The effects of cortisol on the reward system may be partly
mediated through increases in insulin, NPY, and leptin. Insulin
has acute effects inhibiting the reward system [76] and we
speculate that chronic exposure to circulating insulin may stimulate
the reward system, as in the case of insulin resistance. The
effect of those mediators on the brain reward center may contribute
to a state of hedonic withdrawal, leading to the subsequent
drive to relieve this negative state. People have learned that
intake of highly palatable food can do just that. The natural
reward of highly palatable food can directly or indirectly reduce
activity of the HPA axis [5]. This has been described as ‘self
medication’ with food [5,119]. Changes in neuroendocrine
balance (high cortisol and insulin) from eating when under stress
might further sensitize the reward center of the brain, leading to a
positive feedback loop drive to maintain opioid stimulation from
palatable food (not shown in Fig. 1). Thus, stress eating is a feed
forward process. In the end, it is unclear whether continued stress
is even necessary to maintain the drive for palatable food, since
hedonic withdrawal may be enough to sustain continued drive
without stress. Lastly, given that cortisol and eating stimulate
insulin, the combination of stress and highly palatable food
intake sets up potent conditions for visceral fat storage. While
this model is speculative, the data at this point show that human's
stress related energy intake is not very different than that of the
rat. Further, a recent review suggests that stress induced cortisol
exposure may impair right prefrontal cortex activity, thus impeding
the more reflective cognitive control over eating that is
distinct to humans [120]. While recent research has elucidated
likely pathways for stress-eating, there is much progress to be
made in trying to understand an