Appetitive interoception, the hippocampus and western-style diet

Metabolic disorders, like type 2 diabetes and obesity, impose a looming threat to our well-being and overall health. One of the reasons behind this is the excessive intake of sugars and saturated fats, which are hallmark features of the dietary pattern known as the Western-style diet (WD). In this publication by Davidson & Stevenson (2022), the authors outline the underlying mechanism behind the relationship between WD intake and brain substrate modulations that play a role in interoceptive hunger and satiety signal processing. The authors present current evidence from human and rat studies supporting this theoretical mechanism, demonstrating how the ability of these interoceptive signals to alter eating and appetitive behaviors is dependent on hippocampal learning memory operational coherence, in particular, operations that utilize contextual information in the recall of memories linked to other experiences. Taking this concept in mind, the authors postulate that satiety interoceptive signals halt the reward perception after food intake in animals, regardless of the existence of further food cues or appetitive behaviors, which then become ineffective in recalling memories of reward. The authors comment that these results substantiate that WD intake (with elevated content of sugar and saturated fat) leads to physiological derangements, particularly in the hippocampus, encumbers the ability of interoceptive contextual stimuli of hunger and satiety from controlling dietary behavior, and interferes with hippocampal-dependent learning and memory (HDLM). Finally, the authors postulate that owing to the negative impacts of the WD pattern, a vicious cycle could emerge, potentiating further WD patterns, obesity, and worsening cognitive derangement. [NPID: Eating, inhibition, memory, obesity, satiety]

Year: 2022

Reference: Davidson, T. L., & Stevenson, R. J. (2022). Appetitive interoception, the hippocampus and western-style diet. Reviews in endocrine & metabolic disorders, 23(4), 845–859. https://doi.org/10.1007/s11154-021-09698-2