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Commentary
April 25, 2007

The Right Brain Hypothesis for Obesity

Author Affiliations
 

Author Affiliations: Berenson-Allen Center for Noninvasive Brain Stimulation, Behavioral Neurology Unit, Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass.

JAMA. 2007;297(16):1819-1822. doi:10.1001/jama.297.16.1819

The prevalence of obesity continues to increase exponentially worldwide. In the United States, where the majority of the adult population is at least overweight, this condition accounts for an economic burden in billions of dollars per year. Despite increased awareness and determined efforts, the epidemic remains uncontrolled and constitutes a global public health problem. Moreover, the current state of knowledge may not include critical aspects of the etiology of obesity.

Research during the past decades has drawn attention to the role of the brain in the regulation of food intake and the pathogenesis of obesity. The current paradigm, derived from carefully studied animal models, emphasizes neuroendocrine circuits involved in the control of appetite, with the hypothalamus as the main orchestrator. Peripheral information from the gastrointestinal tract, the pancreas, and adipose tissue is provided to the hypothalamus and brainstem via the vagus nerve and hormonal mediators, such as ghrelin, insulin, and leptin (Figure). As a result, adjustments in feeding and energy expenditure take place to ensure an adequate balance that matches bodily needs. Aside from satiating appetite, eating provides feelings of gratification, and palatable foods stimulate brain circuits of reward and motivation, engaging limbic and paralimbic areas under the modulatory influence of neurotransmitters and releasing neuropeptides, such as dopamine and endorphins. Beyond genetic predispositions and metabolic needs, hedonic aspects of food intake are important to understand body weight regulation and the genesis of obesity.

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