Article

Chronic stress exposure may affect the brain's response to high calorie food cues and predispose to obesogenic eating habits

Department of Nutrition, University of California, Davis, CA 95616, USA.
Physiology & Behavior (Impact Factor: 3.03). 08/2013; 120. DOI: 10.1016/j.physbeh.2013.08.010
Source: PubMed

ABSTRACT Exaggerated reactivity to food cues involving calorically-dense foods may significantly contribute to food consumption beyond caloric need. Chronic stress, which can induce palatable "comfort" food consumption, may trigger or reinforce neural pathways leading to stronger reactions to highly rewarding foods. We implemented functional magnetic resonance imaging (fMRI) to assess whether chronic stress influences activation in reward, motivation and executive brain regions in response to pictures of high calorie and low calorie foods in thirty women. On separate lab visits, we also assessed food intake from a snack food buffet and circulating cortisol. In women reporting higher chronic stress (HCS), pictures of high calorie foods elicited exaggerated activity in regions of the brain involving reward, motivation, and habitual decision-making. In response to pictures of high calorie food, higher chronic stress was also associated with significant deactivation in frontal regions (BA10; BA46) linked to strategic planning and emotional control. In functional connectivity analysis, HCS strengthened connectivity between amygdala and the putamen, while LCS enhanced connectivity between amygdala and the anterior cingulate and anterior prefrontal cortex (BA10). A hypocortisolemic signature and more consumption of high calorie foods from the snack buffet were observed in the HCS group. These results suggest that persistent stress exposure may alter the brain's response to food in ways that predispose individuals to poor eating habits which, if sustained, may increase risk for obesity.

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    • "Furthermore, for many people, stress alters food selection towards eating a greater proportion of calories from highly-palatable foods (i.e. tasty, caloricallydense foods containing high amounts of sugars, other carbohydrates and/or fats) (Groesz et al., 2012; Kim et al., 2013; Laugero et al., 2011; McCann et al., 1990; Oliver & Wardle, 1999; Tryon et al., 2013), and this shift can even occur in individuals who reduce their total caloric intake during stress (Oliver & Wardle, 1999). This altered food selection is often referred to as eating ''comfort food'' – a term that reflects the idea that palatable food intake reduces stress responses, thereby providing a potential means for people to ''self-medicate'' for stress relief. "
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    ABSTRACT: This manuscript summarizes the proceedings of the symposium entitled, "Stress, Palatable Food and Reward", that was chaired by Drs. Linda Rinaman and Yvonne Ulrich-Lai at the 2014 Neurobiology of Stress Workshop held in Cincinnati, OH. This symposium comprised research presentations by four neuroscientists whose work focuses on the biological bases for complex interactions among stress, food intake and emotion. First, Dr Ulrich-Lai describes her rodent research exploring mechanisms by which the rewarding properties of sweet palatable foods confer stress relief. Second, Dr Stephanie Fulton discusses her work in which excessive, long-term intake of dietary lipids, as well as their subsequent withdrawal, promotes stress-related outcomes in mice. Third, Dr Mark Wilson describes his group's research examining the effects of social hierarchy-related stress on food intake and diet choice in group-housed female rhesus macaques, and compared the data from monkeys to results obtained in analogous work using rodents. Finally, Dr Gorica Petrovich discusses her research program that is aimed at defining cortical-amygdalar-hypothalamic circuitry responsible for curbing food intake during emotional threat (i.e. fear anticipation) in rats. Their collective results reveal the complexity of physiological and behavioral interactions that link stress, food intake and emotional state, and suggest new avenues of research to probe the impact of genetic, metabolic, social, experiential and environmental factors on these interactions.
    Stress (Amsterdam, Netherlands) 08/2015; DOI:10.3109/10253890.2015.1062981 · 3.46 Impact Factor
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    • "Chronic stress influences feeding behaviors and energy homeostasis and can lead to depression-like behaviors such as anhedonia, which is considered the main symptom of human depression; this can be reproduced in animal models through decreased consumption of palatable solutions (Der-Avakian and Markou, 2012; Willner et al., 1987). Research has shown that chronic stress promotes the consumption of palatable and energy-dense (comfort) foods and elevates sugar consumption, leading to obesity in animal models (Adam and Epel, 2007; Pecoraro et al., 2004) and humans (Tryon et al., 2013). The neural mechanisms recruited by stress are complex and involve different nuclei of the hypothalamus. "
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    ABSTRACT: Chronic stress, whether associated with obesity or not, leads to different neuroendocrine and psychological changes. Obesity or being overweight has become one of the most serious worldwide public health problems. Additionally, it is related to a substantial increase in daily energy intake, which results in substituting nutritionally adequate meals for snacks. This metabolic disorder can lead to morbidity, mortality, and reduced quality of life. On the other hand, brain-derived neurotrophic factor (BDNF) is widely expressed in all brain regions, particularly in the hypothalamus, where it has important effects on neuroprotection, synaptic plasticity, mammalian food intake-behavior, and energy metabolism. BDNF is involved in many activities modulated by the hypothalamic-pituitary-adrenal (HPA) axis. Therefore, this study aims to evaluate the effect of obesity associated with chronic stress on the BDNF central levels of rats. Obesity was controlled by analyzing the animals' caloric intake and changes in body weight. As a stress parameter, we analyzed the relative adrenal gland weight. We found that exposure to chronic restraint stress during 12 weeks increases the adrenal gland weight, decreases the BDNF levels in the hippocampus and is associated with a decrease in the calorie and sucrose intake, characterizing anhedonia. These effects can be related stress, a phenomenon that induces depression-like behavior. On the other hand, the rats that received the hypercaloric diet had an increase in calorie intake and became obese, which was associated with a decrease in hypothalamus BDNF levels. Copyright © 2015. Published by Elsevier Ltd.
    Neuropeptides 02/2015; 51. DOI:10.1016/j.npep.2015.01.002 · 2.55 Impact Factor
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    • "Gottfried et al. showed that neural responses induced by a conditioned stimulus in amygdala is modulated by hunger and the activation of amygdala to food cues decreases as a function of satiety [16]. It is known that chronic stress may induce higher palatable food intake [27]. Rudenga et al. investigated whether an inducible stress might potentiate amygdala response to food cues in overweight women with chronic stress. "
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    ABSTRACT: Obesity is increasing worldwide and is triggered, at least in part, by enhanced caloric intake. Food intake is regulated by a complex mechanism involving the hypothalamus and hindbrain circuitries. However, evidences have showing that reward systems are also important in regulating feeding behavior. In this context, amygdala is considered a key extra-hypothalamic area regulating feeding behavior in human beings and rodents. This review focuses on the regulation of food intake by amygdala and the mechanisms of insulin resistance in this brain area. Similar to the hypothalamus the anorexigenic effect of insulin is mediated via PI3K (phosphoinositide 3-kinase)/Akt (protein kinase B) pathway in the amygdala. Insulin decreases NPY (neuropeptide Y) and increases oxytocin mRNA levels in the amygdala. High fat diet and saturated fatty acids induce inflammation, ER (endoplasmic reticulum) stress and the activation of serine kinases such as PKCθ (protein kinase C theta), JNK (c-Jun N-terminal kinase) and IKKβ (inhibitor of nuclear factor kappa-B kinase beta) in the amygdala, which have an important role in insulin resistance in this brain region. Overexpressed PKCθ in the CeA (central nucleus of amygdala) of rats increases weight gain, food intake, insulin resistance and hepatic triglycerides content. The inhibition of ER stress ameliorates insulin action/signaling, increases oxytocin and decreases NPY gene expression in the amygdala of high fat feeding rodents. Those data suggest that PKCθ and ER stress are main mechanisms of insulin resistance in the amygdala of obese rats and play an important role regulating feeding behavior. Copyright © 2015 Elsevier B.V. All rights reserved.
    Behavioural Brain Research 01/2015; 282. DOI:10.1016/j.bbr.2015.01.003 · 3.39 Impact Factor
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