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Appetite 58 (2012) 717721

Contents lists available at SciVerse ScienceDirect

Appetite
journal homepage: www.elsevier.com/locate/appet

Short communication

What is eating you? Stress and the drive to eat q


Lisa M. Groesz a,, Shannon McCoy b, Jenna Carl c, Laura Saslow d, Judith Stewart a, Nancy Adler a,
Barbara Laraia a, Elissa Epel a,
a

UCSF, Department of Psychiatry, 3333 California St, San Francisco, CA 94118, United states
UMaine, Department of Psychology, 301 Little Hall, Orono, Maine 04469, United states
c
Boston University, Department of Psychology, 64 Cummington St., Boston, MA 02215, United states
d
UC Berkeley, Department of Psychology, Tolman Hall, Berkely, CA 94720, United states
b

a r t i c l e

i n f o

Article history:
Received 11 August 2010
Received in revised form 8 November 2011
Accepted 29 November 2011
Available online 4 December 2011
Keywords:
Stress
Drive to eat
Restraint
Disinhibition
Binge eating
Reward based eating

a b s t r a c t
Non-human animal studies demonstrate relationships between stress and selective intake of palatable
food. In humans, exposure to laboratory stressors and self-reported stress are associated with greater
food intake. Large studies have yet to examine chronic stress exposure and eating behavior. The current
study assessed the relationship between stress (perceived and chronic), drive to eat, and reported food
frequency intake (nutritious food vs. palatable non-nutritious food) in women ranging from normal
weight to obese (N = 457). Greater reported stress, both exposure and perception, was associated with
indices of greater drive to eatincluding feelings of disinhibited eating, binge eating, hunger, and more
ineffective attempts to control eating (rigid restraint; rs from .11 to .36, ps < .05). These data suggest that
stress exposure may lead to a stronger drive to eat and may be one factor promoting excessive weight
gain. Relationships between stress and eating behavior are of importance to public health given the concurrent increase in reported stress and obesity rates.
2011 Elsevier Ltd. All rights reserved.

Introduction
A recent national survey found that nearly 50% of people report
feeling greater stress now than 5 years ago and 43% report using food
to cope with stress (American Psychological Association Press Release, 2007). The high prevalence of stress-related eating may contribute to the increasing prevalence of overweight and obesity in
the US, where 72.3% of adult men and 64.1% of adult women are
overweight or obese (Flegal, Carroll, Ogden, & Curtin, 2010). Women
report signicantly more stress-related eating than men (Greeno &
Wing, 1994), especially of high fat and high sugar foods (Wansink,
Cheney, & Chan, 2003). Here we examine whether women who report greater life stress (stress perception or stress exposure) also report a greater drive to eat and consumption of palatable food.
Relationship between stress and eating
Non-human animal studies show that chronic stress exposure
increases consumption of palatable food (Dallman et al., 2003;
q
Lisa Groesz was supported in part by the NIMH T32 MH019391 grant and by the
Marchionne Foundation.
Corresponding authors.
E-mail addresses: [email protected] (L.M. Groesz), Shannon.mccoy@
umit.maine.edu (S. McCoy), [email protected] (J. Carl), laura_saslow@berkeley.
edu (L. Saslow), [email protected] (J. Stewart), [email protected] (N.
Adler), [email protected] (B. Laraia), [email protected] (E. Laraia),
[email protected] (E. Epel).

0195-6663/$ - see front matter 2011 Elsevier Ltd. All rights reserved.
doi:10.1016/j.appet.2011.11.028

Wilson et al., 2008). Following laboratory exposure to ego threats,


people exhibiting high negative affect or greater cortisol reactivity
eat more sweet and high fat food (Epel, Lapidus, McEwen, &
Brownell, 2001; Rutters, Nieuwenhuizen, Lemmens, Born, &
Westerterp-Plantenga, 2009). Outside the laboratory, when faced
with more daily stressors, people with high cortisol reactivity report greater snack food intake (Newman, OConnor, & Conner,
2007).
Experiencing drive to eat, in the absence of true caloric need, is
common, but there are large individual differences in the strength
of the drive to eat (Greeno & Wing, 1994). Type of stressor, restraint and disinhibition differentially impact amount eaten both
in the laboratory and in the real world. For example, only people
who scored high on both disinhibition and restraint ate more following a negative mood induction (Yeomans & Coughlan, 2009).
While an anticipated electric shock did not increase eating in people who scored high on restraint, ego threats signicantly increased eating in high restraint people (Heatherton, Herman, &
Polivy, 1991). In another study, people who endorsed restrained
or emotional eating consumed equivalent amounts of high and
low fat foods following both an ego-threatening and a neutral task
(Wallis & Hetherington, 2009).
Dietary restraint involves efforts to control food intake for the
purpose of weight loss or maintenance. However, people endorsing
higher levels of dietary restraint show little difference in calorie intake compared to people with low restraint, or in food intake when
unobtrusively observed in the laboratory (Stice, Sysko, Roberto, &

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L. M. Groesz et al. / Appetite 58 (2012) 717721

Allison, 2010) and naturalistically (Stice, Fisher, & Lowe, 2004).


Some types of dietary restraint may be more effective than others.
Researchers have differentiated exible restraint (which may prevent excessive consumption of palatable non-nutritious food) versus rigid restraint (which may be ineffective and eventually lead to
overeating). Using the Eating Inventory (Stunkard & Messick,
1985), people higher on exible restraint, compared to those higher on rigid restraint, displayed less overeating in the laboratory following a milkshake preload (Westenhoefer, Broeckmann, Munch, &
Pudel, 1994). People who maintain rigid rules around food appear
less attentive to physiological cues of hunger and satiety, leading to
overeating after a preload (Heatherton, Polivy, & Herman, 1989).
Lastly, among people with binge eating disorder undergoing
behavioral treatment, increases in exible but not rigid restraint
predicted both abstinence from binging and weight loss (Blomquist & Grilo, 2010).
Although strong drive to eat and the brake on drivehigh levels of restraintare important factors determining food intake
there has been little empirical work examining their relationship
to stress, and specically whether stress may increase drive to
eat as well as be related to ineffective efforts at dietary restraint.
The drive to eat is an understudied factor underlying obesity. Stress
may impair inhibition and is known to trigger relapse of unwanted
behaviors such as smoking (Shiffman, Paty, Gnys, Kassel, &
Hickcox, 1996). Stress can result in feeling out of control while
eating. For example, for people actively trying to restrain food
intake, the depletion of resources caused by stressors may further
impair inhibitory control, thus increasing the likelihood of
overeating (Westenhoefer et al., 1994).

Current study
To determine the impact of stress exposure on eating behavior
as well as on rigid and exible restraintthe current study tested
cross-sectional associations between perceived stress, stressor
exposure, and indices of drive to eat in a large sample of community women. We hypothesized that women who reported greater
life stress would report greater drive to eat (hunger, disinhibition),
greater intake of palatable food high in fat and sugar, and greater
levels of rigid (vs. exible) restraint.

Method
Participants
Women (N = 561) were recruited from the Northern California
via advertisements, email list serves, and community yers to participate in an online study on Womens Health. Our focus was on
normal weight, overweight and obese women; women who reported Body Mass Index (BMI) less than 18 were excluded from
our analyses (n = 20). Eighty-four people did not report relevant
study variables leaving a nal sample of 457 with Mage = 28.50
(SD = 6.75; range: 20.0056.00) and MBMI = 24.20 (SD = 4.87;
range: 18.5150.11). Participants identied as 59.2% Caucasian,
17.3% Asian-American, 5.6% Latino, 7.1% African American, 2.6% Indian, 1.1 % Native American, and 6.7% other.

Procedures and measures


Participants, after providing informed consent online, completed an online survey that included questions on age, weight,
stress, and eating behavior. Participants were not compensated
for participation. The protocol was approved by the UCSF IRB.

Sociodemographics
To measure education, participants responded on a 17 scale
from some high school to a completed doctoral degree. Self-reported annual household income data was collected from
participants.
Anthropometrics
Self-reported height and weight was used to calculate body
mass index (BMI = kg/M2), a proxy measure of body fat recommended by the World Health Organization as a universal criterion
of adult weight (WHO, 1995). BMI values of P25 and P30 were
used as criteria to indicate overweight and obesity, respectively.
Perceived stress
The Perceived Stress Scale (Cohen & Williamson, 1988), a 10item scale assesses unpredictability, uncontrollability, and overloading, including items such as In the last month, how often have
you been upset over something that happened unexpectedly, and
In the last month, how often have you been angered because of
things that were outside of your control? Responses were averaged to create an indicator of perceived stress (a = .87; mean
range: 0.003.70). The current study mean of 1.68 is comparable
to a national sample of women from 2009 (M = 1.6; Cohen & Janicki-Deverts, in press).
Chronic stressor exposure
The Social Stress Index was used to assess multiple domains of
chronic stress, including 51 items measuring stressors associated
with work, family, and relationships (Wheaton, 1994). Endorsed
stressors, such as The place you live is too noisy or too polluted,
were added to create a stress index that ranged from 0 to 51. Reliability was a = .90 (range: 051) in the current study, indicating
high inter-item reliability, showing that stressors tend to cluster
together.
Restraint, disinhibition, and hunger
The Eating Inventory (Stunkard & Messick, 1985) was used to
assess cognitive restraint, disinhibition, and susceptibility to hunger. We used the 21 item measure of restraint (a = .83), the 16 item
measure of disinhibition (e.g. I usually eat too much at social
occasions like parties or picnics; a = .84) and the 14 item measure
of hunger (a = .78). To determine the utility in identifying different
types of restraint, we created exible and rigid restraint subscales
based on Westenhoefer et al. (1994). In the current study, four
items were added to the exible scale and eight items were added
to the rigid restraint scale to fully encompass restraint, resulting in
an 11 item measure of exible restraint (a = .73), and a 15 item
measure of rigid restraint (e.g., I avoid some foods on principle
even though I like them; a = .75). We also examined the original
scale of restraint with the additional items, creating a 33 item measure of restraint (overall restraint, a = .86). The exible restraint
and rigid restraint scales were signicantly intercorrelated but
not totally redundant with each other (r = .581, p < .001).
Binge eating
The Binge Eating Scale (Gormally, Black, Daston, & Rardin, 1982)
was used to assess behavioral manifestations and feelings surrounding a binge episode. Items examined frequency of eating
when bored, when guilty, ability to control eating urges, as well
as preoccupation with eating. We removed ve items assessing
non-eating behavior (e.g., body dissatisfaction) because our interest was binge eating. In the current study, the 11 remaining items
were summed and averaged (a = .85).

L.M. Groesz et al. / Appetite 58 (2012) 717721

719

Table 1
Descriptives (Means, SD) and Pearson Correlations.a

Note. N = 457 unless otherwise noted.


a
Correlations are zero order except the partial correlations (shaded). The partial correlations between stress and drive to eat indices control for age, BMI, education, and
income. The partial correlations between stress and rigid restraint also control for exible restraint and correlations between stress and exible restraint control for rigid
restraint.
+
p < .10.

p < .05.

p < .01.

Food frequency
The frequency of intake of particular food items was measured
by a questionnaire adapted from Wardle and colleagues (Potischman et al., 1999). Participants were presented with food categories
and asked to rate How often do you eat the following foods? on a
6-item Likert scale from never to more than once a day. The
questionnaire included items such as burgers, pizza and hot dogs
and whole grain bread, pasta, and brown rice. Answers were
averaged within categories delineated by a factor analysis that
found two reliable factors: palatable non-nutritious food, and
nutritious food. The palatable non-nutritious food scale included
four food groupings: chips; burgers (pizza, hotdogs); fried foods;
and soda (regular soda, sweetened drinks; a = .71; M = 2.08,
SD = .63; range: 15). The nutritious food scale included four food
groups: legumes (e.g. peas); vegetables (e.g. salad); fruit; and
whole grains (a = .71; M = 3.86, SD = .86; range: 1.255.75).
Analysis strategy
SPSS, Version 17 was used. Partial correlations examined the
relationships between stress exposure and perceived stress on eating patterns, controlling for BMI, education, income, and age. Analyses of variance were used for group comparisons. Signicance was
determined to occur at p < .05. See Table 1 for descriptive data and
correlations between all variables. When examining the relationship between stress and the two types of restraint we controlled
for one while examining the other in order to look at unique
effects.

(r = .096, p = .040). Additionally, perceived stress was related to


an increased lack of control over eating (r = .321, p < .001), greater
hunger (r = .327, p < .001), and more frequent binge eating
(r = .362, p < .001). Although perceived stress was not related to
the original version of the restraint subscale (r = .068, p = .146)
or overall restraint that included additional items (r = .007,
p = .887), it was related to the sub-category of rigid restraint. Controlling for exible restraint, perceived stress was related to greater levels of rigid restraint (r = .106, p = .023). Controlling for rigid
restraint, perceived stress was negatively related to exible restraint (r = .094, p = .045).
Stress exposure
Similarly, stress exposure was related to drive to eat indices,
controlling for age, BMI, income, and education. Stress exposure
was related to reported higher palatable non-nutritious food intake
(r = .165, p = .0001), but not with nutritious food intake (r = .071,
p = .129). Further, increased stress exposure was related to lack of
control over eating (r = .233, p < .001), hunger (r = .254, p < .001),
and binge eating (r = .289, p < .001). As with perceived stress, stress
exposure was not related to the original scale of restraint
(r = .068, p = .149) or overall restraint using additional items
(r = .010, p = .833), but was related to the sub-categories. Controlling for exible restraint, stress exposure related to greater levels
of rigid restraint (r = .167, p < .001). Conversely, controlling for rigid restraint, stress exposure was related to lower exible restraint
(r = .135, p = .004).

Results
BMI status and stress
Perceived stress
Partial correlations, controlling for age, BMI, income, and education, revealed that perceived stress was related to drive to eat. Specically, increased perceived stress was related to reported higher
palatable non-nutritious food intake (r = .154, p = .001), and there
was a signicant negative association with nutritious food intake

Finally, we explored a counter hypothesis that overweight may


induce greater stress and drive to eat. To test this, we compared
normal weight, overweight, and obese participants on our two
stress measures. A one-way analysis of variance found no differences based on BMI status on perceived stress [F(456) = 2.150,
p = .143] or on stress exposure [F(456) = .331, p = .565].

720

L. M. Groesz et al. / Appetite 58 (2012) 717721

Discussion
This is the rst study to test, in a large sample, associations between stress exposure and indices of increased drive to eat. As
hypothesized, stress was related with the drive to eat as measured
by reported disinhibited eating, binge eating, and intake of palatable non-nutritious food. Additionally, stress was related to increased rigid restraintthe form of restraint more frequently
associated with overeating. Those reporting greater stress, regardless of whether it was perceptions of stress, or presence of more
objective exposures, also reported greater drive to eat across several indices (disinhibition, hunger, and binge eating) and more frequent palatable non-nutritious food consumption (e.g. chips,
hamburgers, and soda). Results were remarkably consistent across
both types of stress, perceived stress and the chronic stressor exposures, despite the limited overlap between measures (only 25%
shared variance).
This study supports previous ndings linking stress with greater
palatable or comfort food intake. Perceived stress was associated
with signicantly decreased healthy eating (e.g. vegetables and
whole grain foods), possibly as a result of the increased intake of
highly palatable food. In non-human animal models, palatable
non-nutritious food has a calming effect on the HPA axis stress response (e.g. Warne, 2009). Humans tend to eat more in a laboratory
setting following an acute stressor than in a control session, if high in
cortisol reactivity and negative affect (Epel, Lapidus, McEwen, &
Brownell, 2001). Sugar and fat target the brain similar to opiates
and are often sought during times of stress (see Cota, Tschop, Horvath, & Levine, 2006, for review; Newman, OConnor, & Conner, 2007;
Oliver, Wardle, & Gibson, 2000). Food is an inexpensive resource for
providing relief; these highly palatable, low nutrient dense foods can
offer short term pleasure and relief from discomfort (Dallman,
Pecoraro, & la Fluer, 2005). The results of the current study appear
consistent with previous experimental and non-human animal research on the stress-related eating relationship.
The empirical separation of restraint into exible and rigid subscales (Westenhoefer, 1991) proved to be useful in this study as
well. It is striking that the total restraint scale, was not related to
either stress measure, and we may have concluded null ndings
if we had not separated out rigid and exible restraint. Although
the subscales are related to each other, each subscale provided unique variance and related to stress measures in opposite directions.
Greater stress exposure (controlling for age, BMI, socioeconomic
status, and exible restraint), accounted for signicantly higher rigid restraint. Greater exposure to chronic stress affects brain regulation of emotions and impulses, downregulating activity in the
prefrontal cortex, reducing executive control, and upregulating
activity in the amygdala and hypothalamus (Epel, Tomiyama, &
Dallman, 2011). Greater perceived stress can promote less conscious control over volitional behavior and greater hedonic drive
via impairment of prefrontal cortex (Arnsten, 2009). Lack of control
over situations in ones life could lead to the desperate but ineffective attempts to control eating such as deprivation from a particular food followed by later overeating.
Directionality cannot be determined from the analyses. For
example, overweight may lead to both increased stress and increased eating. To examine this counter hypothesis, we tested potential stress differences based on BMI status. The relationship
was not supported, in alignment with a recent meta-analysis nding
no consistent cross sectional relationship between stress and adiposity, although the longitudinal studies showed an effect of stress
on weight (Wardle, Chida, Gibson, Whitaker, & Steptoe, 2010). Another hypothesis is that genetic factors may predispose one to both
excessive weight and stress. Such relationships could be mediated
by differences in the glucocorticoid receptor gene. Some studies

have found that certain variants are associated with both greater
cortisol reactivity to stress and greater body mass index (Kumsta
et al., 2007; Rosmond et al., 2000).
There are limitations to this study, including the relatively small
effect size, a community sample of premenopausal who do not
necessarily well represent the highest levels of stress, and potential
problems inherent in internet data collection. The small observed
effect sizes, from .106 to .362, indicate that the real world signicance of these relationships still needs to be determined. In addition, while this samples endorsement of mild to moderate levels
of stress is equivalent to a national sample of women in 2009 (Cohen & Janicki-Deverts, in press), we were unable to detect the potential relationship between people endorsing high stress and
frequency of unhealthy food intake. Although there are advantages
to internet data collection including reduced social desirability in
self-report (Nosek, Banaji, & Greenwald, 2002), internet data collection is vulnerable to haphazard answers and rapid responding.
This study tests the concept of a stress-related drive to eat in a
large sample, in a preliminary fashion, and represents the tip of the
iceberg in understanding the role of drive to eat. Our study is consistent with ndings from known neural networks linking stress to
a drive for dense calories (Chandler-Laney et al., 1997; Dallman
et al., 2003). It underscores the need for studies more directly
examining the relationship between stress and vulnerability to
obesity, with increased drive to eat serving as a potential mediator.
This question has become increasingly important as more basic research is uncovering the central role of reward circuitry and wanting palatable food in compulsive overeating (Corwin, Avena, &
Boggiano, 2011; Davis et al., 2011; Finlayson, King, & Blundell,
2007). Future human research could incorporate real-time ecological momentary assessment paradigms to determine directionality
in the relationships between stress, restraint and palatable food intake to inform weight loss treatment studies.

References
American Psychological Association Press Release. (2007, October 24). Stress a
major health problem in the US, warns APA. Retrieved April 26, 2010, from
<http://www.apa.org/news/press/releases/2007/10/stress.aspx>.
Arnsten, A. F. T. (2009). Stress signaling pathways that impair prefrontal cortex
structure and function. Nature Reviews Neuroscience, 10, 410422.
Blomquist, K. K., & Grilo, C. M. (2010). Predictive signicance of changes in dietary
restraint in obese patients with binge eating disorder during treatment.
International Journal of Eating Disorders.
Chandler-Laney, P. C., Castaneda, E., Viana, J. B., Oswald, K. D., Maldonado, C. R., &
Boggiano, M. M. (1997). A history of human-like dieting alters serotonergic
control of feeding and neurochemical balance in a rat model of binge-eating.
International Journal of Eating Disorders, 40, 136142.
Cohen, S., & Williamson, G. (1988). Perceived stress in a probability sample of the
US. In S. Spacapam & S. Oskamp (Eds.), The social psychology of health. Claremont
symposium on applied social psychology. Newbury Park, CA: Sage.
Cohen, S., & Janicki-Deverts, D. (in press). Whos stressed? Distributions of
psychological stress in the US in probability samples from 1983, 2006, and
2009. Journal of Applied Social Psychology.
Corwin, R. L., Avena, N. M., & Boggiano, M. M. (2011). Feeding and reward. A
perspective from three rat models of bingeing. Physiology & Behavior, 104,
8797.
Cota, D., Tschop, M. H., Horvath, T. L., & Levine, A. S. (2006). Cannabinoids, opioids,
and eating behavior. The molecular face of hedonoism? Brain Research Review,
51, 85107.
Dallman, M. F., Akana, S. F., Laugero, K. D., Gomez, F., Manalo, S., Bell, M. E., &
Bhatnagar, S. (2003). A spoonful of sugar. Feedback signals of energy stores and
corticosterone regulate responses to chronic stress. Physiology and Behavior, 79,
312.
Dallman, M. F., Pecoraro, N. C., & la Fluer, S. E. (2005). Chronic stress and comfort
foods. Self-medication and abdominal obesity. Brain, Behavior, and Immunity, 19,
275280.
Davis, C., Curtis, C., Levitan, R. D., Carter, J. C., Kaplan, A. S., & Kennedy, J. L. (2011).
Evidence that food addiction is a valid phenotype of obesity. Appetite, 57(3),
711717.
Epel, E. S., Lapidus, R., McEwen, B., & Brownell, K. (2001). Stress may add bite to
appetite in women. A laboratory study of stress-induced cortisol and eating
behavior. Psychoneuroendocrinology, 26, 3749.

L.M. Groesz et al. / Appetite 58 (2012) 717721


Epel, E. S., Tomiyama, A. J., & Dallman, M. (2011). Stress and reward neural
networks, eating, and obesity. In: K. Brownell, & M. Gold (Eds.), Handbook of
food addiction. Oxford: Oxford University Press.
Flegal, K. M., Carroll, M. D., Ogden, C. L., & Curtin, L. R. (2010). Prevalence and trends
in obesity among US adults, 19992008. Journal of the American Medical
Association, 303, 235241.
Finlayson, G., King, N., & Blundell, J. E. (2007). Liking vs. wanting food. Importance
for human appetite control and weight regulation. Neuroscience and
Biobehavioral Reviews, 31(7), 9871002.
Gormally, J., Black, S., Daston, S., & Rardin, D. (1982). The assessment of binge eating
severity among obese persons. Addictive Behavior, 7, 4755.
Greeno, C. G., & Wing, R. R. (1994). Stress-induced eating. Psychological Bulletin, 115,
444464.
Heatherton, T. F., Polivy, J., & Herman, C. P. (1989). Restraint and internal
responsiveness. Effects of placebo manipulations of hunger state on eating.
Journal of Abnormal Psychology, 98, 8992.
Heatherton, T. F., Herman, C. P., & Polivy, J. (1991). Effects of physical threat and ego
threat on eating behavior. Journal of Personality and Social Psychology, 60,
138143.
Kumsta, R., Entringer, S., Koper, J. W., van Rossum, E. F., Hellhammer, D. H., & Wust,
S. (2007). Sex specic associations between common glucocorticoid receptor
gene variants and hypothalamus-pituitary-adrenal axis responses to
psychosocial stress. Biological Psychiatry, 62, 863869.
Newman, E., OConnor, D. B., & Conner, M. (2007). Daily hassles and eating behavior.
The role of cortisol reactivity status. Psychoneuroendocrinology, 32, 125132.
Nosek, B. A., Banaji, M. R., & Greenwald, A. G. (2002). E-Research. Ethics, security,
design, and control in psychological research on the internet. Journal of Social
Issues, 58, 161176.
Oliver, G., Wardle, J., & Gibson, E. L. (2000). Stress and food choice. A laboratory
study. Psychosomatic Medicine, 62, 853865.
Potischman, N., Carroll, R. J., Iturria, S. J., Mittl, B., Curtin, J., Thompson, F. E., &
Brinton, L. A. (1999). Comparison of the 60- and 100-item NCI-Block
Questionnaires with validation data. Nutrition and Cancer, 34, 7075.
Rosmond, R., Chagnon, Y. C., Holm, G., Chagnon, M., Perusse, L., Lindell, K., Carlsson,
B., Bouchard, C., & Bjorntorp, P. (2000). A glucocorticoid receptor gene marker is
associated with abdominal obesity, leptin, and dysregulation of hte
hypothalamicpituitaryadrenal axis. Obesity Research, 8, 211218.
Rutters, F., Nieuwenhuizen, A. G., Lemmens, S. G., Born, J. M., & WesterterpPlantenga, M. S. (2009). Acute stress-related changes in eating in the absence of
hunger. Obesity, 17, 7277.

721

Shiffman, S., Paty, J. A., Gnys, M., Kassel, J. A., & Hickcox, M. (1996). First lapses to
smoking: Within-subjects analysis of real-time reports. Journal of Consulting and
Clinical Psychology, 64, 366379.
Stice, E., Fisher, M., & Lowe, M. R. (2004). Are dietary restraint scales valid measures
of acute dietary restriction? Unobtrusive data suggest not. Psychological
Assessment, 16, 5159.
Stice, E., Sysko, R., Roberto, C. A., & Allison, S. (2010). Are dietary restraint scales
valid measures of dietary restriction? Additional objective behavioral and
biological data suggest not. Appetite, 54, 331339.
Stunkard, A. J., & Messick, S. (1985). The three-factor eating questionnaire to
measure dietary restraint, disinhibition, and hunger. Journal of Psychosomatic
Research, 29, 7183.
Wallis, D. J., & Hetherington, M. M. (2009). Emotions and eating. Self-reported and
experimentally induced changes in food intake under stress. Appetite, 52,
355362.
Wansink, B., Cheney, M. M., & Chan, N. (2003). Exploring comfort food preferences
across age and gender. Physiology & Behavior, 79, 739747.
Wardle, J., Chida, Y., Gibson, E. L., Whitaker, K. L., & Steptoe, A. (2010). Stress and
adiposity. A meta-analysis of longitudinal studies. Obesity. Epub.
Warne, J. P. (2009). Shaping the stress response. Interplay of palatable food choices,
glucocorticoids, insulin, and abdominal obesity. Molecular and Cellular
Endocrinology, 300, 137146.
Westenhoefer, J. (1991). Dietary restraint and disinhibition. Is restraint a
homogenous construct? Appetite, 16, 4555.
Westenhoefer, J., Broeckmann, P., Munch, A. K., & Pudel, V. (1994). Cognitive control
of eating behaviour and the disinhibition effect. Appetite, 23, 2741.
Wheaton, B. (1994). Sampling the stress universe. In W. R. Avison & I. G. Gotlib
(Eds.), Stress and mental health. Contemporary issues and prospects for the future
(pp. 77114). New York: Springer.
WHO (1995). Physical status: The use and interpretation of anthropometry.
Report of a WHO Expert Committee. WHO Technical Report Series 854.
Geneva: WHO.
Wilson, M. E., Fisher, J., Fischer, A., Lee, V., Harris, R. B., & Bartness, T. J. (2008).
Quantifying food intake in socially housed monkeys. Social status effects on
caloric consumption. Physiology and Behavior, 94, 586594.
Yeomans, M. R., & Coughlan, E. (2009). Mood-induced eating. Interactive effects of
restraint and tendency to overeat. Appetite, 52, 290298.

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