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HCl is produced by the parietal cells of the stomach. To begin with, water (H2O) and carbon dioxide (CO2) combine within the parietal cell cytoplasm to produce carbonic acid (H2CO3), which is catalysed by carbonic anhydrase. Carbonic acid then spontaneously dissociates into a hydrogen ion (H+) and a bicarbonate ion (HCO3–).
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The hydrogen ion that is formed is transported into the stomach lumen via the H+– K+ ATPase ion pump. This pump uses ATP as an energy source to exchange potassium ions into the parietal cells of the stomach with H+ ions.
The bicarbonate ion is transported out of the cell into the blood via a transporter protein called anion exchanger which transports the bicarbonate ion out the cell in exchange for a chloride ion (Cl–). This chloride ion is then transported into the stomach lumen via a chloride channel.
This results in both hydrogen and chloride ions being present within the stomach lumen. Their opposing charges leads to them associating with each other to form hydrochloric acid (HCl).
At rest, the number of H+– K+ ATPases present within the parietal cell membrane is minimal. The rest are sequestered within tubulovesicles in the parietal cell. Upon stimulation the vesicles fuse with the cell membrane which leads to the increased insertion of H+– K+ ATPase into the membrane, hence allowing for the increased movement of hydrogen ions into the stomach thus increasing acid production.
There are three ways in which acid production is increased. The first of these is via ACh, which is released from the vagus nerve. This is released firstly during the cephalic phase of digestion, which is activated upon seeing or chewing food, leading to direct stimulation of parietal cells via the vagus nerve. It is also produced during the gastric phase of digestion when intrinsic nerves detect distension of the stomach, stimulating the production of ACh by the vagus nerve.
The main regulation pathway involves the hormone gastrin which is secreted from G cells in the stomach. G cells are activated by the vagus nerve, gastrin related peptide, and by peptides in the stomach lumen produced via protein digestion. Activation of the G cells leads to the production of gastrin which is released into the blood and travels through the blood until it reaches the parietal cells. Gastrin binds to CCK receptors on the parietal cells which also elevates calcium levels causing increased vesicular fusion.
Finally, enterochromaffin-like cells in the stomach secrete histamine which binds to H2 receptors on the parietal cells. These cells release histamine in response to the presence of gastrin and ACh. This leads to increased fusion however it is via the secondary messenger cAMP as opposed to calcium in the other methods.
There are a number of ways in which acid production can be decreased.
The first of these is via accumulation of acid in the empty stomach between meals. This increase in acid leads to a lower pH within the stomach, which inhibits the secretion of gastrin, via the production of somatostatin from D cells. Once food has been broken down into chyme, it passes into the duodenum, triggering the enterogastric reflex. This reflex can be stimulated by distention of the small bowel, if there is excess acid in the upper intestine, the presence of protein breakdown products as well as excess irritation to the mucosa. Inhibitory signals are sent to the stomach via the enteric nervous system, as well as signals to the medulla – reducing vagal stimulation of the stomach. The enterogastric reflex is important in slowing down gastric emptying when the intestines are already filled.
The presence of chyme within the duodenum also stimulates entero-endocrine cells to release cholecystokinin and secretin, both of which play a variety of important roles in completing digestion, but also inhibit gastric acid secretion. Secretin is released by the S cells of the duodenum when there is excessive acid production in the stomach.
Other hormones including glucose-dependent insulinotropic peptide (GIP) and vasoactive intestinal polypeptide also work to decrease acid production in the stomach.
Excessive secretion of stomach acid can lead to the formation of peptic ulcers. Potential complications of peptic ulcers include excessive bleeding due to erosion through a blood vessel. There are two main drugs used to prevent excessive acid formation. H2 antagonists such as ranitidine bind to the H2 receptors preventing the binding of histamine and thus reduce acid secretion.
It is important to note that the other two pathways for stomach acid secretion still operate, thus acid secretion is only reduced and not completely inhibited. Proton pump inhibitors (PPIs) such as omeprazole bind to the H+– K+ ATPase (proton pump), hence preventing the transportation of hydrogen ions into the stomach lumen. PPIs completely prevent stomach acid formation due to hydrogen ions not being able to react with chloride ions in the stomach.
This is a state where there is a decrease in the volume of stomach acid produced. Achlorhydria can result in an increased risk of salmonella and cholera. There are a variety of causes and further tests must be undertaken to ascertain the cause to allow for a targeted treatment regime.
Most of us don’t give stomach acid a second thought, but some of us are reminded of its power when it leaks into our esophagus and causes heartburn.
The fact that your body contains an acidic liquid that could burn your skin is pretty impressive, right?
Here, we’ll answer these questions and more. So get ready to fall in love with your amazing stomach.
Stomach acid is essentially hydrochloric acid.
Scientists measure how acidic something is using the pH scale. This runs from 1–14, with 14 being highly alkaline, 7 being neutral, and 1 being highly acidic.
Alongside acid, your stomach produces a cocktail of digestive compounds, including enzymes like lipase, which breaks down fat, and pepsin, which breaks down protein.
Together, this heady mixture is called gastric juice. Incredibly, your stomach produces around 17 cups (4 liters) of the stuff each day.
Stomach acid is a dangerous thing to have sloshing around inside your body, so whatever it’s doing, it must be important.
Stomach acid occurs in nearly all fishes, amphibians, reptiles, birds, and mammals. So, evolutionarily speaking, it’s been around for a very long time. Evolution clearly holds this spicy juice in high regard.
It does this directly and also by activating enzymes that chop up compounds in your freshly swallowed lunch.
Stomach acid also helps the body absorb minerals, like magnesium, calcium, and iron, and other nutrients, like vitamin B12.
Although it's best known for its culinary skills, one of stomach acid’s most important jobs is to be a protector.
Bacteria and other pathogens are all around us. They would dearly love to enter our guts and set up shop among our “good” gut bugs.
That’s why people who take heartburn medications for long periods are more prone to infections and other complications.
These drugs, such as proton pump inhibitors, reduce the acidity in your stomach. So, bacteria from your mouth can work their way through your less hostile stomach and make it into your gut.
In general, the pH of the stomach stays at or below 4. According to experts, this level is — not coincidentally — “the pH level essential to kill potential microbiological invaders.”
Stomach acid is produced by parietal cells, which sit in pits in your stomach lining. And because this colorless fluid is dangerous, your body controls its release very carefully.
It can’t just flow freely all day. Stomach acid needs to be released at the right time.
The brain has a direct link to the stomach through the vagus nerve. When you’re expecting to eat or simply smell some delicious muffins, your brain sends a message to your stomach to release a hormone called gastrin.
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Gastrin helps trigger the release of gastric acid.
Gastrin is also released in response to certain components entering your stomach — particularly protein. And when your stomach is full, its walls stretch, and this also triggers gastrin’s release.
Alongside gastrin, a wide range of other compounds and hormones make sure stomach acid is pumped out at the right time. These include histamine and ghrelin, the so-called hunger hormone.
How does the stomach protect itself from acid?As we've mentioned, your brain, hormones, and other messengers keep a tight rein on your stomach acid. But it’s still released multiple times a day, so how does your stomach not get digested?
And scientists are still uncovering other compounds that help keep your stomach from digesting itself.
Some of these lesser-known actors are prostaglandins, a group of lipids that help repair damaged tissues and have a range of other jobs. Scientists now think that they also help protect the stomach from itself.
Other protective chemicals may include:
Nitric oxide: This gas acts as a biological messenger and may inhibit gastric acid secretion.
Hydrogen sulfide: This gas also acts as a messenger. There's evidence that it can reduce pH in the stomach and increase the amount of protein in the mucus lining.
Calcitonin gene-related peptide: This small protein is involved in everything from increasing blood flow to transmitting pain signals. It might also help reduce levels of gastric acid.
Overall, scientists have identified a whole host of compounds that can help dial up or down the amount of gastric acid in your stomach.
Aside from this incredible selection of signals, your stomach has other defenses, too.
For instance, the cells that line your stomach are tough — they're surprisingly resistant to acid, compared with cells elsewhere in your body. So, even if they are exposed to the acid, they can survive longer than most cells would.
And if all of the above fails, the lining of your stomach is excellent at repairing itself swiftly. The whole internal lining of the stomach is replaced every 2–4 days.
We hope, if nothing else, that this article has given you a new love for your stomach and its acid.
Not only can stomach acid help you digest food and absorb nutrients, it can also help fend off microbes that want to make you sick.
So, next time you have one of those burps where you feel a bit of acid coming up, don’t grimace; smile. But if the problem persists, make sure you talk with your doctor about your symptoms.
Stomach acid has a pH of between 1 and 3, which means it's highly acidic. It's more acidic than lemon juice and vinegar, which is 2–3 pH, but not as acidic as battery acid, which is around 0.8 pH.
Gastric acid and stomach acid are just different names for the same thing. "Gastric" is just the scientific word for something that is associated with the stomach.
Stomach acid is a hydrochloric acid solution.
High or low levels of gastric acid can be caused by many factors. For instance, low levels might be due to aging, stress, some medications, or zinc deficiency.
High levels of stomach acid can be caused by H. pylori infection, an excess of certain hormones, and certain health conditions.
Acid reflux, or heartburn happens when acid flows up into your esophagus (food pipe) and damages the sensitive lining.
A number of factors increase the risk of experiencing this unpleasant sensation, including being overweight, consuming fatty foods or alcohol, smoking, being pregnant, taking some medications, and lying down straight after eating.
For more information about the causes and how to find relief, try this episode of the ZOE Science & Nutrition podcast.
If left untreated, GERD increases the risk of developing:
ulcers
an inflamed esophagus (esophagitis)
narrowing of the food pipe (esophageal strictures)
changes in the lining of the esophagus (Barrett's esophagus)
esophageal cancer
GERD can be managed through dietary changes and medications, though. So, speak with your doctor.
If you produce too much stomach acid, you might experience heartburn, a sour taste in your mouth, or nausea. You might also bring up some sick or develop a cough.
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