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Commentary |

The Right Brain Hypothesis for Obesity

Miguel Alonso-Alonso, MD, MPhil; Alvaro Pascual-Leone, MD, PhD
JAMA. 2007;297(16):1819-1822. doi:10.1001/jama.297.16.1819.
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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.

Corresponding Author: Alvaro Pascual-Leone, MD, PhD, Department of Neurology, Beth Israel Deaconess Medical Center, 330 Brookline Ave, KS 452, Boston, MA 02215 (apleone@bidmc.harvard.edu).

Financial Disclosures: Dr Alonso-Alonso reports that he was accepted in the Clinical Investigator Training Program, which supports his salary and provides formal training in various aspects of clinical research. This program was set up as a joint venture of the Harvard-MIT Division of Health Sciences and Technologies and the Beth Israel Deaconess Medical Center, supported by unrestricted educational grants from Pfizer and Merck Inc. During 2006, he was funded by the Fundación para la Investigación y Desarrollo del Complexo Hospitalario Universitario de Vigo (FICHUVI), Galicia, Spain. Dr Pascual-Leone reported no financial disclosures.

Funding/Support: The work on this article was partly supported by grants from the Boston Obesity and Nutrition Research Center (P30 DK46200), National Institutes of Health grant K24 RR018875, and the CITP Program.

Role of the Sponsor: None of the funding organizations played a role in the design and conduct of this work; collection, management, analysis, interpretation of the data; or the preparation, review, and approval of the manuscript.

Acknowledgment: We thank Clifford B. Saper, MD, PhD, Harvard Medical School and Beth Israel Deaconess Medical Center; Eleftheria Maratos-Flier, MD, Harvard Medical School and Beth Israel Deaconess Medical Center; Christos Mantzoros, MD, DSc, Harvard Medical School and Beth Israel Deaconess Medical Center; and Jeffrey S. Flier, MD, Harvard Medical School and Beth Israel Deaconess Medical Center, for valuable comments and suggestions. None received compensation for their feedback in the development of this article.

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Figure. Brain Areas Involved in the Regulation of Food Intake and Schematic Representation of Their Interactions in the Proposed Model
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The regulation of food intake in humans involves 3 hierarchical levels of control: cognition, homeostasis, and reward. Information on nutritional status is transmitted from the periphery to lower brain centers by neural and humoral signals. Indirect evidence suggests that peripheral mediators may also act on the cerebral cortex (dotted line). Extensive interconnectivity between these regulatory pathways allows precise and integrated control of food intake according to internal and external factors. These interactions are complex and may be inhibitory or facilitatory. Homeostatic and reward circuits (reflexive eating mode) tend to favor food intake. Brain areas involved in cognition (reflective eating mode), especially the right prefrontal cortex (PFC), tend to decrease food intake. Under normal circumstances, reflective areas can override and suppress reflexive areas (thick arrows). When activity of the right PFC is diminished, however, cognitive control of food intake decreases, favoring obesogenic habits.

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