Coincident with increased prevalence and severity of psychological stress in the general population [1
], the prevalence of overweight and obesity has reached epidemic levels [3
]. Understanding the connections between stress and obesity are critically important. Psychological stress is an increasingly well-established factor implicated in the development of obesity [4
]. A key mechanism through which stress likely leads to weight gain and obesity is stress-induced eating
. Stress-induced eating of palatable foods is conserved across species. Both humans [5
] and animals [8
] have been documented to increase their food intake following stress or negative emotion, even if the organism is not hungry [9
]. Further, the type of food eaten tends to be high in sugar or fat, or both [11
], commonly referred to as “comfort food.”
Various psychological and other factors predispose people to stress-induced eating. For example, being female, overweight, or scoring high in dietary restraint (a measure of chronic dieting) puts one at risk for increased food intake in response to a psychological laboratory stressor [5
]. As for what physiological
factors underlie stress-induced eating, prior research has focused on the stress-responsive hypothalamic-pituitary-adrenocortical (HPA) axis and glucocorticoids. In one study, for example, subjects who responded with the greatest amount of cortisol in response to a laboratory stressor, compared to a session with no stressor, consumed the greatest amount of high fat, sugary food [12
]. Furthermore, glucocorticoid administration studies in humans and rodents have documented increased food intake as well as a shift in preference toward sweet and fatty foods [16
]. Although some studies suggest that glucocorticoids directly increase preference of sweet and high fat food [17
], stress affects most bodily systems through multiple pathways [12
] and accumulating evidence exists suggesting the role of other systems in modulating consumption during stress towards sweet and fatty foods [8
Although understanding what triggers increases in eating after stress is important, it is equally important to understand what might protect an individual from stress eating. That is, we must also understand what physiological factors might underlie less food consumption following stress.
One possible modulator of stress eating is leptin, the protein product of the ob
]. Leptin circulates in the bloodstream, reflects the amount of fat stores, recent energy balance and dietary macronutrient composition [24
]. Leptin provides a signal to the hypothalamus of body fat reserves and recent energy intake [21
], and appears to act as a long-term hormonal signal in the regulation of energy homeostasis [30
]. Leptin contributes to body weight regulation by affecting both feeding behavior and energy expenditure. In rodents, leptin upregulates thermogenesis in brown adipose tissue. Leptin also exerts effects within the hypothalamus, regulating homeostatic food intake [30
], and in the ventral tegmental area, reducing dopamine neurotransmission and extinguishing the reward value of food [34
]. Paradoxically, obese humans tend to have higher levels of leptin, suggesting a state of leptin resistance [21
Circulating leptin concentrations increase 4–6 hours after meals in response to nutrient-induced insulin secretion [27
]. However, leptin may also be acutely responsive to psychological stress [12
]. Brydon et al. [19
] exposed subjects to psychological stress and measured plasma leptin concentrations at baseline, immediately after the stressor, and 45 minutes post-stressor. They found a small but significant increase of leptin, which peaked at 45 minutes following exposure to the stressor and was not correlated with cortisol response to the same task.
These stress-related changes in leptin may also modulate stress-induced eating. One study has examined leptin, stress, and eating together [37
] and reported that higher circulating serum leptin concentrations over one day were related to less overall food consumption following stress compared with days on which the subjects were not exposed to stress. This study suggests that tonic
serum concentrations of leptin may be linked to both stress and to decreased consumption.
A remaining question is whether acute changes in leptin under conditions of stress might affect subsequent food intake, or “stress eating.” In the current study, we tested whether leptin modulates stress eating by exposing women to a standardized laboratory stressor, discreetly measuring their food choices and amount eaten following the stressor, and measuring leptin throughout the session. Given the prior research implicating leptin in decreased food consumption, we hypothesized that leptin responses to stress would be negatively associated with comfort food consumption. We also measured cortisol to assess whether leptin effects associated with stress eating were independent of, or associated with, the known effects of cortisol on stress-induced eating behavior.