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: 2.98). 08/2013; 120. DOI: 10.1016/j.physbeh.2013.08.010
Source: PubMed


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; 18(4):1-19. DOI:10.3109/10253890.2015.1062981 · 2.72 Impact Factor
    • "One strategy that many individuals adopt is the intake of highly palatable 'comfort' foods. During times of stress, both humans (McCann et al. 1990; Oliver and Wardle 1999; Laugero et al. 2011; Groesz et al. 2012; Kim et al. 2013; Tryon et al. 2013a) and rodents (Pecoraro et al. 2004; Ulrich-Lai et al. 2007; Packard et al. 2014) preferentially consume highly palatable foods that are generally high in sugars, other carbohydrates, and/or fats relative to more nutritious, less-tasty alternatives. Moreover, a history of eating these types of foods confers stress relief—it improves mood and sense of well-being and reduces glucocorticoid levels following stress in both humans (Markus et al. 2000; Gibson 2006; Macht and Mueller 2007; Tomiyama et al. 2011; Tryon et al. 2013b) and rodents (Shide and Blass 1989; Strack et al. 1997; Suchecki et al. 2003; Pecoraro et al. 2004; la Fleur et al. 2005; Ulrich-Lai et al. 2007, 2010). "
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    ABSTRACT: A history of eating highly palatable foods reduces physiological and emotional responses to stress. For instance, we have previously shown that limited sucrose intake (4 ml of 30 % sucrose twice daily for 14 days) reduces hypothalamic-pituitary-adrenocortical (HPA) axis responses to stress. However, the neural mechanisms underlying stress relief by such 'comfort' foods are unclear, and could reveal an endogenous brain pathway for stress mitigation. As such, the present work assessed the expression of several proteins related to neuronal activation and/or plasticity in multiple stress- and reward-regulatory brain regions of rats after limited sucrose (vs. water control) intake. These data were then subjected to a series of statistical analyses, including Bayesian modeling, to identify the most likely neurocircuit mediating stress relief by sucrose. The analyses suggest that sucrose reduces HPA activation by dampening an excitatory basolateral amygdala-medial amygdala circuit, while also potentiating an inhibitory bed nucleus of the stria terminalis principle subdivision-mediated circuit, resulting in reduced HPA activation after stress. Collectively, the results support the hypothesis that sucrose limits stress responses via plastic changes to the structure and function of stress-regulatory neural circuits. The work also illustrates that advanced statistical methods are useful approaches to identify potentially novel and important underlying relationships in biological datasets.
    Brain Structure and Function 08/2015; DOI:10.1007/s00429-015-1092-x · 5.62 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 · 2.64 Impact Factor
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