The Second Brain goes delightfully deep into the regulatory signals involved in gastric acid production. . The stomach is made up of several parts, which I am going to give diminutive summaries. There’s the cardiac region (the heartburn prevention valve), the corpus (food storage area), the fundus (backup food storage, primary burp storage unit), and the pyloric antrum (home of actual digestion). The cells that produce HCl (parietal cells) are in the corpus and fundus areas, where food sits and waits its turn to be digested. This means they don’t have very good information about how much acid is needed. Other parts of the body can send them information using three signals: acetylcholine (source: vagus nerve), histamine (enterochromassin-like cells), and gastrin (G cells).
Of these, gastrin appears to be the best understood. G cells live in the pyloric (“digesty”) region of the stomach. Based on a variety of signals, including pH and stimulation from the vagus nerve, they release gastrin to signal a variety of digestion-related cells to release that digestion is happening. Parietal cells release gatric acid, chief cells release pepsinogen, the valve between the small and large intestine opens (to create room for new food), and the valve between the stomach and throat close (to prevent heartburn).
Those of us who once had allergies so bad they kept us home from school will remember histamine as the thing that simultaneously put us to sleep and created itching so painful we could not sleep through it.* The digestive histamine is the same chemical, but is secreted within the stomach and so (I assume) does not risk what we classicly think of as an allergic reaction.** Histamine is not so much a signal to produce gastric acid as the absence of histamine signals cells not to produce it, no matter what other signals they get. Histamine is produced by Enterochromaffin-like cells, which are intermixed with the parietal cells (along with other enteroendocrine cells) in the corpus and fundus gastric regions. ECL cells are stimulated to produce histamine via gastrin (the same gastrin that stimulates HCl production directly) and pituitary adenylate cyclase-activating peptide which, if I’m reading this correctly, can act as both a neurotransmitter and a hormone (which is rare but apparently not unheard of. I will refer to this dual-purpose molecules as ballerina-astronaut messengers). Dr. Internet is curiously silent on the topic of what cells release pituitary adenylate cyclase-activating peptide. If it’s reaching G cells as a neurotransmitter it must be coming from the vagus nerve, but there may be other mechanisms as well.
Lastly there is directly nerve stimulation, coming from our friend the vagus nerve, delivered via third and more traditional neurotransmitter, acetylcholine. So the inputs to the system appear to be signals from the digesting food, and a tiny wizard sending out electrical sparks via the vagus nerve. This wizard can be encouraged to do so via things like chewing and thinking about food, but we do yet not understand his simple yet beautiful language.
Here’s the interesting things: the parietal cells that produce HCl also produce something called intrinsic factor, which preps vitamin B12 for digestion. This is very, very rare. Almost all cells in the body do exactly one thing. These two things aren’t even related. The Second Brain is a little vague on what stimulates intrinsic factor production: it says it uses the same signalling molecules as HCl, but not that they’re triggered by the same receptors, or that they react identically to the signal. It’s the kind of vagueness that makes me think we don’t know for certain.
But it seemed plausible that they might be related, and thus the same factors that cause a gastric acid shortage could cause a B12 shortage. I have a gastric acid shortage. Could I have a B12 shortage? I checked the symptoms: it’s a complete grab bag, because B12 is used for DNA synthesis and energy production, and there is no system that does not affect. I pull out my last blood test results: B12 was high normal. It’s seven months old, but there’s every reason to believe my B12 has gone up since then.
There are two categories of explanations for why I produce insufficient HCl: either the signal to produce is not reaching my parietal cells, or my cells don’t react to the signal properly. The signal to the parietal cells to release intrinsic factor seems to work thus fine. If it’s the same signal (which I need to research more), this strongly suggests the problem lies inside the cell rather than in the signal. This is disappointing because my “mumble mumble vagus nerve” hypothesis was both interesting and led to a pleasant treatment plan (keep up the sensory integration work aimed at my misophonia). Now I will have to investigate the intracellular manufacture of HCl.
*”Us” is an optimistic term. I am very rare in finding histamines fatiguing, and I sure hope very few people experienced allergic pain like I did.
**Nor do anti-histamines like Claritin, whose makers I once pledged my hypothetical firstborn child to, interfere with digestion. Drugs marketed as anti-histamines act on only one of three possible histamine receptors (H1), and it’s not the one you find in the stomach. Drugs that affect that receptor (H2) are marketed as anti-heartburn medications.
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