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Food cravings mediate the relationship between chronic stress and body mass index

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Abstract

This study examined the relationships between chronic stress, food cravings, and body mass index. A community-based sample of adults (N = 619) completed a comprehensive assessment battery and heights and weights were measured. Chronic stress had a significant direct effect on food cravings, and food cravings had a significant direct effect on body mass index. The total effect of chronic stress on body mass index was significant. Food cravings partially mediated the relationship between chronic stress and body mass index. These findings are consistent with research that chronic stress may potentiate motivation for rewarding substances and behaviors and indicate that high food cravings may contribute to stress-related weight gain. © The Author(s) 2015.
Journal of Health Psychology
2015, Vol. 20(6) 721 –729
© The Author(s) 2015
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DOI: 10.1177/1359105315573448
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Currently, 34.9 percent of adults in the United
States are obese, and little progress has been
made in reducing the number of individuals
with this complex problem (Ogden et al., 2014).
The increasing societal burden of obesity has
prompted the development of numerous inter-
ventions for prevention and treatment. While
these interventions are multifaceted and hetero-
geneous, with varied behavioral and biological
targets, lifestyle modifications form the founda-
tion of prevention and treatment options.
Obesity interventions are diverse in terms of
delivery and duration, although the conventional
cornerstones are dietary, physical activity, and
behavioral changes (Jensen et al., 2013). Many
obesity interventions focus on strategies to improve
nutrition, increase physical activity, and decrease
sedentary behavior (e.g. self-monitoring calorie
intake, increasing fruit and vegetable intake,
decreasing fat intake, goal setting pertaining to
physical activity, and learning to read nutrition
labels). Although there are a multitude of obesity
interventions, many result in only modest and
short-term improvements in weight (Lemmens
et al., 2008; Seo and Sa, 2008).
There are multiple reasons why only modest
and short-term improvements result from cur-
rent obesity interventions, including the chal-
lenges of finding the correct fit between
treatments and individuals. Solutions to this
challenge require a more nuanced understanding
of the mechanisms related to obesity. Studying
Food cravings mediate the
relationship between chronic stress
and body mass index
Ariana Chao1, Carlos M Grilo2, Marney A White2
and Rajita Sinha2,3
Abstract
This study examined the relationships between chronic stress, food cravings, and body mass index. A
community-based sample of adults (N = 619) completed a comprehensive assessment battery and heights
and weights were measured. Chronic stress had a significant direct effect on food cravings, and food cravings
had a significant direct effect on body mass index. The total effect of chronic stress on body mass index was
significant. Food cravings partially mediated the relationship between chronic stress and body mass index.
These findings are consistent with research that chronic stress may potentiate motivation for rewarding
substances and behaviors and indicate that high food cravings may contribute to stress-related weight gain.
Keywords
body mass index, eating behaviors, food cravings, obesity, stress
1Yale University School of Nursing, USA
2Yale University School of Medicine, USA
3Yale Stress Center, USA
Corresponding author:
Ariana Chao, Yale University School of Nursing, 400
West Campus Drive, Orange, CT 06477, USA.
Email: Ariana.Chao@yale.edu
573448HPQ0010.1177/1359105315573448Journal of Health PsychologyChao et al.
research-article2015
Article
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722 Journal of Health Psychology 20(6)
mechanisms of behaviors is crucial to interven-
tion development and enhancement. It can allow
for amplification, optimization, and targeting of
interventions to relevant processes. In addition,
studying mechanisms can help advance what is
known about a problem, develop solutions, and
simplify complex interventions. One such rela-
tionship in which further clarification is needed
is that between chronic stress and obesity.
Chronic stress and obesity
Stress is a complex and multidimensional con-
cept referring to a real or perceived disruption in
homeostasis (Chrousos and Gold, 1992). While
there are some studies that demonstrate the rela-
tionship between increased stress and higher
body mass index (BMI), the literature is mixed
(Torres and Nowson, 2007; Wardle et al., 2011).
This is partially due to the varying conceptual-
izations and measures of stress. While some
focus on specific stress events (e.g. traumas, lay-
offs, divorce; Udo et al., 2014), this study will
focus on the role of chronic stress, the subjective
experience of continuous stressors or ongoing
life problems and hassles that can last for months
to years (Turner and Lloyd, 1995).
While it is recognized that chronic stress is
associated with obesity (Chen and Qian, 2012;
Kouvonen et al., 2005; Wardle et al., 2011), the
mechanisms underlying this process are unclear.
There are several potential mechanisms that
may contribute to the relationship between
chronic stress and obesity including decreased
physical activity, increased sedentary behavior,
changes in stress-related hormones, changes in
eating patterns, decreased sleep duration, and
increased food cravings. The current study
focuses on a possible mechanism in which there
is a paucity of literature and that may provide
beneficial knowledge for obesity intervention
development: food cravings.
Stress and food cravings
The etiology of food craving, defined as an
intense and specific desire to consume a certain
food or food type that is difficult to resist
(Weingarten and Elston, 1990, 1991), has gener-
ated much interest from the research commu-
nity: multiple theories pertaining to the etiology
of food cravings have been proposed.
Physiological theories include those pertaining
to nutritional and energetic homeostatic mecha-
nisms and the psychoactive influences of com-
ponents of craved foods on neurotransmitter
systems (Pelchat, 2002). For example, some
researchers have found that food deprivation
increases food cravings (Massey and Hill, 2012)
while others have found no relationship between
food deprivation and cravings (Pelchat and
Schaefer, 2000; Polivy et al., 2005). Learning
theories posit that food cravings are conditioned
to food-related cues. These may be emotional
cues or external food cues such as a location or
the smell or sight of a food (Jansen et al., 2011).
Psychological and affect-based theories include
the roles of mood and emotional states such as
stress (Nijs et al., 2007; Rogers and Smit, 2000).
According to the Reward Based Stress
Eating Model and Selye’s Theory of Stress,
stress results in physiological responses to pre-
pare the body to cope with stress, including
activation of the hypothalamic–pituitary–
adrenocortical (HPA) axis (Adam and Epel,
2007; Selye, 1956). Activation of the HPA axis
results in the secretion of cortisol, a steroid
hormone that regulates eating behaviors and
choices (Pacák and Palkovits, 2001). Although
acute stress typically results in decreased food
intake, chronic activation of the HPA axis may
result in the prolonged action of cortisol and a
subsequent orexigenic response (Dallman
et al., 2003; Torres and Nowson, 2007). This
response may manifest as cravings for certain
foods: neurobiological mechanisms related to
stress may potentiate motivation and reward of
highly palatable foods thus increasing food
cravings and the risk for overeating (Sinha and
Jastreboff, 2013). In prior studies, researchers
have found that after HPA axis activation,
there is an increase in sweet cravings in indi-
viduals with binge eating disorder (Rosenberg
et al., 2013).
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Chao et al. 723
Food cravings and BMI
Food cravings are a commonly experienced
phenomenon among the general population
(Weingarten and Elston, 1991). Although not
all food cravings are pathological, cravings are
typically for foods that are high in fat, sugar,
and carbohydrates such as chocolate, pizza, and
fast foods (White et al., 2002). Researchers
have also found that higher food cravings are
associated with higher intake of respective food
types craved and higher BMIs (Chao et al.,
2014; Martin et al., 2008). Given the observed
relationships among stress, food cravings, over-
eating, and BMI, it is possible that food crav-
ings mediate the relationship between chronic
stress and BMI.
The primary aim of this study was to exam-
ine the relationships between chronic stress,
food cravings, and BMI. Based on prior litera-
ture, we hypothesized that food cravings would
mediate the relationship between chronic stress
and BMI.
Materials and methods
Design
The hypothesis was tested using a cross-sec-
tional design from a large observational data set
obtained from a collaborative, interdisciplinary
set of studies that examined the effects of stress
and self-control on the maladaptive behaviors
of overeating, excessive alcohol use, and nico-
tine smoking.
Participants
The sample for this study is a convenience sam-
ple of adult men and women who were recruited
from weekly advertisements in local newspapers
and flyers at community centers and churches in
and around New Haven, Connecticut. Participants
include individuals from a variety of racial and
socioeconomic backgrounds. Some individuals
have the addictive behaviors of cigarette smok-
ing, alcohol drinking, and/or overeating, while
others do not engage in these behaviors. Inclusion
criteria were that participants were between the
ages of 18–50 years and were able to read English
at least at the sixth-grade level. Exclusion criteria
were dependence on any drug other than alcohol
or nicotine, use of prescribed medications for any
psychiatric disorders, pregnancy, and medical
conditions that would preclude participation in
the study (e.g. current cancer, type 1 diabetes,
major head trauma). Study procedures were con-
ducted at the Yale Stress Center, and participants
received compensation for completion of assess-
ment sessions.
The mean age of the sample was 29.55
(standard deviation (SD) = 9.06) years with a
mean BMI of 27.42 (SD = 5.53) kg/m2. A little
more than half (54.9%) of the sample was
female. The sample was 67.0 percent White,
20.9 percent Black, and 12.2 percent “other.”
Procedures
The Yale University Institutional Review Board
approved the parent study protocol. Potential
participants completed an initial screening over
the telephone or in person to determine eligibil-
ity based on inclusion and exclusion criteria.
Following screening, eligible participants met
with a research assistant for an intake session to
obtain informed consent. Participants then
completed an assessment battery including
physical examinations, diagnostics, and cogni-
tive and psychological assessments. Heights
were collected using a height rod and weight
was collected using a standard procedure.
Measures
Chronic stress. Chronic stress was measured using
the chronic stress subscale of the Cumulative
Adversity Interview (Turner and Lloyd, 1995).
The Cumulative Adversity Interview is a well-
established, 140-item interview that assesses for
the accumulation of stressful life events over a
lifetime. The chronic stress subscale consists of
62 items relating to the subjective experience of
continuous stressors or ongoing life problems and
hassles. Items are on a 3-point Likert-type scale
ranging from not true to very true and refer to per-
ceived difficulties with ongoing interpersonal,
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724 Journal of Health Psychology 20(6)
social, and financial relationships and responsi-
bilities including difficulties in the work and
home environment and relationships with family
and significant others. A 3-month test–retest reli-
ability for the chronic stress subscale was .79
(Ansell et al., 2012). The use of interview tech-
niques is recommended to decrease participant
recall bias (Dohrenwend et al., 2006).
Food cravings. Food cravings were measured
using the Food Craving Inventory (FCI; White
et al., 2002). The FCI is a 28-item self-report
measure that assesses general and specific types
(high fat foods, complex carbohydrates/starches,
sweets, and fast-food fats) of food cravings. Par-
ticipants are asked to rate how often each food
was craved over the past month using a 5-point
Likert-type scale ranging from 1 (never) to 5
(always/almost every day; White et al., 2002).
The FCI has established content validity from
experts in the field of eating behaviors (White
et al., 2002). Concurrent validity has been estab-
lished with the Conceptual Craving Scale (Hill
et al., 1991) and disinhibition and hunger scales
of the Three-Factor Eating Questionnaire
(TFEQ; Stunkard and Messick, 1985), and dis-
criminant validity with the restraint scale of the
TFEQ. The FCI has demonstrated acceptable
internal consistency reliability and test–retest
reliability in adults (White et al., 2002) as well as
diverse community and clinical samples (Barnes
and Tantleff-Dunn, 2010; Barnes and White,
2010; White and Grilo, 2005). In the current
study, Cronbach’s alpha was .93 for general food
cravings.
BMI. BMI was calculated from measured
heights and weight using the formula weight
(kg)/[height (m)]2.
Age, gender, race/ethnicity. Age, gender, and race/
ethnicity were assessed using a demographic
questionnaire designed for this study.
Statistical analysis
We calculated descriptive statistics and exam-
ined the bivariate associations using Pearson’s
correlations for continuous variables, point-bise-
rial correlations for a dichotomous and continu-
ous variable, and phi coefficients for two
dichotomous variables. To test our primary
hypothesis, we used a mediation analysis with
bootstrapping as recommended by Preacher and
Hayes (2008). We used the SPSS macro pro-
vided by Preacher and Hayes (2008) to calculate
direct and indirect effects using 1000 bootstrap
samples and a 95 percent confidence interval.
For the mediation model (Figure 1), chronic
stress was the independent variable, food crav-
ings (FCI total score) was the mediator variable,
and BMI was the dependent variable. All models
were estimated with and without adjusting for
age, gender, and race/ethnicity.
Chronicstress
Food cravings
BMI
a
.02(.004)***
b
.02(.004)***
a
1.29(.36)***
b
.85(.36)*
Total effect:
a
.18(.04)***;
b
.13(.03)***
Direct effect:
a
.15(.04)***;
b
.12(.04)**
Figure 1. Food cravings mediate the effect of chronic stress on body mass index (BMI; n = 619).
Unstandardized coefficients are provided. Total effect = effect of chronic stress on BMI. Direct effect = effect of chronic
stress on BMI after controlling for food cravings.
aUnadjusted.
bAdjusted for age, gender, and race/ethnicity.
*p < .05; **p < .01; ***p < .001.
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Chao et al. 725
Results
Descriptive statistics
The mean score on the chronic stress subscale
was 10.03 (SD = 5.93) and the mean of the food
cravings (FCI) total score was 1.95 (SD = 0.62).
Almost all participants (97.9%) endorsed hav-
ing at least one food craving over the past
month.
Correlations
The correlations between study variables are
shown in Table 1. Chronic stress was positively
correlated with food cravings, BMI, age, and
Black race/ethnicity (r(617) = .14 to .24,
p < .001) and negatively correlated with White
race/ethnicity and being male (r(617) = −.24
and −.14, p < .001, respectively). Food cravings
were positively correlated with BMI, age, and
Black race/ethnicity (r(617) = .12 to .28,
p < .001) and negatively associated with White
race/ethnicity (r(617) = −.27, p < .001).
Mediation analysis
Results from the bootstrapped analysis sup-
ported the hypothesis that food cravings mediate
the relationship between chronic stress and
BMI. Figure 1 displays the mediation models
with and without adjusting for age, gender, and
race/ethnicity. Unadjusted results demonstrated
that chronic stress had a significant direct effect
on food cravings (B = .03 ± .004; p < .001), and
food cravings had a significant direct effect on
BMI (B = 1.29 ± .36, p < .001). The total effect of
chronic stress on BMI was significant
(B = .18 ± .04, p < .001). Food cravings partially
mediated the relationship between chronic stress
and BMI (effect of chronic stress on BMI con-
trolling for food cravings was B = .15 ± .04,
p < .001; unadjusted, bootstrapped 95 percent
bias-corrected confidence interval of .01 to .06).
Both unadjusted and adjusted confidence inter-
vals exclude 0, suggesting mediation (Preacher
and Hayes, 2008).
Discussion
These findings from a large and diverse commu-
nity sample of adults support our hypothesis that
food cravings statistically mediate the relation-
ship between chronic stress and increased BMI
albeit the effect size was small. To our knowl-
edge, this is one of the first studies to examine
the role of food cravings as a statistical mediator
of this relationship. These results serve to gener-
ate hypotheses about possible mechanisms
underlying the association between chronic
stress and BMI and demonstrate the potential
effect of food cravings in this relationship.
This work supports the Reward Based Stress
Eating Model and Selye’s Theory of Stress
(Adam and Epel, 2007; Selye, 1956) and builds
Table 1. Correlations among study variables (n = 619).
1 2 3 4 5 6 7
1. Chronic stress
2. Food cravings .24**
3. BMI .19** .18**
4. Age .14** .12** .21**
5. White −.24** −.27** −.17** −.05
6. Black .20** .28** .22** .13** −.73**
7. Male −.14** −.05 .03 −.02 .09* −.04
BMI = body mass index.
The following statistics were used: Pearson correlations for continuous variables, point-biserial correlations for a
dichotomous and continuous variable, and phi coefficients for two dichotomous variables.
*p < .05; **p < .001.
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726 Journal of Health Psychology 20(6)
upon previous research exploring eating-
related correlates and mechanisms related to
chronic stress and BMI. Researchers have
found that stress-related eating is associated
with greater preference for calorie-dense and
highly palatable foods (Dallman, 2010; Epel
et al., 2004; Laitinen et al., 2002). Furthermore,
stress has been shown to potentiate brain moti-
vation and habit regions that are active under
craving for high calorie foods (Page et al.,
2011; Pelchat et al., 2004). Thus, we have pos-
ited that stress and brain food and reward cir-
cuits overlap significantly and stress potentiates
food craving via activation of habit-based cir-
cuits as in other types of addictions (Sinha and
Jastreboff, 2013). Our results are in concord-
ance with this research as well as research
demonstrating that perceived stress and chronic
stressor exposure are associated with an
increased drive to eat as measured by disinhibi-
tion, hunger, binge eating, and palatable, non-
nutritious food consumption (Groesz et al.,
2012). Our findings support this relationship
and add to the literature by demonstrating the
relationship with food cravings. Food cravings
are differentiated from other constructs such as
hunger and food consumption as a food craving
is a subjective experience that is intense and
specific for a certain food (Hill, 2007; White
et al., 2002). Although food cravings are asso-
ciated with increased consumption of craved
foods (Chao et al., 2014; Martin et al., 2008),
food cravings are not synonymous with
increased consumption, and food cravings can
occur in the absence of hunger (Hill, 2007;
Weingarten and Elston, 1990).
Few studies have examined mediators and
mechanisms relating chronic stress to increased
BMI. Aligning with our results, researchers
have suggested that among older adults, poor
health habits (i.e. low physical activity, high
sedentary activity, and unhealthy dietary intake)
mediate the relationship between chronic stress
and the metabolic syndrome (Vitaliano et al.,
2002). Our results also align with findings from
basic research demonstrating the role of reward
circuitry and hedonic mechanisms in the con-
sumption of unhealthy foods and obesity
(Corwin et al., 2011; Finlayson et al., 2007;
Jastreboff et al., 2013; Patterson and Abizaid,
2013).
Given the suggestion that there are differ-
ences in stress and obesity by gender and race/
ethnicity, it is of note that although there was
some attenuation, the statistical mediation
remained after controlling for these factors.
Researchers have demonstrated that the rela-
tionships between stress, weight gain, and obe-
sity are stronger in women than men (Laitinen
et al., 2002; Sinha and Jastreboff, 2013; Udo
et al., 2014). There is evidence indicating that in
comparison to Whites, Blacks have higher lev-
els of stress (Geronimus et al., 2006; Troxel
et al., 2003) and obesity (Ogden et al., 2014).
Our results suggest that food cravings may be
an important factor accounting for the relation-
ship between stress and obesity across these
groups.
The results of this study must be interpreted
in light of several limitations. First, this study
was cross-sectional and non-experimental;
thus, causality and temporality cannot be
inferred. The cross-sectional nature of these
data does not allow us to discriminate between
our hypothesis and alternative hypotheses.
Additionally, alternative hypotheses were not
tested statistically as the FCI assesses food
craving over the past month whereas the
Cumulative Adversity Interview assesses
chronic stress over months to years. Thus, the
results from this analysis would not have been
theoretically valid (Iacobucci et al., 2007).
Longitudinal and experimental studies are nec-
essary to provide more insight into the direc-
tionality of these relationships and alternative
models cannot be ruled out. Second, despite the
diversity and size of the sample, a convenience
sampling approach was used which may limit
generalizability. Third, there are several poten-
tial mechanisms that may contribute to the rela-
tionship between stress and obesity-related
metabolic abnormalities including behavioral
changes in eating behaviors and physical activ-
ity, sympathetic nervous system activation, and
changes in HPA axis function (De Vriendt et al.,
2009; Kyrou and Tsigos, 2009).
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Chao et al. 727
Previous work has established that chronic
stress is associated with increased BMI, but to
our knowledge, this study is one of the first
studies to propose and demonstrate that food
cravings statistically mediate this relationship.
These findings suggest that creating interven-
tions to help adults cope with stress and with
food cravings may help them attain a healthier
weight. Further longitudinal and experimental
studies as well as exploration of behavioral and
physiological mechanisms related to chronic
stress, food cravings, and BMI are needed.
Acknowledgements
The authors gratefully acknowledge all participants
in this study and research staff. The authors would
also like to thank their funding sources. Study con-
cept and design: A.C., C.M.G., M.A.W., R.S.
Acquisition and collection of data: R.S. Analysis of
data: A.C. Obtained funding for study: R.S.
Administrative, technical, and material support: R.S.
All authors were involved in writing and revising the
article and provided final approval of the article.
Funding
This study was funded by The National Institute on
Drug Abuse/National Institute of Health (NIH) grants
PL1-DA024859 and UL1-DE019859. A.C. was
funded by pre-doctoral fellowships from the Jonas
Center for Nursing Excellence and the National
Institute of Nursing Research/NIH (T32-NR00834610;
F31-NR014375). C.M.G. was funded, in part, by
NIDDK/NIH (K24-DK070052).
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... A risk factor of emotional eating development is activation of hypothalamic-pituitaryadrenal axis by both acute and chronic stress and its impact regarding both the reward/ motivation system and the inhibitory-control pathways [16,17]. Increased subjective appetite or food cravings and preferences for high-calorie snacks (e.g., sweets and chocolate) by negative mood states or chronic stress has also been observed [18][19][20][21]. In addition, the meta-analysis of 13 studies including 8925 children suggest that the effect of stress on unhealthy eating may begin as early as 8 or 9 years old [22]. ...
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Obesity is one of the most dangerous epidemics of the 21st century. In 2019, the COVID-19 pandemic began and caused many deaths among patients with obesity with and without complications. Simultaneously, the lockdown related to the COVID-19 pandemic caused a host of emotional problems including anxiety, depression, and sleep disturbances. Many people began to cope with their emotions by increasing food (emotional eating) and alcohol consumption and in combination with decreased physical activity, promoted the development of overweight and obesity. Emotional eating, also known as stress eating, is defined as the propensity to eat in response to positive and negative emotions and not physical need. It should be noted that emotional eating may be the first step in the development of binge eating disorder and its extreme subtypes such as food addiction. Interestingly in some post-bariatric surgery patients, an increased frequency of addictive disorders has been observed, for example food addiction replaced by alcohol addiction called: “cross addiction” or “addiction transfer”. This data indicates that obesity should be treated as a psychosomatic disease, in the development of which external factors causing the formation of negative emotions may play a significant role. Currently, one of these factors is the COVID-19 pandemic. This manuscript discusses the relationships between the COVID-19 pandemic and development of emotional eating as well as potential implications of the viral pandemic on the obesity pandemic, and the need to change the approach to the treatment of obesity in the future.
... Fifth, even though the standardization of the diet across groups is a strength, we cannot rule out that some of the differences found among groups, especially bariatric groups versus controls, is due to transitory changes in postoperative physiology, including fluid shifts and changes in absorption and metabolism. Finally, stress is a potential mediator for appetite and food cravings [44], and given that this study was carried out under unusual circumstances (COVID-19 pandemic), stress could have affected our outcome variables. ...
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... According to a study there is a relationship between chronic stress, food cravings, and body mass index (BMI). [24] A community-based sample of 619 adults was collected and their heights and weights were measured. Chronic stress had a major direct impact on food cravings, and food cravings had a major direct impact on body mass index. ...
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... In conclusion, the quantity of food intake is more or less affected by negative emotions [19]. The effect of emotions on the type of food eaten has also been documented [20][21][22][23][24]. For example, studies have shown that individuals in a positive emotional state tend to consume healthy food, while negative emotions have been associated with a tendency to consume junk food [25][26][27]. ...
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... 22 Other studies have reported that high levels of psychological variables cause craving and intake of unhealthy foods and snacks. 23,24 However, our study showed that depressive mood, anxiety, and sleep disturbance were not associated with weight gain during the COVID-19 pandemic. Some reports shown that individuals with high levels of stress lost weight during the COVID-19 lockdown. ...
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... Although the mechanisms of acute stress-induced relapse have been studied in animals using the classical reinstatement model [3], the possibility that chronic stress may impact relapse vulnerability has received relatively little attention. Indeed, chronic stress may contribute to food craving and obesity [4] due to long-lasting neurochemical and morphological alteration in medial prefrontal cortex (mPFC) [5], a brain region whose activation is critical to the expression of acute stress-and food priming-induced reinstatement of palatable food seeking [6]. ...
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Obesity is a major contributor to many chronic diseases and a risk factor for cardiovascular disease. It is also associated with increased risk of all-cause and cardiovascular disease (CVD) mortality. Toward the goals of the American College of Cardiology (ACC) and American Heart Association (AHA) for preventing CVD and promoting cardiovascular health, the ACC and AHA have collaborated with the National Heart, Lung, and Blood Institute and professional organizations to develop the "2013 AHA/ACC/TOS Guideline for the Management of Overweight and Obesity in Adults". The 2013 guideline is the second edition of the 'Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: the Evidence Report' published in 1998. The new guideline maintains its focus on primary care practitioners (PCPs) and their patients in an effort to manage obesity more effectively and to reduce cardiovascular risk. The new guideline limits its scope by using five critical questions (CQs) and provides a summary of evidence-based recommendations and a treatment algorithm derived from the five CQs. The five CQs deal with the risks of overweight and obesity and the benefits of weight loss, and evaluate the following three treatment areas: diet, behavioral therapy, and surgical therapy. The recommendations and treatment algorithm serve as a guide for PCPs in the evaluation, prevention, and management of being overweight and obesity.
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Stress is defined as the behavioral and physiological responses generated in the face of, or in anticipation of, a perceived threat. The stress response involves activation of the sympathetic nervous system and recruitment of the hypothalamic-pituitary-adrenal (HPA) axis. When an organism encounters a stressor (social, physical, etc.), these endogenous stress systems are stimulated in order to generate a fight-or-flight response, and manage the stressful situation. As such, an organism is forced to liberate energy resources in attempt to meet the energetic demands posed by the stressor. A change in the energy homeostatic balance is thus required to exploit an appropriate resource and deliver useable energy to the target muscles and tissues involved in the stress response. Acutely, this change in energy homeostasis and the liberation of energy is considered advantageous, as it is required for the survival of the organism. However, when an organism is subjected to a prolonged stressor, as is the case during chronic stress, a continuous irregularity in energy homeostasis is considered detrimental and may lead to the development of metabolic disturbances such as cardiovascular disease, type II diabetes mellitus and obesity. This concept has been studied extensively using animal models, and the neurobiological underpinnings of stress induced metabolic disorders are beginning to surface. However, different animal models of stress continue to produce divergent metabolic phenotypes wherein some animals become anorexic and loose body mass while others increase food intake and body mass and become vulnerable to the development of metabolic disturbances. It remains unclear exactly what factors associated with stress models can be used to predict the metabolic outcome of the organism. This review will explore a variety of rodent stress models and discuss the elements that influence the metabolic outcome in order to further our understanding of stress-induced obesity.
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In this paper, we suggest ways to improve mediation analysis practice among consumer behavior researchers. We review the current methodology and demonstrate the superiority of structural equations modeling, both for assessing the classic mediation questions and for enabling researchers to extend beyond these basic inquiries. A series of simulations are pre- sented to support the claim that the approach is superior. In addition to statistical demonstra- tions, logical arguments are presented, particularly regarding the introduction of a fourth construct into the mediation system. We close the paper with new prescriptive instructions for mediation analyses.
Chapter
The cued overeating model that is presented in this chapter states that cues that reliably signal highly palatable food intake – such as the sight, smell, and taste of highly palatable foods – and also the context in which (over)eating takes place – like place and time and feelings and thoughts – may start to act as conditioned stimuli. This means that soon after, the cues alone can trigger food cue reactivity and food cravings. The learned cue reactivity increases the probability of (over)eating and might sabotage dieting. It is argued that for successful dieting it is necessary to extinguish learned cue reactivity. To reach that goal, the way of dieting is relevant: dieters who avoid highly palatable food cues and dieters who intermittently keep eating high-calorie high-fat palatable foods will remain cue reactive. Only dieters who expose themselves to highly palatable food cues without eating them are expected to show the desired extinction of cue reactivity. Extinction of cue reactivity can be accelerated by prolonged cue exposure with response prevention. During the exposure the overeater is exposed to the cues (e.g., smell and sight of tasty foods) that elicit appetite or craving. The exposure is long lasting and without eating. Whether cue exposure with response prevention is an effective intervention that promotes successful dieting remains to be studied.
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Harmon S. Jordan, ScD, Karima A. Kendall, PhD, Linda J. Lux, Roycelynn Mentor-Marcel, PhD, MPH, Laura C. Morgan, MA, Michael G. Trisolini, PhD, MBA, Janusz Wnek, PhD Jeffrey L. Anderson, MD, FACC, FAHA, Chair , Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect , Nancy M. Albert, PhD, CCNS, CCRN,
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Although certain commonalities exist between eating and drug use (mood effects, external cue-control of appetites, reinforcement, etc.), it is argued that the vast majority of cases of (self-reported) food craving and food “addiction” should not be viewed as addictive behavior. An explanation is proposed that instead gives a prominent role to the psychological processes of ambivalence and attribution, operating together with normal mechanisms of appetite control, the hedonic effects of certain foods, and socially and culturally determined perceptions of appropriate intakes and uses of those foods. Ambivalence (e.g., “nice but naughty”) about foods such as chocolate arises from the attitude that it is highly palatable but should be eaten with restraint. Attempts to restrict intake, however, cause the desire for chocolate to become more salient, an experience that is then labelled as a craving. This, together with a need to provide a reason for why resisting eating chocolate is difficult and sometimes fails, can, in turn, lead the individual to an explanation in terms of addiction (e.g., “chocoholism”). Moreishness (“causing a desire for more”) occurs during, rather than preceding, an eating episode, and is experienced when the eater attempts to limit consumption before appetite for the food has been sated.