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.
Keywords: Dopamine; Hippocampus; Memory; Obesity; Overeating; Reward; Stress.
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