psychophysiological factors as a function of BED and Obesity status.

control group did not allow for a full understanding of the impact
consumed

of BED above and beyond that of obesity. Future studies utilizing


r = −0.04

r = −0.07
Calories

r = 0.28
r = 0.48

r = 0.11
r = 0.11

this control in addition to a fourth normal weight BED group are


warranted in order to further isolate the effects of BED from the
effects of obesity on motivation for palatable food following stress.
Brain imaging studies have revealed the clinical relevance of
(n = 9)

r = −0.10

r = −0.01
r = 0.73#
Calories
poured

r = 0.13
r = 0.32
r = 0.10

differential activation in regions associated with ‘liking’ versus


‘wanting’. Recent reports have shown that obesity is associated
with increased brain activation in reward-based corticolimbic-
% poured food

striatal regions in response to palatable food and stress cues


(Jastreboff et al., 2013) as well as greater motivation for, but not
consumed

r = −0.34

r = 0.41
r = 0.10

r = 0.04
r = 0.08

r = 0.04

liking of, palatable food following stress and in the absence of


hunger (Lemmens, Rutters, Born, & Westerterp-Plantenga, 2011).
Additionally, Bohon and Stice (2012) found an association between
NW non-BED

greater negative affect and brain activity related to reward-based


learning and habit formation during anticipation of palatable food
consumed

r = −0.60#
r = −0.55+
r = −0.29
Calories

intake, but not during actual consumption in women with bulimia


r = 0.66*
r = 0.29
r = 0.34

(Bohon & Stice, 2012). Altogether, these findings suggest that the
relative strength of motivational versus pleasurable aspects of food
intake may be predictors of stress-induced eating in vulnerable
r = −0.66#

r = −0.60#
(n = 12)

r = −0.33

populations.
Calories

r = 0.76*
poured

r = 0.28
r = 0.29

Alternatively, it is possible that obese women in our study ate


a smaller percentage of the snack food they poured because they
felt more limited by the controlled laboratory environment and the
Post-Stress Negative Affect

time constraints of the food consumption period than the normal


weight group of women. As opposed to exhibiting a reduction in
Post-Stress Anxiety
Post-Stress Hunger

Change in Cortisol

pleasure from eating the food, they may have simply lacked the
Dietary Restraint

Stress-Induced

Stress-Induced

disinhibition to finish the snacks they poured. In contrast, the nor-


Change in HR

mal weight non-BED women showed positive correlations between


p ≤ 0.05.
p < 0.01.

p < 0.10.

post-stress hunger ratings and both calories poured and consumed,


Table 3

indicating that their stress-induced snacking behaviors were more


*

closely aligned with their level of hunger than the obese groups.
104 R.R. Klatzkin et al. / Biological Psychology 131 (2018) 96–106

Our findings that both anxiety and negative affect following ative affect, and anxiety compared to normal weight non-BED
stress were associated with the amount of calories poured, but women, levels were not significantly different from obese non-BED
not consumed, indicate that psychological factors may be more women. Consequently, overall greater psychological impairment is
relevant to the motivational aspects of snacking rather than the unlikely to explain this distinction between obese BED and non-
pleasurable aspects for women in general. Because psychological BED groups. Instead, results indicate that dietary restraint, and
dysfunction such as heightened negative affect and anxiety are to a lesser extent, stress-induced changes in anxiety and cortisol,
more prevalent in obese BED versus obese non-BED individuals are associated with snack food intake in obese women with BED.
(Klatzkin et al., 2015), a greater understanding of the mechanisms Specifically, the smaller percentage of poured snack food that was
by which motivation for food following stress contributes to the consumed in the obese BED group may be explained by an enhanced
etiology and maintenance of BED is needed to inform prevention stress-induced motivational drive to eat coupled with the influence
and treatment efforts. of dietary restraint on caloric consumption.
Toward this end, one goal of the current study was to explore In contrast, physiological factors in addition to homeostatic
the psychophysiological moderators of the relationship between hunger were associated with stress-induced snacking in NW non-
stress and eating behaviors as a function of BED and obesity sta- BED women. Specifically, greater stress-induced changes in heart
tus. Findings revealed that hunger following stress was associated rate and cortisol were associated with less calories poured and
with eating behaviors in both non-BED groups, but not in the obese consumed. Although heightened physiological responses to stress
BED group, indicating a potential dysregulation of homeostatic reg- are typically linked with enhanced food consumption, individ-
ulation of energy intake in BED. Homeostatic mechanisms in the ual differences contribute to variance in the relationship between
hypothalamus and peripheral organs contribute to the regulation stress and eating (Adam & Epel, 2007). Stress has been linked
of food consumption, but under certain circumstances (e.g. stress, to both under- and over-eating, a phenomenon known as the
heightened emotion, or the presence of palatable food) the brain stress-eating paradox. Individual difference factors such as obesity,
reward system may override homeostatic control mechanisms to dietary restraint, and chronic perceived stress contribute to this
promote food intake (Berthoud, 2011; Dallman, 2010). Our correla- variance, with greater levels being associated with stress-induced
tional results in the obese BED group, coupled with studies showing overeating (Adam & Epel, 2007). In the present study, these mea-
enhanced reward sensitivity to palatable food images in over- sures were lower in NW non-BED women compared to Obese BED
weight BED women versus overweight and normal weight non-BED women and thus may have contributed to the negative relationship
women (Schienle, Schäfer, Hermann, & Vaitl, 2009), suggest that between physiological stress and snacking behaviors in the NW
the reward system may be overriding the influence of homeostatic non-BED group. Future studies assessing the impact of psychophys-
hunger mechanisms in BED to influence eating behaviors. iological factors on stress-induced eating as a function of obesity
The uncoupling of physiological hunger mechanisms and food and BED status are warranted to further explicate this notion.
intake in obese BED women may also be explained by the height- Strengths of the current study include our nuanced analysis of
ened impact of psychological factors on eating behaviors. Results snacking behaviors. Incorporating new methods for the assessment
suggested that only in obese BED women is greater caloric intake of eating are imperative in order to elucidate factors that distin-
associated with lower dietary restraint as well as greater anxiety. guish obesity, BED, and other eating disorders, and subsequently
These findings are in line with evidence for a relationship between inform diagnostic and treatment strategies (Herzog, Douglas,
disordered eating behaviors and increased dietary restraint (Davis, Kissileff, Brunstrom, & Halmi, 2016). An additional strength of
Freeman, & Garner, 1988; Engelberg, Gauvin, & Steiger, 2005; the current study was the strategy used to recruit women with
Steiger et al., 2005), negative mood (Goldschmidt et al., 2014; BED. Participant expectations susceptible to influencing food con-
Ivanova et al., 2015; Schulz & Laessle, 2010), and ratings of per- sumption (Robinson, Kersbergen, Brunstrom, & Field, 2014) that
ceived stress (Goldschmidt et al., 2014; Pinaquy et al., 2003; are inherent to studies recruiting from treatment facilities or clin-
Rosenberg et al., 2013) in BED as well as bulimia. ics were reduced by enrolling members of the community in a
Although these psychological measures are also commonly metropolitan area who were blind to the study’s focus on BED.
linked to stress-induced eating in non-clinical samples (Epel et al., Furthermore, the racial and ethnic diversity of our participants
2001; Freeman & Gil, 2004; Roberts, Troop, Connan, Treasure, & increased the applicability of our findings to community samples,
Campbell, 2007; Wardle, Steptoe, Oliver, & Lipsey, 2000; Zellner particularly in light of the evidence that non-Hispanic black women
et al., 2006), their effects are potentiated in individuals with eat- have the highest obesity rates in the United States, adjusting for age
ing disorders. For instance, negative mood has been shown to be (Flegal, Carroll, Kit, & Ogden, 2012). The present study also included
a strong antecedent of binge eating in BED and bulimia, but not of a food anticipation period post-stress to more closely resemble real
binge-eating episodes or regular eating in healthy controls (Greeno world scenarios in which the ability to consume palatable foods
et al., 2000; Hilbert & Tuschen-Caffier, 2007). Additionally, dietary may not be possible immediately following a stressor. Findings for
restraint is negatively associated with neural activation in brain obesity- and BED-related differences in eating behaviors and dif-
regions responsible for impulse control in obese BED, but not in ferential moderators of the relationship between stress and caloric
obese non-BED individuals (Balodis et al., 2013). Furthermore, a consumption were documented in light of this delay, indicating
relationship between desire to binge eat and anxiety ratings fol- that long term effects of acute stress may have unique implications
lowing stress was reported in obese BED patients, but not obese in obese and BED populations.
or normal weight non-BED controls (Rosenberg et al., 2013). The Despite its strengths, the present study was not without its
present study builds upon these previous reports by being the first limitations, including the inability to compare eating behaviors
to assess the relationship between psychophysiological factors and following both stress and rest. It is possible that the reported dif-
measurable snack food intake, as opposed to self-reported eating ferences in the ratio of snack food poured to consumed may have
behaviors, following a mental stress manipulation as a function of been present regardless of the stress manipulation and this should
obesity and BED status. be investigated in future studies. In addition, we measured con-
Our findings for a connection between psychological factors and sumption of only one preferred snack food 45 min post-stress, and
stress-induced snacking only in obese BED women may at first thus our findings cannot be extrapolated to stress-induced binge
seem to be a result of the heightened levels of dietary restraint, eating, per se. The fact that our participants were not asked to binge
negative affect, and anxiety found in this group. While obese BED eat, but only given the option to eat, may alternatively be consid-
women did in fact report greater levels of dietary restraint, neg- ered a strength given the demand characteristics associated with
R.R. Klatzkin et al. / Biological Psychology 131 (2018) 96–106 105

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