
How Food Choices Shape Memory, Cognition & Cravings | Dr. Scott Kanoski
Dr. Scott Kanoski, professor at USC, studies how diet impacts memory, cognition, and appetite. In this episode, he discusses the interplay between hunger, food choices, and brain function, from GLP-1 drugs to artificial sweeteners and the microbiome.
GLP-1 and Appetite Control- GLP-1 (glucagon-like peptide 1) is a natural incretin hormone released from the gut (and also produced in the brainstem). It suppresses appetite and helps regulate blood glucose.
- GLP-1 drugs (e.g., Ozempic, Wegovy) superphysiologically elevate GLP-1 levels, leading to weight loss but also side effects like nausea.
- Appetite suppression partly occurs via the vagus nerve (paracrine signaling). Reducing "food noise" may involve higher brain regions (hippocampus, prefrontal cortex), but the exact mechanisms are still under investigation.
- The evidence on artificial sweeteners is mixed. Three camps exist: harmless, harmful, or uncertain.
- Preclinical studies by Kanoski showed that juvenile rats consuming artificial sweeteners (stevia, Ace‑K, saccharin) within FDA limits later exhibited memory deficits and altered glucose regulation as adults – even after the sweeteners were discontinued.
- These rodent findings are not directly translatable but raise caution, especially for developing brains.
- Memory of recent meals influences subsequent eating: recalling a meal leads to less consumption later.
- A "magic soup bowl" experiment (unbeknownst refilling/emptying) revealed that satiety initially depends on actual intake, but hours later it depends on perceived (remembered) intake.
- Unhealthy diets (Western diet: high sugar and saturated fat) cause hippocampus-dependent memory deficits in rodents, persisting even after switching to healthy chow.
- Heat-treated food (Maillard reaction) produces Advanced Glycation Endproducts (AGEs). In a preprint study, an AGE-rich diet impaired memory in rats; this could be reversed by reintroducing a specific Lactobacillus strain.
- Gut bacteria populations change with diet. In the high-sugar model, Parabacteroides increased and correlated with worse memory. Enriching this bacterium in otherwise healthy animals induced memory deficits.
- Conversely, Lactobacillus was depleted by heat treatment and positively correlated with memory; replenishing it rescued the impairment.
- The microbiome field is still young – we cannot yet list specific "good" or "bad" bacteria.
- The vagus nerve carries signals from the gut to the brain. Vagotomy (cutting the nerve) can cause memory problems in both rats and humans (suggested by epidemiological data).
- Kanoski’s lab identified a three‑step pathway: vagus → medial septum → hippocampus, using acetylcholine as a key neurotransmitter.
- Fiber photometry shows acetylcholine release in the hippocampus ramps up during eating and stays elevated post‑meal – likely to encode the memory of the eating episode.
- Notably, artificial sweeteners (e.g., stevia) do not trigger this acetylcholine release; actual nutrients are required.
- Oxytocin is best known for bonding and appetite reduction.
- However, in the hippocampus and during social contexts, oxytocin can actually increase food intake (social facilitation of eating). This illustrates the complexity of neuroendocrine regulation.
- Diet profoundly shapes memory and cognition through gut–brain signaling, the microbiome, and neurotransmitter systems.
- The reward system is plastic: shifting to healthier foods can recalibrate preferences, making ultra‑processed foods seem overly sweet or unappealing.
- Dr. Kanoski emphasizes that many questions remain – especially regarding GLP‑1 mechanisms and specific gut bacteria – but the research offers actionable insights for maintaining brain health through nutrition.





