Interactions with the Stress Circuitry. Effects of Stress on Food Intake

During stress, several neuropeptides and hormones are affected that are part of the previously described neural circuitry involved in feeding behavior. CRH in the PVN plays an initiating role in hypothalamic- pituitary-adrenocortical (HPA) axis activity and is increased with acute stress and decreased with chronic stress (through feedback effects of released glucocorticoids). In addition, acute stress increases NPY mRNA in the arcuate nucleus.

In the amygdala, which is also part of processing taste information, NPY mRNA will decrease whereas CRH mRNA will increase after a stressful event. Thus, during stress, depending on the anatomical site, anorexigenic (CRH) as well as orexigenic (NPY) signaling is increased. This might result in conflicting food intake signals. Interestingly, some eat more while others eat less following stressful experiences. The individual sensitivity and reactivity in these different neural circuits may underlie the response of food intake to a stressful situation.

It has also been shown that NPY induces changes in the daily rhythm of circulating corticosterone (which shows a rhythm over the day- night cycle) when rats’ food intake is restricted. Interestingly, AgRP, but not NPY, mRNA levels are reduced following a stressful event. Thus, although both orexigenic neuropeptides are colocalized in the arcuate nucleus and their expression appears similarly affected following fasting, their expression is differently regulated following a stressor.

Also, a-MSH interacts with the stress circuitry; central administration of a-MSH stimulates grooming and the release of ACTH and corticosterone in rats, and this activation is further increased in stressed rats.

Another overlapping system for food intake and stress responsivity is the catecholaminergic pathway between the brain stem and the hypothalamus, which is involved in feeding behavior as well as in stress responsivity. Physiological evidence that these systems indeed interact is provided by data showing effects of stress on food intake and vice versa.

Effects of Stress on Food Intake. Human studies showed that the psychophysiological response to stress is related to greater food consumption. Stress is the main trigger for obese patients to start binge eating. Moreover, people that release more cortisol due to a stressor are consuming more calories and eat significantly more sweet foods across days. Stress eaters gain more weight and are at greater risk for cardiovascular disease and type II diabetes.

In Cushing’s disease as well as in patients treated with corticosteroids for longer periods, a typical visceral form of obesity is induced. Generally, adrenal insufficiency is accompanied by reduced food intake and body weight. Removal of the adrenal glands in rodents results in reduced food intake and body weight, which demonstrates that corticosteroids are essential for maintaining a normal body weight.

More severe traumatic environmental stressors (e.g., the loss of a spouse) can have an opposite effect, decreasing food intake and fat stores. Stress is also thought to play a central role in anorexia nervosa. The neurodevelopmental model of anorexia nervosa proposes that chronic stress in predisposed individuals results in (maladaptive) hyperactivity of the HPA axis, resulting in a loss of nutritional homeostasis.

Other models, however, state that the principles of anorexia nervosa are starvation and physical activity, and that the consequential activation of the HPA axis is rewarding for the patient.

In animal models, the influence of stress (ranging from physical stress to social stress) on food intake has been studied extensively. The typical response of rodents to a wide range of stressors is to decrease food intake. Only in Syrian hamsters has it been shown that social stress increases food intake and fat stores.

Most experiments studying effects of stress on food intake in rats and mice have been done using normal lab chow, which is balanced, healthy, and high in carbohydrates. In daily society, however, humans have choices, and often have easy access to cheap foods with high fat and sugar content.

Providing rats with a greater choice of food results in different food intake responses when animals are subjected to a chronic stressor. Rats were given access to normal lab chow, lard, and a bottle of 1 M sugar water and were repeatedly restrained for 5 days, 3 h/day. Rats increased their intake of the more palatable items, lard and sugar, and consumed more of those as compared to the nonstressed animals.