Crush Cravings Naturally: How Beta-Glucan Harnesses the Gut–Brain Link to Suppress Hunger
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Beta glucan can influence the brain to reduce or stop cravings by modyfying gut hormones and, to a lesser extent, by influencing central neuroimmune and neurotrophic pathways.
In human studies, oral intake of beta-glucan-enriched foods acutely affects two key hormones: it increases plasma peptide YY (PYY) and decreases ghrelin concentrations, both of which affect which appetite and satiety: PYY promotes satiety, while ghrelin stimulates hunger. The net result of beta-glucan is a reduction in subjective hunger and a decrease in subsequent energy intake, as demonstrated in controlled feeding studies with beta-glucan-enriched bread.
Beta glucan can also influence central nervous system pathways involved in mood and reward that in turn then affect food cravings. In mice, beta glucan administration stimulates the growth of cells in the hippocampus, leading to increased brain-derived neurotrophic factor (BDNF) synthesis. Increased BDNF signaling is associated with improved mood and reduced depression-like behaviors, which are often linked to emotional eating and cravings. However, it is important to note that these central effects have been demonstrated in animal models only and their direct relevance to human food cravings remains to be established.
Human data are limited but suggest possible improvements in psychological wellbeing and mood states, with a favorable safety profile, though optimal dosing and long-term effects in humans remain to be established.
Beta glucan also improves gut barrier function, reshaping the intestinal microbiota, and in turn increasing production of short-chain fatty acids, collectively reducing inflammation and improving cognitive outcomes animal models of obesity and Alzheimer’s disease.
In summary, the primary mechanism by which beta glucan reduces or stops cravings is through by increasing a hormone that promotes satiety and decreasing a hormone that leads to hunger. Overall, this leads to enhanced satiety and reduced appetite. Secondary central effects on neuroimmune and neurotrophic signaling may also contribute, particularly in the context of stress or mood-related eating behaviors.
-Dr. Diana Rucker
References:
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