Memory and eating: A bidirectional relationship implicated in obesity

• Published in: Neuroscience and biobehavioral reviews Vol. 132; pp. 110 - 129
• Main Authors: Parent, Marise B., Higgs, Suzanne, Cheke, Lucy G., Kanoski, Scott E.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 01-01-2022
• Subjects: Amnesia; Appetite; Cognition; Diet; Eating; Episodic memory; Feeding Behavior - physiology; Food intake; Hippocampus; Hippocampus - physiology; Humans; Interoception; Obesity; Satiation; Appetite; Diet; Interoception; Food intake; Cognition; Amnesia; Episodic memory; Hippocampus
• ISSN: 0149-7634; 1873-7528; 1873-7528
• DOI: 10.1016/j.neubiorev.2021.10.051

•Meal-related memory inhibits eating in humans.•Amnesia is associated with overeating and impaired interoception in humans.•Research in rodents and humans implicates the hippocampus in these effects.•Obesity disrupts memory and hippocampal functioning in rodents and humans.•These effects of obesity may create a vicious cycle that perpetuates obesity.
This paper reviews evidence demonstrating a bidirectional relationship between memory and eating in humans and rodents. In humans, amnesia is associated with impaired processing of hunger and satiety cues, disrupted memory of recent meals, and overconsumption. In healthy participants, meal-related memory limits subsequent ingestive behavior and obesity is associated with impaired memory and disturbances in the hippocampus. Evidence from rodents suggests that dorsal hippocampal neural activity contributes to the ability of meal-related memory to control future intake, that endocrine and neuropeptide systems act in the ventral hippocampus to provide cues regarding energy status and regulate learned aspects of eating, and that consumption of hypercaloric diets and obesity disrupt these processes. Collectively, this evidence indicates that diet-induced obesity may be caused and/or maintained, at least in part, by a vicious cycle wherein excess intake disrupts hippocampal functioning, which further increases intake. This perspective may advance our understanding of how the brain controls eating, the neural mechanisms that contribute to eating-related disorders, and identify how to treat diet-induced obesity.