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Early satiety and fullness

Early satiety is the defined as the sensation of fullness after eating before one would normally expect. It is often, but not always accompanied by weight loss and loss of appetite (anorexia). The triggers for development of the sensation of fullness are complex. The normal mechanisms for triggering satiety involve neural, hormonal and psychological factors which all interact with each other and may be influenced by other genetic and. Usually after eating satiety is triggered by a combination of gastric distension and the movement of food through the small bowel which leads to the release of a number of hormones, the most influential ones being CCK and glucagon like peptide – 1 (GLP-1). CCK is released in response to meals containing fat and protein entering the duodenum, it slows the emptying og the stomach, stimulates the pancreas to produce digestive enzymes and triggers feelings of satiety in the brain. GLP-1 is  slows gastric emptying when food containing fat and carbohydrate reaches the distal small bowel (ileum), this leads to further gastric distension and the sensation of satiety. Both genetics, an individuals micobiome (the bugs that live within us) and other environmental factors influence when and how these hormones are released. During periods of stress most mammals including humans loose the ability of their upper stomachs to relax in response to distension (a process known as accommodation). Similarly psychological stress delays the emptying of food from the stomach and this too leads to early satiety.

Whilst early satiety may be associated with weight loss this is not always the case. Early satiety is often transient, lasting for a single meal or a day or two, reduced intake can be easily corrected in subsequent meals. The human body is amazingly good at adjusting food intake to match caloric consumption over periods of two to four weeks. As a consequence significant weight loss is unusual in the absence of significant illness (either psychological or physical). Over longer periods other hormones, including leptin and ghrelin have an impact on satiety and appetite control. Ghrelin is produced in response to a number of stimuli including starvation or sleep deprivation and tends to drive increased appetite, particularly for foods of high calorific value. Leptin is released by fat cells in response to increasing adiposity and tends to reduce appetite, but both of these hormones are influenced by a wide variety of neural and metabolic triggers, rather than simple “feast or famine”.

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