Changes in food composition and availability have contributed to the dramatic 
increase in obesity over the past 30-40 years in developed and, increasingly, in 
developing countries. The brain plays a critical role in regulating energy 
balance. Some human studies have demonstrated increased preference for high fat 
and high sugar foods in people reporting greater stress exposure. We have 
examined neurochemical changes in the brain in rodent models during the 
development of obesity, including the impact of obesity on cognition, reward 
neurocircuitry and stress responsiveness. Using supermarket foods high in fat 
and sugar, we showed that such a diet leads to changes in neurotransmitters 
involved in the hedonic appraisal of foods, indicative of an addiction-like 
capacity of foods high in fat and/or sugar. Importantly, withdrawal of the 
palatable diet led to a stress-like response. Furthermore, access to this 
palatable diet attenuated the physiological effects of acute stress (restraint), 
indicating that it could act as a comfort food. In more chronic studies, the 
diet also attenuated anxiety-like behavior in rats exposed to stress (maternal 
separation) early in life, but these rats may suffer greater metabolic harm than 
rats exposed to the early life stressor but not provided with the palatable 
diet. Impairments in cognitive function have been associated with obesity in 
both people and rodents. However, as little as 1 week of exposure to a high fat, 
high sugar diet selectively impaired place but not object recognition memory in 
the rat. Excess sugar alone had similar effects, and both diets were linked to 
increased inflammatory markers in the hippocampus, a critical region involved in 
memory. Obesity-related inflammatory changes have been found in the human brain. 
Ongoing work examines interventions to prevent or reverse diet-induced cognitive 
impairments. These data have implications for minimizing harm caused by 
unhealthy eating.