The<unk><unk>  reduces the size of the stomach by well over 90%. A normal stomach can stretch, sometimes to over 1000 mL, while the pouch of the<unk><unk>  may be 15 mL in size. The<unk><unk>  pouch is usually formed from the part of the stomach which is least susceptible to stretching. That, and its small original size, prevents any significant long-term change in pouch volume. What does change, over time, is the size of the connection between the stomach and intestine and the ability of the small intestine to hold a greater volume of food. Over time, the functional capacity of the pouch increases; by that time, weight loss has occurred, and the increased capacity should serve to allow maintenance of a lower body weight. When the patient ingests just a small amount of food, the first response is a stretching of the wall of the stomach pouch, stimulating nerves that tell the brain that the stomach is full. The patient feels a sensation of fullness, as if they had just eaten a large meal—but with just a thimble-full of food. Most people do not stop eating simply in response to a feeling of fullness, but the patient rapidly learns that subsequent bites must be eaten very slowly and carefully, to avoid increasing discomfort or vomiting. Food is first churned in the stomach before passing into the small intestine. When the lumen of the small intestine comes into contact with nutrients, a number of hormones are released, including cholecystokinin from the duodenum and PYY and GLP-1 from the ileum. These hormones inhibit further food intake and have thus been dubbed "satiety factors". Ghrelin is a hormone that is released in the stomach that stimulates hunger and food intake. Changes in circulating hormone levels after<unk><unk>  have been hypothesized to produce reductions in food intake and body weight in obese patients. However, these findings remain controversial, and the exact mechanisms by which<unk>  reduces food intake and body weight have yet to be elucidated. For example, it is still widely perceived that<unk><unk>  works by mechanical means, i.e. food restriction and/or malabsorption. Recent clinical and animal studies, however, have indicated that these long-held inferences about the mechanisms of Roux-en-Y<unk><unk>  (RYGB) may not be correct. A growing body of evidence suggests that profound changes in body weight and metabolism resulting from RYGB cannot be explained by simple mechanical restriction or malabsorption. One study in rats found that RYGB induced a 19% increase in total and a 31% increase in resting energy expenditure, an effect not exhibited in vertical sleeve<unk> tomy rats. In addition, pair-fed rats lost only 47% as much weight as their RYGB counterparts. Changes in food intake after RYGB only partially account for the RYGB-induced weight loss, and there is no evidence of clinically significant malabsorption of calories contributing to weight loss. Thus, it appears RYGB affects weight loss by altering the physiology of weight regulation and eating behavior rather than by simple mechanical restriction or malabsorption. To gain the maximum benefit from this physiology, it is important that the patient eat only at mealtimes, 5 to 6 small meals daily, and not graze between meals. Concentration on obtaining 80–100 g of daily protein is necessary. Meals after surgery are ¼–½ cup, slowly getting to 1 cup by one year. This requires a change in eating behavior and an alteration of long-acquired habits for finding food. In almost every case where weight gain occurs late after surgery, capacity for a meal has not greatly increased. Some assume the cause of regaining weight must be the patient's fault, e.g. eating between meals with high-caloric snack foods, though this has been debated. Others believe it is an unpredictable failure or limitation of the surgery for certain patients (e.g. reactive hypoglycemia).
Gastric bypass surgery
Endoscopic sleeve gastroplasty
Vertical banded gastroplasty surgery
Sleeve gastrectomy
Adjustable gastric band
Collis gastroplasty
SILS gastric banding
Bariatric surgery