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Updated: Jul 11, 2026

Intermittent Binge-Intake Model in Mice
Published on: January 10, 2025
Binge eating is associated with right orbitofrontal-insular-striatal atrophy in frontotemporal dementia
J D Woolley1, M-L Gorno-Tempini, W W Seeley
1Memory and Aging Center, Department of Neurology, University of California San Francisco, 1779 Turk St., San Francisco, CA 94115, USA. jwoolley@memory.ucsf.edu
Background:
Neurophysiologic studies on human and nonhuman primates implicate an orbitofrontal-insular-striatal circuit in high-level regulation of feeding. However, the role of these areas in determining feeding disturbances in neurologic patients remains uncertain.
Objective And Methods:
To determine brain structures critical for control of eating behavior, we performed a prospective, laboratory-based, free-feeding study of 18 healthy control subjects and 32 patients with neurodegenerative disease. MR voxel-based morphometry (VBM) was used to identify regions of significant atrophy in patients who overate compared with those who did not.
Results:
Despite normal taste recognition, 6 of 32 patients compulsively binged, consuming large quantities of food after reporting appropriate satiety. All six patients who overate were clinically diagnosed with frontotemporal dementia (FTD), a disorder previously associated with disordered eating, while the nonovereaters were diagnosed with FTD, semantic dementia, progressive aphasia, progressive supranuclear palsy, and Alzheimer disease. VBM revealed that binge-eating patients had significantly greater atrophy in the right ventral insula, striatum, and orbitofrontal cortex.
Conclusion:
Binge eating can occur despite reported satiety and is associated with damage to a right-sided orbitofrontal-insular-striatal circuit in humans. These findings support a model in which ventral insular and orbitofrontal cortices serve as higher-order gustatory regions and cooperate with the striatum to guide appropriate feeding responses.
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