Article: Satiety, that elusive feeling of fullness, supports mental health and controls appetite.

Food noise, the persistent mental chatter about food, decreases with satiety, the feeling of fullness after a meal. Satiety is triggered by gut-derived anorexigenic hormones like Glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK), and peptide tyrosine-tyrosine (PYY). Studies show that microbiome health and diet play crucial roles in effective hormone signaling essential to achieve that ever elusive feeling of fullness.

 Recently, the American Society of Nutrition defined food noise as

“Persistent thoughts about food that are perceived by the individual as being unwanted and/or dysphoric and may cause harm to the individual, including social, mental, or physical problems.”

However, questions remain. How can food noise be measured? What differentiates food noise from normal thoughts about food? While research is ongoing there is general consensus that food noise subsides when satiety is reached. This observation has gained momentum with the increasing popularity of GLP-1 drugs, which promote the feeling of fullness. Individuals consistently report that satiety reduces the persistent, unwanted mental chatter about food.

Satiety is triggered by gut-derived anorexigenic hormones like Glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK), and peptide tyrosine-tyrosine (PYY). Conversely, ghrelin, an orexigenic hormone, enhances appetite. These gut-derived hormones influence satiety via the bi-directional communication of the gut-brain axis. Gut-derived signals are transmitted through the vagus nerve to the brainstem and hypothalamus which in turn registers satiety sending efferent signals back out to the body that regulate food intake and maintain metabolism.

Several clinical trials show that protein increases anorexigenic hormone levels while decreasing orexigenic hormone levels, resulting in increased satiety signaling. Further, studies indicate that high protein intake increases energy expenditure by triggering downstream metabolic pathways in the liver (hepatic gluconeogenesis and ketogenesis) that also contribute to increased satiety.

Additionally, short-chain fatty acids (SCFAs), produced by gut bacteria enhance the stimulation of gut-derived hormones, PYY and GLP-1. Dietary fiber, primarily derived from plants, is the main food component that affects the production of SCFAs. Gut bacteria in the large intestine, primarily the proximal colon, convert dietary fiber into SCFAs (propionate, butyrate and acetate) via anaerobic fermentation. Further, SCFA production occurs downstream in the digestion process, commencing approximately 6 hours after food intake, extending the feeling of fullness. Effective SCFA production is directly proportional to diet and microbiome health.

A compromised microbiome triggers immune responses, systemic inflation and breakdown of the gut barrier. Poor gut health interferes with gut-brain axis communication and the ability to effectively signal satiety with emerging evidence linking dysbiosis to neurological disorders. Fermented foods such as yogurt and kefir provide probiotics that enhance gut health and microbiome diversity. Probiotics, as part of a healthy balanced diet that includes protein and dietary fiber, boost microbiome health creating an environment poised to support gut-brain axis communication.

In summary, individuals report a decrease in food noise when satiety, the feeling of fullness, is achieved. Satiety is triggered by gut-derived anorexigenic hormones. A healthy microbiome and a well-balanced diet play a crucial role in effective hormone signaling. Both protein and dietary fiber promote satiety. In the presence of a healthy microbiome, these nutrients trigger a cascade of gut-brain axis signals that enhance the feeling of fullness and help control appetite.