When I was first diagnosed with low gastric acid, I assumed that the acid was needed to physically break down the food, which never quite made sense because protein itself is mildly acidic. It turns out that I was wrong, and that the primary effects of gastric acid are to denature protein (which a protein loses its shape without losing any of the covalent bonds between amino acids) and to activate digestive enzymes.
[Backing up a step: enzymes are biological catalysts. Given the right materials, they make chemical reactions happen faster. But enzymes are not perfectly specific, and can do a lot of damage in the wrong environment. For example, food enzymes digesting your food is good. Food enzymes digesting your stomach is bad. One way to maximize positive effects and minimize negative effects, or simply waste, is to produce the enzyme in an inactive form (known as a zymogen) that can be activated once the enzyme has moved to the correct environment or the correct raw materials are available.]
There are many digestive enzymes, but the one of interest to me right now is pepsin. Pepsin is one of three primary enzymes that digest protein, and the only one produced in the stomach. Or rather, the stomach produces it’s zymogen, pepsinogen. Pepsinogen is useless until it’s turned into pepsin by gastric acid, which is also produced in the stomach (but in a different cell type). Pepsin can also be inactivated by high concentrations of the products of the reactions it’s catalyzes, a common pattern called a negative feedback loop.
So high gastric pH/low gastric acid inhibits protein digestion by keeping pepsin in its inactive form. It’s possible that what I have is not low gastric acid but low pepsin levels. All HCl supplements contain significant amounts of pepsin, so that could be why they help. Digestive enzymes didn’t do me any good until I started HCl, so I don’t think that’s the explanation, but I can’t rule it out with the current data.
Gastric acid production is stimulated by the hormone gastrin (note that this is far from the only effect of gastrin release), which is itself stimulated to production by gastrin-release peptide. GRP is stimulated to production by “the vagus nerve”, which is technically true but not informative, because nerves are mere messengers, and the real question is who is sending the message. There is the research pointing to a link between sensory input and digestive chemicals. Other research pointing to a link between gastric flora and gastrin (more). But the honest answer is that we don’t know.
Which puts the question in good company. This post barely scratches the surface of what we know about the chemistry of digestion, and there’s a lot of we don’t know, and that we don’t know we don’t know.