A recent review by Rajita Sinha and Ania Jastreboff from the Yale Stress Center, New Haven, CT, USA, provides an integrative perspective on the neurohormonal mechanisms by which stress affects reward pathways, and how the interactions between the stress and reward systems may contribute to the epidemic of obesity.
In spite of the well-known link between stress and obesity, the nature of this association remains poorly understood, including why is it some people lose weight when stressed, whereas others gain weight?
Animal research indicates that stress in most cases is related to a reduction in food intake. Interestingly, in rats, when given a choice of highly palatable food, such as lard or sugar, stress, in fact, increases intake of that palatable food. In humans, most individuals increase their food intake during stress yet a much smaller number of people, roughly 30%, are able to reduce food intake and lose weight during or after stress (cf. TC Adam & ES Epel, Physiol Behav, 2007, 91: 449).
In addition, an increasing body of evidence indicates that the brain reward circuitry may play a major role in stress-induced food intake (TC Adam & ES Epel, Physiol Behav, 2007, 91: 449). Furthermore, hedonic systems in brain influence food intake and excessive consumption of palatable food can trigger neuro-adaptive responses in brain reward circuitries similar to drug abuse (PJ Kenny, Neuron, 2011; 69: 664).
As with drug abuse, palatable food can activate the brain reward system, comprising opioid, dopamine and endocannabinoid signaling. This, in turn, produces a powerful behavioral reinforcement for both acquisitions of drugs as well as palatable food (TC Adam & ES Epel, Physiol Behav, 2007, 91: 449).
In their review Drs. Sinha and Jastreboff sum up recent research indicating the involvement of brain reward regions in obesity. They discuss how stress and glucocorticoids potentiate dopaminergic transmission, while stress-induced release of orexigenic neuropeptide Y (NPY) and the increased NPY messenger RNA expression in the hypothalamus, amygdala, and hippocampus increase feeding but also decrease anxiety and stress.
These overall changes increase food craving, motivation and intake of highly palatable (HP) foods. Thus, stress has been reported to increase binge eating and the consumption of fast food, snacks, and calorie dense and HP foods. In addition, the craving for desserts, snacks, and higher HP food intake, particularly, in overweight individuals and/or obese women increase as well.
The authors suggest a heuristic model of how HP foods, food cues, and stress exposure through alterations of metabolic, stress, and reward-motivation pathways in the brain are able to drive increased HP food motivation and intake. This includes:
Stress- and metabolic- related hormones influencing brain reward regions and prefrontal cortical circuits involved in reward prediction, self-control, and decision making;
With weight-related adaptations in neurohormonal and behavioral responses, a vulnerable individual becomes highly susceptible to food cues-related and stress-related HP food craving, predicting HP food intake;
Promotion of weight gain, and increased sensitization of brain motivation pathways, to raise HP food motivation and intake, exceptionally under conditions of food cue or stress exposure.
The authors conclude that despite some advances in behavioral and pharmacological obesity treatment, it is unclear how they relate to normalizing stress, metabolic, and reward disturbances in susceptible obese individuals.
This research is in its infancy, but given the current world-wide obesity epidemic, it may require greater attention in the future.
“People may very well choose to trade off years of their life, or the possibility of disease or injury, in exchange for the current pleasure, excitement, or stress relief they get from food”