Comfort food is comforting to those most stressed: Evidence of the chronic stress response network in high stress women
Introduction
Obesity and obesity-related disease states such as metabolic syndrome are highly prevalent (Crawford et al., 2010). Concurrently, the United States is faced with historically high levels of psychological stress (American Psychological Association, 2009). Both of these trends are taking place within a “toxic” food environment that promotes overeating—particularly overeating of calorie-dense, nutrient-poor foods (Wadden et al., 2002). There are robust and complex connections between obesity, psychological stress, and eating behavior (Adam and Epel, 2007, Dallman, 2010, Warne, 2009). The role of stress in promoting eating and obesity has been relatively well characterized. For example, stress has been shown to promote both obesity (Dallman, 2010, McEwen, 2008, Wardle et al., 2010) and food intake (Born et al., 2010, Epel et al., 2001, Pecoraro et al., 2004, Rutters et al., 2009). In the former, abdominal obesity is most affected by stress due to the role of prolonged stress-induced glucocorticoid secretion in promoting abdominal fat deposition (Bjorntorp and Rosmond, 2000, Dallman et al., 2005). In the latter, also primarily driven by glucocorticoids, stress promotes consumption of highly palatable, nutrient-dense foods high in sugar and fat (Adam and Epel, 2007, Torres and Nowson, 2007, Warne, 2009). Further, acute and chronic stress can interact to exacerbate stress eating. For example, those who are under chronic stress tend to eat more under acute stress conditions (Gibson, 2006).
In the current study, we focus on the converse—eating and obesity affecting stress responses. Although this converse relationship is undoubtedly equally important, it has to date only been directly studied in non-human animal models (Dallman, 2010, Pecoraro et al., 2004). In this model, termed the chronic stress response network model, rats exposed to repeated chronic restraint stress that are then given lard or sucrose demonstrate attenuated stress responses compared to those given chow. Specifically, the otherwise expected CRF expression and ACTH secretion in response to stress is reduced (Foster et al., 2009, la Fleur et al., 2005, Pecoraro et al., 2004). Similarly, rats given sucrose show attenuation of stress-induced activation of the lateral septum (Martin and Timofeeva, 2010). Early life stressors such as maternal separation in rats also appear to activate the chronic stress response network. A palatable cafeteria high-fat diet normalized the effects of prolonged maternal separation in rats, reversing increases in anxiety and depressive behaviors, increased cortisosterone, increased hypothalamic CRH, and increased hippocampal glucocorticoid receptor expression (Maniam and Morris, 2010). In other words, it appears that rats are “self-medicating” through the use of food to regulate their stress responses—specifically their hypothalamic–pituitary–adrenocortical (HPA) axis responses.
These rats, over time, develop greater mesenteric fat, and this mesenteric fat has been found over multiple studies to be negatively correlated with CRF mRNA expression in the paraventricular nucleus (Dallman et al., 2003a, Dallman et al., 2003b, Laugero et al., 2001). This process is one purported mechanism explaining how, over time, chronically stressed humans appear to have hypocortisolism (Fries et al., 2005), but this has not yet been directly tested in humans. One study (Arce et al., 2009) found evidence of the chronic stress response network in rhesus monkeys: subordinate females consumed more calories, gained more weight, and subsequently showed lower diurnal cortisol responses and dampened cortisol responses to an acute social separation stressor.
In sum, greater mesenteric fat, likely developed through repeated consumption of palatable foods, appears to dampen the activity of the HPA axis in chronically stressed rodents and appears to be conserved across species to monkeys. The chronic stress response network has to date only been tested in non-human animal species, and thus we test the potential relevance of this model to humans in the current study. Prior studies of eating, obesity, and stress responses have not directly tested for evidence of the chronic stress response network, and instead have focused on a main effects model whereby greater stress and cortisol is associated with greater obesity. Indeed, in community samples, there may be and have been documented (Epel et al., 2004, Newman et al., 2006) positive associations between abdominal fat and cortisol output in response to acute stress. There is reason to believe, however, that in highly stressed humans we might find the opposite relationship due to the chronic stress response network. These individuals likely have coped with high levels of stress by engaging in stress-eating, thereby developing blunted HPA axis responses like the rats given the opportunity to consume comfort food. Here, we isolate a very high stress group and test for evidence supporting the chronic stress response network.
Given that the prior studies show greater intake of comfort food during stress and recovery from stress, greater mesenteric fat pads, and the amount of the pad is directly related to lowered CRF in the brain and lowered HPA axis response to acute stress, we can make several hypotheses about what to expect in humans under stress who have recruited the chronic stress response network. Specifically, if the chronic stress response network is activated in humans, we would expect the following observations, cross-sectionally:
- 1.
Those with high stress will have greater self-medication with palatable food, and thus will thus report higher scores on self-reported emotional eating.
- 2.
Those with high stress should have greater abdominal fat distribution, as measured by sagittal diameter and overall adiposity as measured by BMI.
- 3.
If those with high stress do tend to have greater abdominal fat distribution, they should also show dampened HPA axis activity in response to acute stress, and diurnally and greater sensitivity to dexamethasone.
Section snippets
Sample
Fifty-nine healthy premenopausal women aged 20–50 participated in this study. To capture a wide range of chronic psychological stress, this sample contained caregivers of chronically ill children (n = 40) and caregivers of healthy children (n = 19). Exclusion criteria included post-menopausal status, heavy drinking (7+ drinks per week), major depression, and chronic health conditions except controlled hypertension with beta blockers or ACE inhibitors (n = 2) and controlled hypothyroidism with
Descriptive statistics
Participants were on average 39 years old (SD = 6.03), with an average BMI of 25.04 (SD = 3.97) and sagittal diameter of 20.20 in. (SD = 4.92). The mean emotional eating score was 2.65 (SD = 1.05) and the mean perceived stress score was 15.70 (SD = 4.92). The women in the top quartile of perceived stress (n = 17) had an average score of 21.5, which is considered “high stress” according to normed values for adults older than 20 years from a poll of a representative U.S. sample (Cohen and Williamson, 1988).
Discussion
Is comfort food truly comforting? Past findings show that in rats, chronic stress induces high cortisol output in response to acute stress, selective intake of “comfort food” (lard and sucrose), and preferential storage of abdominal fat. Consequently, in these rats, the greater the abdominal fat pad, the lower the subsequent HPA axis reactivity to acute stress. This has been labeled the chronic stress response network (Dallman et al., 2003a, Dallman et al., 2003b, Dallman et al., 2004, Dallman
Role of funding source
This research was supported by the following: Robert Wood Johnson Foundation (RWJF) Health and Society Scholars Program, National Institute of Mental Health Award K08 MH64110-01A1; RWJF and NIMH had no further role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication.
Conflict of interest
The authors declare no conflicts of interest.
Acknowledgements
We gratefully acknowledge Drs. Eli Puterman and Aoife O’Donovan for their comments on the manuscript. We also acknowledge Drs. Melvin Heyman, Bryna Siegel, and Paul Harmatz for help recruiting clinic participants, and the busy mothers for donating their time.
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