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The Digestive Cascade: What Happens When Food Enters the Stomach?



When a swallow of food passes through the LES and enters the stomach, it triggers a highly coordinated series of events designed to optimize digestion (see Figure 1)

Digestive Cascade
figure 1:Digestive Cascade


•   The stomach lining stretches a bit.
•   The stretching is sensed by nerve fibers that signal G cells to begin secreting gastrin.
•   Gastrin stimulates parietal cells to increase acid secretion and release. It also stimulates ECL cells to secrete histamine, which then stimulates parietal cells to increase acid secretion and release.
•   Parietal cells also release a substance known as intrinsic     factor, which is required for the absorption of vitamin B12.
•   Gastrin also triggers the release of pepsinogens from chief cells in the gastric mucosa.
•   Pepsinogens, in the presence of sufficient HCl, are converted into pepsin, the primary stomach enzyme responsible for breaking down proteins into amino acids. (The conversion of pepsinogen to pepsin occurs optimally when the pH of the stomach is 4 or less. If the pH should rise to 5 or higher [less acidic], pepsinogens are inactivated, and no pepsin is formed.)
•   While all this is going on, gastrin also signals the stomach muscles to begin churning and grinding away, helping to mix the contents and to move them along. Once the stomach’s contents (chyme) have been “fully acidified,” the processing of proteins and many other vitamins and minerals can move ahead at an optimal rate.
•   By the time the chyme reaches the lower reaches of the stomach, the pH begins to rise so that the digestion and absorption can take place in the small intestine. The acidity of the stomach is reduced in the lower regions of the stomach—the antrum and pylorus. This occurs by two main mechanisms. First, available acid stimulates D cells in the antrum to begin secreting the hormone somatostatin. Somatostatin feeds back to G cells to slow the production of gastrin. Less gastrin means less histamine and less acid secretion from parietal cells. Second,acidified chyme contacting the lining of the duodenum stimulates the release of the hormone secretin.
•   Secretin, in turn, signals the pancreas (a large gland best known for secreting the hormone insulin) to release a variety of digestive enzymes as well as ions of bicarbonate. Bicarbonate produced by the pancreas is actually the same as the “bicarb” that (i.e., sodium bicar bonate, or baking soda) that people have long used to relieve heartburn by neutralizing stomach acid (raising the pH).
•   Thehormone cholecystokinin (CCK) is released in the small intestine at the same time as secretin. It travels to the gallbladder, where it stimulates the release of bile—essential for the proper digestion of fats—into the small intestine.
This has been a highly simplified description of a vastly more complex process. Nevertheless, it serves to make five extremely important points about acid and GI function:
1.  These essential digestive functions can occur only within a very narrow range of pH, and that range shifts depending on the stage of digestion.
2.  “Blocking” or “neutralizing” stomach acid interrupts the normal digestive cascade at a crucial juncture. It removes the “acid trigger” that makes virtually every subsequent event in the sequence possible. Reducing acid means less pepsinogen, less pepsin, less secretin, less CCK, less pancreatic enzymes, and less bile.
3.  With less acid to feed back and turn down gastrin production, gastrin levels soar. As we discuss below, the excessively high levels of gastrin have been linked to a form of stomach cancer.
4.  Since the absorption of many vitamins, minerals, proteins, and amino acids occurs only within a narrow range of pH, disrupting the gastric digestive environment by reducing acidity (raising pH) adversely affects the processing and absorption of many of these nutrients.
5.  Consequently, even if we eat an excellent diet, if stomach acid levels are very low, we may be unknowingly partially starving ourselves. Not surprisingly, nutritional deficiencies are a common finding in people with long-standing atrophic gastritis as well as in people taking certain acid-suppressing drugs.











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