Last month I watched Home, a documentary about a charity offering homes to poor people (maybe just poor single mothers?) at a significant discount. It focuses specifically on one woman who applied for help and the case worker assigned to her. Watching it, I was struck by how much the case worker defined her goal as getting this woman this house, rather than helping her, or giving the house to the person to whom it would do the most good. I thought it was a case of cargo cult, another friend described it as a cultural fixation on helping the poor by making them middle class rather than making being poor bearable. Either way, it seemed to me like an example of misapplied charity.
Last week I started training to volunteer for a crisis hotline. One of the things they drill into us is that most callers have a lot of problems we can’t solve. We have very few tools: occasionally we make referrals if they have certain specific issues (e.g. we’ll offer LGBTQ kids the number for the Trevor Project, or suggest they call 211 to get referrals to programs that could help their material problems), but mostly we listen. That is what we do. We are to apply that one tool as best we can. If it helps, great. If not, we end the conversation anyway. There’s a weird tension between “Anything is a crisis if it feels like one to you. We’re here to listen to anyone, any time, for any reason.” and “Some people are just black holes, cut them off after 45 minutes. But they can call back tomorrow.”
The only way I can justify this is by thinking “We have one tool. It’s impossible to know if this tool is what this person needs. Even when it is, there are diminishing returns to using the tool. After 45 minutes, the marginal returns to further use are 0. Therefore, treating everyone as receptive at minute 0 and no one as receptive at minute 45 is the optimal use of our time.”
I still think the case worker in the movie was pushing her tool too hard, and not listening when the person she was nominally trying to help brought up very reasonable concerns. But I’m a lot more sympathetic to the myopia now.
The library took away The Second Brain and there’s a long wait to get it back, so we’ll be putting digestive issues aside for a moment and talking more about sensory stuff. While I have a variety of issues that are in retrospect sensory, the driving complaint that drove me to seek treatment was misophonia. You know how nails on a chalkboard or a crying baby creates a kind of aural pain you can’t block out? Misophonia is having that reaction to sounds normally considered safe. http://misophonia-meerkat.tumblr.com/ is full of people are driven to thoughts of self harm or even suicide by very common sounds, like breathing, low bass, and typing. Luckily, I’m not nearly that bad. But I also find it almost impossible to concentrate when people are talking, and work in an open office.
I have a new SI therapist (who I have yet to compare to a Guantanamo Bay interrogator, which makes her much better than the last one) who says my problem lies in my vestibular system, so let’s do some recon on that. The vestibular system has two parts: a series of canals that track rotational acceleration, and two sacs that track acceleration in a single direction. I wrote several paragraphs explaining exactly how these work, but ultimately I don’t think I added much over wikipedia, so I’m just going to summarize. The canals and sacs are constructed differently but operate on the same physical principle: if you have a rigid container holding a liquid, the atoms in the solid share momentum/inertia with each other but not the atoms in the liquid. That’s why you can spill water by moving a glass very quickly, even if it’s perfectly level the whole time. The canals and sacs detect this somewhat differently- the canals are filled with an electrically charged fluid (endolymph) that interacts with electrically sensitive hairs when you spin, which triggers a signal to the relevant nerve. You have three canals, each of which detects rotation in a different plane. Do not bother reading the descriptions of which plane each covers, they do not make any sense. Instead, read this article on the axes of rotation for airplanes. The theory is equivalent and the pilots have much better diagrams.
The sacs have a number of stones or crystals sitting in a gel, and nervous system is triggered when the stone hits the sac wall, bending the hairs on it. Both sacs provide information on both horizontal and verticle movement, but the uticle is more sensitive to vertical movement and the saccule more sensitive to horizontal.
Note that both of these track changes in movement, not movement itself. In order to track speed, your brain needs to keep track of your existing state and then calculate the change indicated by the vestibular organs. It then automagically triggers the necessary changes in posture and eye movement to keep you upright and looking at your target. That is why you can read when shaking your head, but not when someone moves your book.
Motion sickness is caused by a disagreement between your vestibular system and your eyes about how fast you are moving, which means my trick of looking at a fixed point in the vehicle was exactly wrong. What I need to do is look outside so my eyes track motion.
At this point, I have two questions: what can go wrong in these systems, and how to do they relate to misophonia, which is a hearing thing, not a balance thing?
I alluded to my terrible, horrible, no good very bad allergies in my post on parietal cell signaling, and it struck me that I haven’t worried about my allergies in a very long time . They were the first medical problem of mine that I cured, and I cured them so thoroughly I’d forgotten they were ever an issue. There probably won’t be any long posts explaining allergic mechanisms because I don’t have a use case for the data, but I thought I could at least tell you what cured me.
To set the stage: it was my senior year in college. I was on three different medications for my allergies (a rhinocort inhaler, hydroxyzine, and a rotating anti-histamine like Zyrtec or Claritan). Those kept me from sleeping 14 hours a day or developing debilitating hives, and it even controlled the sinus headaches as long as I didn’t do anything stupid like get on an elevator. It took about two days for the motion sickness from elevator riding to dissipate. That’s nothing compared to pre-treatment, when I would arrange my books so I had to move my head as little as possible because that small movement would give me a headache.
A friend suggested local, unprocessed honey. I had nothing to lose, so I tried it. I almost immediately dropped down to one medication, and felt better than I had on three. When I moved to Seattle at the end of the year, my allergies were entirely controllable by honey, and then just gone. Every once in a while they resurface, I eat some honey, and the problem goes away.
After it worked I started researching. I remember finding a fair amount of scientific support at the time, but when I went looking for this post I failed to find any peer-reviewed support for the notion. Additionally, I realized that I’d been buying honey made from specific pollen based on what tasted best. But I was tested for allergies as a chlid, and I barely had pollen sensitivity: the majority of my symptoms were caused by dust mites. And yet, they had improved.
So I absolutely believe honey worked for me but I have no idea why or how.
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.
This is less about giving you physiological information- there’s nothing here you couldn’t look up yourself in six seconds- and more about demonstrating my process for fact checking information sources.
The Second Brain spends an awful lot of time talking about how miraculous the enteric nervous system (the nerves integrated with the large and small intestines) is (are), because they respond to stimuli in predictable manners even when cut off from the brain. It contrasts this with all other reflexes, with the implication that they do require a connection to the brain. That struck me as not right. I could have sworn the entire point of reflexes was that they worked without the brain.
I checked with Dr. Wikipedia, and I was half right. In humans reflexes are defined by not needing to reach the brain- but they do need to reach the spinal column. What makes the enteric system special is that it keeps operating without any connection to the spinal column or brain at all. That’s still not entirely unique; the heart does it too. But as it turns out, both the heart and intestines receive signals via my new fixation, the vagus nerve. The Second Brain talks as if the vagus nerve is the only connection the enteric system has with the gastrointestinal system, but like its use of the word reflex, I suspect I’m slightly misreading it. I’m very sure the heart has additional connections, because the vagus nerve is responsible for only the slow-down signal, and at a bare minimum there must be something to send a speed-up signal.
This one will be short because the alternative is that it be very, very long. The short version is that our brain does a lot of work we are not consciously aware of to make sensory input make sense. More than that, different input takes a varying amount of work, and the areas of the brain that do that work can become exhausted to the point they cannot function, just like a muscle. The tests for sensory integration issues involve stimuli specifically designed to overwork these regions and observing what fails first (each region producing different characteristics mistake).
[As an aside, if you are getting tested for sensory processing issues, don’t plan on doing much afterwords. The whole point of the test is not only to mentally exhaust you, but to do so in a way your conscious brain is blind to. I am convinced hardened spies would reveal anything if you interrogated them after a sensory integration test.]
People with sensory integration issues find this processing more taxing- either because they’re fed more or noisier input, their brains have a lower capacity, or their brains are attempting to do more processing on the data. My most obvious symptom is some noise sensitivity, but there’s also a school of thought that sensory and digestive issues are linked. I wish I could tell you more on this, and I will, eventually, but I don’t have very good sources. My (now ex-) sensory integration therapist gave me a book that referred to thimerosal causing autism as if it was an undisputed fact.* I’d burn it if the exercises weren’t so helpful. So we’re going to put a pin in this and I’ll tell you more when I know it.
I mentioned sensory issues and digestive issues appear to be linked. Some of it is that a lot of sensory issues seem to relate to the trigeminal nerve, which is also involved in chewing. If the issues make chewing unpleasant, people won’t do it, which has a lot of gastrointestinal consequences. But there’s more than that.
I’m reading a book called The Second Brain, which I will undoubtedly have more to say about when I’m more than five pages in. But already it’s discussing the enteric nervous system and how it appears to perform complex, coordinated behaviors without any input from the brain or spine.** This tickled something I found in my research on the gastric system: the vagus nerve.
I have only minimal neurology, so take this description with a grain of salt, but: the Vagus nerve is a nerve collection that goes straight from the brain to certain parts of the body, without going through the spinal cord. Those parts? The digestive system, the heart, some reproductive and sexual organs, and the trigeminal nerves. This is a long way from conclusive, but it is does suggest that time spent studying the vagus nerve could benefit me.
**It implies that the enteric system is unique in this. I have a vague sense it’s not, or at least that I’m misrepresenting what is unique about it, but I’d need to research it to be sure.