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There is an accumulating body of evidence to indicate that stress leads to the consumption of unhealthy, energy-dense, palatable food, potentially contributing to the alarming global prevalence of chronic diseases, including obesity. However, comparatively little research has been devoted to addressing how best to remedy this growing problem. We provide an overview of the influence of stress on dietary intake, and then explore the novel, yet simple, possibility that regular elicitation of the relaxation response may effectively reduce stress-induced eating via both physiological neuroendocrine and reward pathways and psychological pathways involving emotion regulation, and habitual coping. If shown to be effective, the regular practice of relaxation may provide a convenient, cost efficient, patient-centered therapeutic practice to assist in the prevention of unhealthy weight gain and other negative consequences of unhealthy food intake.

To combat the obesity epidemic, interventions and treatments often recommend low-calorie dieting. Calorie restriction (CR) as a weight intervention, however, is often unsuccessful, as most people cannot sustain the behavior. Yet one small group has maintained extreme CR over years - members of the CR Society and followers of The CR Way. This study examined stable psychosocial characteristics of these individuals to identify traits that may promote success at long-term CR. In 65 participants, we measured diet, eating behaviors, and personality traits comparing calorie restrictors with two age-, gender-, ethnicity-, and education-matched comparison groups (normal weight and overweight/obese). We first tested whether the CR group restricted calories without indications of eating disorder pathology, and second, what crystallized psychosocial characteristics set them apart from their nonrestricting comparisons. Results indicated the CR group averaged 10 years of CR but scored lower than comparison groups on measures of disordered eating (p < .001) and psychopathology (p < .001). Particularly against overweight/obese participants, CR participants scored lower on neuroticism (p < .04) and hostility (p < .01), and were stronger in future time orientation (p < .05). Overall, CR profiles reflected high self-control and well being, except for having few close relationships. This study suggests a potential predisposition for successful long-term CR without disordered eating. Since modifying trait factors may be unrealistic, there may be psychosocial boundaries to the capacity for sustaining CR. Paralleling a movement toward personalized medicine, this study points toward a personalized behavioral medicine model in behavioral nutrition and treatment of overweight/obesity.

Overweight and obese individuals differ in their degree of hedonic eating. This may reflect adaptations in reward-related neural circuits, regulated in part by opioidergic activity. We examined an indirect, functional measure of central opioidergic activity by assessing cortisol and nausea responses to acute opioid blockade using the opioid antagonist naltrexone in overweight/obese women (mean BMI=31.1±4.8) prior to the start of a mindfulness-based intervention to reduce stress eating. In addition, we assessed indices of hedonic-related eating, including eating behaviors (binge eating, emotional eating, external eating, restraint) and intake of sweets/desserts and carbohydrates (Block Food Frequency); interoceptive awareness (which is associated with dysregulated eating behavior); and level of adiposity at baseline. Naltrexone-induced increases in cortisol were associated with greater emotional and restrained eating and lower interoceptive awareness. Naltrexone-induced nausea was associated with binge eating and higher adiposity. Furthermore, in a small exploratory analysis, naltrexone-induced nausea predicted treatment response to the mindfulness intervention, as participants with more severe nausea at baseline maintained weight whereas those with little or no nausea responses tended to gain weight. These preliminary data suggest that naltrexone-induced cortisol release and nausea may help identify individuals who have greater underlying food reward dependence, which leads to an excessive drive to eat. Future research is needed to confirm this finding and to test if these markers of opioidergic tone might help predict success in certain types of weight management programs.

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 eat— including feelings of disinhibited eating, binge eating, hunger, and more ineffective attempts to control eating (rigid restraint; r’s from .11 to .36, p ’s < .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.

Ghrelin regulates homeostatic food intake, hedonic eating, and is a mediator in the stress response. In addition, ghrelin has metabolic, cardiovascular, and anti-aging effects. This cross-sectional study examined associations between total plasma ghrelin, caloric intake based on 3 day diet diaries, hedonic eating attitudes, stress-related and metabolic factors, and leukocyte telomere length in overweight (n=25) and obese women (n=22). We hypothesized associations between total plasma ghrelin and eating behaviors, stress, metabolic, cardiovascular, and cell aging factors among overweight women, but not among obese women due to lower circulating ghrelin levels and/or central resistance to ghrelin. Confirming previous studies demonstrating lowered plasma ghrelin in obesity, ghrelin levels were lower in the obese compared with overweight women. Among the overweight, ghrelin was positively correlated with caloric intake, giving in to cravings for highly palatable foods, and a flatter diurnal cortisol slope across 3 days. These relationships were non-significant among the obese group. Among overweight women, ghrelin was negatively correlated with insulin resistance, systolic blood pressure, and heart rate, and positively correlated with telomere length. Among the obese subjects, plasma ghrelin concentrations were negatively correlated with insulin resistance, but were not significantly correlated with blood pressure, heart rate or telomere length. Total plasma ghrelin and its associations with food intake, hedonic eating, and stress are decreased in obesity, providing evidence consistent with the theory that central resistance to ghrelin develops in obesity and ghrelin’s function in appetite regulation may have evolved to prevent starvation in food scarcity rather than cope with modern food excess. Furthermore, ghrelin is associated with metabolic and cardiovascular health, and may have anti-aging effects, but these effects may be attenuated in obesity.