**2. Physiology of human feeding**

The gastrointestinal tract processes ingested food via a complex series of actions in specific organs.

sensation that the stomach feels heavy. Some reports have suggested that delayed gastric

Diet in the Etiology and Management of Functional Dyspepsia

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Visceral hypersensitivity is also an important factor contributing to the feeling of dyspepsia. When a balloon is distended in the stomach of an FD patient, the threshold at which pain is perceived is significantly lower in FD patients compared to normal controls [11]. Such gastric

Different nutrients and food items may modulate gastrointestinal motor and sensory func‐ tions, and so provoke gastrointestinal symptoms. The three basic nutritional components (carbohydrates, proteins and lipids) can contribute to disturbed gastrointestinal function. The individual nutritional components impact gastric emptying and the sensation of fullness differently. 1. Lipids (fat) and proteins exert a negative ("braking") effect on gastric motility. Fat releases enteric hormones (such as CCK) that increase pyloric sphincter tone and delay

Proteins alter gastric motility, leading to a feeling of fullness and this provides satiety. 3.

Carbohydrates and some food chemicals (like salicylates and amines) give rise to an osmotic effect with increased luminal volume. This can result in a sensation of fullness particularly in

In addition to the individual nutrients, the caloric content, the physical form, and the ingested volume of food affect the sensation of satiety and fullness. High meal viscosity has a greater effect on the sense of satiety, whereas high caloric foods delay gastric emptying. [12,13].

Dietary nutrients influence gastrointestinal function and seem to be related to symptom generation. Thus, it seems logical that disturbances of gastrointestinal motor and sensory functions can lead to generation of gastrointestinal symptoms after food ingestion. However, usually mixtures of food items are eaten, creating difficulties when attempting to pinpoint the individual responsible factor and limiting advice in terms of dietary restrictions in patients with dyspepsia. Dietary measures are classically prescribed in the management of patients

**5. Role of meals in the generation of symptoms in functional dyspepsia**

Epidemiologic studies, both in the USA and Europe, have shown that 50 to 80% of subjects with functional dyspepsia indicate that their symptoms are meal-related [5]. Meal ingestion is associated with diverse changes in the environment of the gastrointestinal lumen, the gastro‐ intestinal function and potential physiopathological mechanisms. The two most cited causes of pathology are delayed gastric emptying and visceral hypersensitivity. After ingestion of a

with motility disorders, although they have not been systematically studied.

hypersensitivity relates to symptoms of postprandial pain, belching and weight loss.

emptying may be seen in up to 40% of FD patients [10].

**4. Nutrients and gastrointestinal function**

gastric emptying. 2.

patients with visceral hypersensitivity.

The esophagus propels food into the stomach though a relaxed lower esophageal sphincter that subsequently contracts to prevent gastroesophageal reflux. The functions of the proximal and distal stomach differ remarkably. Initially, the proximal stomach relaxes, providing a reservoir function. The distal stomach regulates the gastric emptying of solids by grinding and sieving the contents until the particles are small enough to pass the pylorus. The small intestine also regulates the gastric emptying rate through a feedback mechanism mediated by vagal nerves, and by physiological changes, such as gastric relaxation and the release of gastroin‐ testinal hormones [3].

The overall process of digestion is coordinated by interactions between the gut and brain. Hunger is the sensation that leads us to seek and consume food, whereas satiety notifies us when to stop feeding.

Food intake is influenced by several types of gastrointestinal signals. These signals, when elicited by receptors in the stomach, provide information to the brain via the vagus nerve [6]. The stomach functions as a food reservoir; its capacity limits food intake. The gastric distention associated with ingestion of food activates tension mechanoreceptors and this generates a feeling of satiety. Pyloric chemoreceptors have an important role in regulating gastric motility, a fixed energy load being emptied into the duodenum at a constant rate regardless of meal composition. Conversely, gastrointestinal peptides, secreted by the stomach and small intestine with meals, primarily exert short–term effects on food intake. The gut peptides that reduce meal size are cholecystokinin (CCK), glucagon, glucagon – like peptide 1, amylin, somatostatin, peptide YY and bombesin. In contrast, ghrelin appears to have the opposite effect, stimulating enhanced food intake [3].
