The digestive chain: how stomach acid, bile and pancreas set each other off

Healthy state

Digestion begins before the first bite is in your mouth. Seeing, smelling and expecting food trigger the cephalic phase via the vagus nerve Vagus nerve The tenth cranial nerve and the most important nerve of the rest-and-digest system. It connects the brainstem and the abdominal organs; most of its fibres tell the brain what is happening in the gut. More in the chapter “The vagus nerve: the data line between belly and head”: saliva flows, the stomach makes acid, the pancreas releases its first enzymes, and even insulin is released in advance. This preparation helps make better use of nutrients.

In the gastric phase, food stretches the stomach, and protein building blocks reach the lining. Both stimulate the G cells to release the hormone gastrin. Gastrin drives the parietal cells to make acid. The acid activates pepsin, which splits protein, and releases vitamin B12 from food. When the stomach becomes very acidic, the hormone somatostatin slows gastrin production again. A feedback loop.

Then the stomach passes the acidic mush on to the duodenum in portions. Now the intestinal phase begins, and this is where two key hormones sit. The acid triggers secretin Secretin A hormone from the duodenum. It is triggered by stomach acid and makes the pancreas and bile ducts release bicarbonate to neutralise it. in the gut wall. Secretin makes the pancreas and the bile ducts release a bicarbonate-rich fluid that neutralises the acid. This is necessary, because the pancreatic enzymes only work at an almost neutral pH.

Fat and protein in the duodenum, by contrast, trigger CCK CCK (cholecystokinin) A hormone from the duodenum. It is released in response to fat and protein, makes the gallbladder contract and calls up digestive enzymes from the pancreas. , cholecystokinin. It was discovered in 1928 because it makes the gallbladder contract. CCK calls up the bile, makes the pancreas release digestive enzymes, slows stomach emptying and signals fullness to the brain. Secretin and CCK reinforce each other.

The pancreas releases its protein enzymes as inactive precursors so that it does not digest itself. Only in the small intestine does an enzyme of the gut wall activate trypsin, and trypsin activates the others. At the end of the small intestine, the ileal Ileum The last section of the small intestine. It recovers bile acids, absorbs vitamin B12 and joins the colon via the ileocaecal valve. More in the chapter “Where the small intestine meets the colon: ileum, valve and caecum” brake closes the circle: if nutrients still arrive there, GLP-1 GLP-1 A hormone from the gut wall that controls insulin release after eating, slows the stomach and makes you feel full. Weight-loss injections mimic it. More in the chapter “GLP-1 from the gut: what bacteria do and what “natural Ozempic” cannot do” and PYY slow the stomach and appetite.

Between meals another signal takes over. The hormone motilin rises in bursts when fasting and triggers the housekeeping wave in the stomach and small intestine, the MMC (migrating motor complex Migrating motor complex A wave of muscle contractions that sweeps the stomach and small intestine empty about every one and a half to two hours when fasting. Eating interrupts it. More in the chapter “Intermittent fasting and meal timing: 16:8, 5:2 and Ramadan”). As soon as you eat, it falls and the wave pauses until the meal has been processed. Gastric emptying is also fed back: fat and acid in the duodenum slow the stomach so that the small intestine is not flooded. So the chain controls not only the start of digestion but also its pace.

Disrupted state: causes and effects

The widespread assumption that “stomach acid triggers the bile” is only partly true. Acid is the main signal for secretin and thus for the neutralising bicarbonate. Bile is called up mainly by fat and protein via CCK. In a small study of 20 healthy people, a single intravenous dose of the acid blocker omeprazole did not change gallbladder emptying after a meal. This says nothing about long-term use.

If stomach acid is lacking, for example because of proton pump inhibitors Proton pump inhibitors (PPIs) Acid blockers such as omeprazole or pantoprazole. They inhibit the acid pump in the stomach lining. More in the chapter “Acid blockers (PPIs): what they change in the gut and how to stop them properly” or inflammation of the lining, the body releases more gastrin. Protein pre-digestion in the stomach becomes weaker, vitamin B12 is released less well, and more germs survive the passage. The pancreas still takes over most of the protein digestion, so major digestive problems are rare. Heartburn, too, does not come from too much acid alone: too little acid can weaken the valve to the oesophagus and make the stomach hold food for longer, which also irritates.

If the bile store is lost, for example after removal of the gallbladder, bile flows constantly in small amounts instead of in a bundle at mealtimes. Most people cope well with this. Some tolerate large, high-fat meals less well or get diarrhoea because more bile acids Bile acids Substances made by the liver that make fat digestible. About 95 percent are reabsorbed in the last part of the small intestine; gut bacteria transform the rest. More in the chapter “Bile acids: when bile causes diarrhoea” reach the large intestine.

If the gallbladder is hardly called on, for example on a very low-fat diet, with long fasting or rapid weight loss, the bile stands still for a long time. Then sludge and stones can form.

If the pancreas does too little, all the signals are of no use: fat stays undigested, and the stool becomes greasy, pale and foul-smelling. This is a condition in its own right that can be measured and treated well.

Self-tests for “too little stomach acid” circulate online, for example with baking soda and the time until you burp, with betaine HCl capsules as the remedy. The baking soda test has not been validated, and there are no good studies of betaine HCl for digestive symptoms. With damage to the lining or ulcers, acid capsules can do harm.

The whole chain hangs on the vagus nerve. If it is damaged, for example in long-standing diabetes (autonomic neuropathy), after stomach surgery that cut the nerve or after some infections, the signals reach the stomach, gallbladder and pancreas more weakly. You then feel full early, have a sense of fullness, and the stomach empties with delay. Lasting stress and hasty eating can also dampen the head phase. That this leads to noticeable symptoms is plausible, but the long-term effect has been little studied.

Around eating, some assumptions persist stubbornly. Drinking with a meal does not “dilute stomach acid” in a way that measurably disturbs digestion; the stomach adjusts acid amount and pace. Separating food groups (food combining) is not necessary, because the stomach and pancreas adapt to mixed meals. And digestion that “does not get going” is far more often down to pace, stress, motility or medication than to a lack of acid.