Lifetime stressor exposure is associated with greater rewarding effects of stress-related eating.

Acute stressors tend to shift preferences toward comfort foods, yet they do not ubiquitously increase the amount of food consumed. Moreover, although many individuals eat more under stress, others eat less or show no change. Although the precise mechanisms explaining this variability in stress-related eating are unknown, they may be driven by individual differences in the rewarding effects of comfort eating, which are enhanced by greater lifetime stressor exposure. To investigate this possibility, we examined whether differences in lifetime stressor exposure predicted reductions in negative affect following snacking (i.e., negative reinforcement) and if this effect was specific to stress-related snacking or snacking in general. Participants were 26 women (23% non-White) between 20 and 45 years old (M = 31), with a mean body mass index of 26, who completed three laboratory visits. Participants completed an assessment of lifetime stressor exposure (i.e., STRAIN) on the first visit and, on two subsequent laboratory visits in counterbalanced order, were given snacks after an acute social stress task (i.e., TSST) or rest period. Greater lifetime stressor exposure was related to greater post-ingestive decreases in negative affect following the acute social stressor but not following the rest period. If stress-related eating is more comforting for women with greater lifetime stressors and contributes to a stronger stress-eating association, then this may inform obesity-related clinical treatments that target behaviors and cognitions related to reward-based learning.

An acute social stressor decreases reinforcing value of both high and low energy-dense food in college students in a randomized controlled trial.

It is well known that a large portion of the population elevates their intake of high energy-dense foods during times of stress; however, it is understudied whether stress affects the reinforcing value of a food reward. Further knowledge of this relationship may help us better understand the positive correlation between reinforcing value of food and obesity. Therefore, it was tested if an acute stressor would increase the reinforcing value of low or high energy-dense food. Participants (N = 70) were randomized to a stress or no-stress condition after which they were allowed to work to gain access to a food reward and reading time. To determine if high energy-dense food was specifically affected, half the participants from each stress manipulation were randomly assigned to work for either grapes or chocolate candies. Participants in the stress condition worked less for food access than those in the no-stress condition, for both low and high energy-dense foods, but stress did not affect the reinforcing value of reading time. These results indicate that, contrary to our hypothesis, in a sample of college students, an acute stressor decreased reinforcing value of food, with no difference between a low and high energy-dense food item.

The effect of acute and chronic scarcity on acute stress: A dyadic developmental examination.

BACKGROUND: Food insecurity, obesity, and psychological stress are interrelated constructs which are thought to be connected through increased energy intake, but the underlying mechanisms for these relationships remain unclear. The current study used experimental methods to investigate how financial losses may influence acute stress in the context of food insecurity for both parents and offspring. This study also sought to examine the effect of acute stress related to financial losses on the reinforcing value of food (RRVfood) and delay discounting (DD). METHODS: One hundred and six families stratified by both offspring age (53 children aged 7-10, 53 adolescents aged 15-17) and household financial resources, visited our laboratory for three separate appointments. Each appointment included the experimental manipulation of financial gains and losses, saliva samples for cortisol assay, continuous heart rate monitoring, self-rated tension, and computer-based DD and RRVfood tasks. Participants also completed surveys to report perceived life stress level and food insecurity status. RESULTS: Among all participants, financial losses were related to decreased heart rates and increased self-rated tension. Among parents reporting food insecurity, acute financial losses resulted in an increase in cortisol levels. Changes in cortisol, heart rate, and tension were not related to RRVfood or DD. CONCLUSION: Food insecure parents are sensitive to financial losses and respond with an increase in cortisol. However, we found no evidence for a relationship between cortisol and RRVfood or DD. This sensitivity to financial losses did not extend to children or adolescents.

Plasma levels of ghrelin and GLP-1, but not leptin or amylin, respond to a psychosocial stressor in women and men.

It is well known that stress elevates intake of total calories and shifts food preference toward unhealthy food choices. There is, however, little known on the physiological mechanisms that drive stress-induced hyperphagia. In order to better understand how to reduce stress eating, it is critical to identify mechanisms in humans that are points of convergence between stress and eating. The feeding-related hormones ghrelin, leptin, glucagon-like peptide-1 (GLP-1), and amylin are likely candidates. It was hypothesized that ghrelin, an orexigenic hormone, would increase in response to an acute laboratory stressor, but that leptin, GLP-1, and amylin (anorexigenic hormones) would decrease after stress. To this aim, participants (n = 47) came into the laboratory and had feeding-related hormones, salivary cortisol and α-amylase, and self-rated anxiety measured. Then they underwent either exposure to a stressor (n = 24), which reliably elevates measures of stress and energy intake, or a no-stress condition (n = 23). Feeding hormones, stress hormones, and self-rated anxiety were measured twice more after the stressor. Elevated self-rated anxiety and α-amylase confirmed the validity of the stressor. Furthermore, there was a time X condition interaction for both ghrelin and GLP-1. Ghrelin was significantly elevated after stress compared to baseline (p = .02) and there was a trend for GLP-1 to be higher in the stress condition over the no-stress condition immediately after the stressor (p = .07). Overall, ghrelin is the most likely candidate driving energy intake after stress in humans.

Increasing water intake influences hunger and food preference, but does not reliably suppress energy intake in adults.

Increasing water intake is often purported to reduce energy intake, and is recommended as a weight loss strategy. The few experimental studies that have been conducted to verify these claims have examined the impact of a single pre-load of water before a meal. Although correlational data indicate a relationship between hydration, energy intake, and weight status, there is very little experimental research in this area. The current studies examined the hypothesis that elevated hydration, through increased water intake, would suppress energy intake. In Experiment 1, participants (n = 49) were asked to consume either one, two, or three 500 ml bottles of water throughout the morning before a lunch buffet in the laboratory. When participants categorized as normal weight drank three bottles of water they consumed less energy at lunch, but there was no effect on participants categorized as overweight or obese. In addition, increased water intake suppressed liking of food items in all participants and hunger in females. A follow-up study (n = 45) was conducted to test if four bottles of water throughout the morning would result in a similar energy suppression in participants categorized as overweight or obese. Surprisingly, in the second experiment, there was no effect of water intake on energy intake at lunch in any of the conditions. There was, however, a similar suppression of hunger and food liking. In conclusion, increasing water intake throughout the morning only suppressed energy intake in individuals categorized as normal weight under certain circumstances, and had no effect on individuals categorized as overweight/obese.

Endogenous glucagon-like peptide-1 reduces drinking behavior and is differentially engaged by water and food intakes in rats.

Glucagon-like peptide-1 (GLP-1) is produced in the ileum and the nucleus of the solitary tract. It is well known that GLP-1 controls food intake, but there is a growing literature indicating that GLP-1 also is involved in fluid intake. It is not known, however, if the observed effects are pharmacological or if endogenous GLP-1 and its receptor contribute to physiological fluid intake control. Accordingly, we blocked endogenous GLP-1 by application of a receptor antagonist and measured subsequent drinking. Furthermore, we measured changes in GLP-1-associated gene expression after water intake, and compared the effects of fluid intake to those caused by food intake. Rats injected with the antagonist exendin-9 (Ex-9) drank more fluid in response to either subcutaneous hypertonic saline or water deprivation with partial rehydration than did vehicle-treated rats. Analysis of licking behavior showed that Ex-9 increased fluid intake by increasing the number of licking bursts, without having an effect on the number of licks per burst, suggesting that endogenous GLP-1 suppresses fluid intake by influencing satiety. Subsequent experiments showed that water intake had a selective effect on central GLP-1-related gene expression, unlike food intake, which affected both central and peripheral GLP-1. Although water and food intakes both affected central GLP-1-relevant gene expression, there were notable differences in the timing of the effect. These results show a novel role of the endogenous GLP-1 system in fluid intake, and indicate that elements of the GLP-1 system can be engaged separately by different forms of ingestive behavior.

Glucagon-like peptide-1 receptor agonists suppress water intake independent of effects on food intake.

Glucagon-like peptide-1 (GLP-1) is produced by and released from the small intestine following ingestion of nutrients. GLP-1 receptor (GLP-1R) agonists applied peripherally or centrally decrease food intake and increase glucose-stimulated insulin secretion. These effects make the GLP-1 system an attractive target for the treatment of type 2 diabetes mellitus and obesity. In addition to these more frequently studied effects of GLP-1R stimulation, previous reports indicate that GLP-1R agonists suppress water intake. The present experiments were designed to provide greater temporal resolution and site specificity for the effect of GLP-1 and the long-acting GLP-1R agonists, exendin-4 and liraglutide, on unstimulated water intake when food was and was not available. All three GLP-1R ligands suppressed water intake after peripheral intraperitoneal administration, both in the presence of and the absence of food; however, the magnitude and time frame of water intake suppression varied by drug. GLP-1 had an immediate, but transient, hypodipsic effect when administered peripherally, whereas the water intake suppression by IP exendin-4 and liraglutide was much more persistent. Additionally, intracerebroventricular administration of GLP-1R agonists suppressed water intake when food was absent, but the suppression of intake showed modest differences depending on whether the drug was administered to the lateral or fourth ventricle. To the best of our knowledge, this is the first demonstration of GLP-1 receptor agonists affecting unstimulated, overnight intake in the absence of food, the first test for antidipsogenic effects of hindbrain application of GLP-1 receptor agonists, and the first test of a central effect (forebrain or hindbrain) of liraglutide on water intake. Overall, these results show that GLP-1R agonists have a hypodipsic effect that is independent of GLP-1R-mediated effects on food intake, and this occurs, in part, through central nervous system GLP-1R activation.