Heart Rate Variability is one of those things that has such an obvious meaning I feel dumb asking follow up questions, but is consistently used in ways that confuse me. It sounds a lot like arrhythmia, which is bad, but The Willpower Instinct consistently refers to it as good. Plus it refers to it changing in ways that must be measured instantaneously, but changes in variability have to be measured over time, right?
Here is what I have figured out: we (I) think of the heart as beating to A Rhythm, which is your BPM. The rhythm can speed up or slow down, but it’s still a rhythm. A deviation from that is an arrhythmia, which is Bad. We (I) think this because the wikipedia article on sinus rhythm basically says it, and because the article on HRV implies it’s measured in five minute increments over 24 hours, which means it’s basically a measure of range. But at least some of the time HRV refers to beat-to-beat variation, and it’s being measured in response to an immediate stimulus (although, maddeningly, no one specifies the time period).
Your parasympathetic (relaxed/restorative) nervous system sends signals to your heart to decrease your heart rate. Your sympathetic (fight/flight/freeze) system sends signals to increase it. High parasympathetic activity also seems to be associated with high variability, at least to a point. My personal guess is that high variability indicates both systems are operating and interacting, while low variability indicates one has taken over, and that your body is somewhat biased towards a higher rate, so it takes a bigger push from the parasympathetic to get the rate down. Having one system dominate is not always bad: when you are running from a tiger, your heart should beat as fast as possible and redirect blood from digestion and immune system to muscles. And when you are truly safe, the parasympathetic tells your body it can safely pay off it’s technical debt. But often having both, and being able to switch between the two, is useful.
There’s a lot of data showing high heart rate variability is increased by known Good Things (meditation, exercise), and low HRV is associated with bad things (alcoholism, PTSD), but I don’t see hard enough data on causality that I’m confident of the direction.
The typical explanation for motion sickness is that your inner ear and your eyes disagree about whether or not you are moving, your body interprets it as food poisoning, and prepares to throw up. This does not quite make sense to me, because it fails to explain any of the following:
Why being a passenger is so much worse than being the driver.
Why playing video games (eyes say movement, ears say stationary), reading in a bus (eyes say stationary, ears say moving) and riding a roller coaster (eyes and ears both say moving very fast) produce the same feeling.
Why smooth rides (subways, no-turbulence airplanes) are so much easier than busses, or why highways are easier than stop and go traffic.
Apparently other people consider nausea a stomach issue, but for me it’s very much a head issue. Motion sickness also gives me headaches. What’s up with that? Why is it so tightly correlated with sinus pressure?
Why does low blood sugar feel so much like motion sickness?
I’ve never experienced this, but television assures me heavy drinking produces the same effect. Why?
Why does motion sickness give me temperature fluctuations.
I’ve heard a partial explanation for #3, which is that your inner ear actually senses acceleration, not movement, so a steady velocity doesn’t feel like movement. And we have a very compelling proximal explanation for #6: the difference in density between water and alcohol stimulates your inner ear both as you get drunk and as you sober up. So obviously the inner ear is very involved in this, but how?
Alternate hypothesis: motion sickness is designed to keep you from eating, because your body is not in a good state to digest. One way that can happen is if your sympathetic nervous system (responsible for fight-or-flight-or-stand-there-being-really-anxious) has kicked in, because it redirects blood flow and energy to things that are immediately useful in escaping from tigers (muscles, senses) and away from things that solve future you problems like digestion and the immune system (which are regulated by the parasympathetic nervous system).
Both the sympathetic and parasympathetic systems are regulated by the hypothalamus. For fun I googled “hypothalamus motion sickness” and the first result was this rat based study,* which put rats in a “animal centrifuge” to induce motion sickness. I couldn’t find video of a rat centrifuge, but NASA helpfully provided video of a dog centrifuge. It looks not quite as bad as a tilt a whirl, although the rats were exposed to double gravity so I should probably cut them some slack.
During their amusement park adventures, the rats experienced a spike in histamine production in the hypothalamus (how cool is it that we can continuously measure that?), and caused the rats to display characteristic motion sick rat behavior. Inhibiting histamine production or removing the inner ear (the part that detects motion) caused both of these to disappear. Histamines also help regulate body temperature, so that’s #7. This suggests that anti-histamines would be useful at fighting motion sickness. The good news is that this is correct, the bad news is that they make you sleepy and possibly give you Alzheimer’s. That’s fine for any one time but I don’t want to make a lifestyle out of taking them.
A website my laptop unfortunately ate the link to has a subtly different explanation: your brain tracks motor movement via an efference copy, creates a prediction of what sensory changes that should create, and they compares that to the actual sensory input. Motion sickness might be your brain saying “these are too different, abort, abort”, or buckling from the intensity of calculation needed to reconcile the input.
I have always wondered why I/people hold my (our) breath during times of stress. Unless you’re being hunted by a xenomorph right that second, oxygen deprivation is not helpful.
The most convincing hypothesis I’ve found is that your brain can only do so many calculations per second, compensating for breathing takes calculation, so you stop breathing. That this rapidly starves your brain of oxygen, lowering the number of calculations you can do, is exactly the kind of long term thinking I expect from the human body which, lest we forget, takes in air and food through the same hole. If both breath-holding and nausea can be caused calculation overload, we would expect the same things to cause them both. I can think of two things that do exactly this off the top of my head- sparring (but not drills) in martial arts, and playing Katamari, both of which involve complex spatial reasoning. These are not great examples because there’s a lot of confounding variables, like extreme physical exertion while being hit in the stomach.
To summarize my speculation: sensory input requiring too high a rate of calculation points you towards your sympathetic nervous system, which makes you nauseous so you won’t eat while you’re not capable of digesting.
This suggests that anything that kicks you towards the parasympathetic system should reduce motion sickness. Unfortunately the parasympathetic and sympathetic systems run on the same neurotransmitters, so looking at the relevant drugs does not provide useful information.
This also suggests that anything that lowers the number of calculations you need to do will be helpful. BCMC tested a heads up display that showed users their head position relative to the horizon.
Studies found it overwhelmingly helpful, although I haven’t dug into that paper in detail yet. Unfortunately there’s no way to purchase the technology, so I’m left hoping someone picks up the patent.
In conclusion: we don’t really know what causes motion sickness and that there’s no known really good treatmen. I am going to experiment with consciously tracking my head position relative to horizon and with rhythm games (which help integrate sensory data).
*The second result appears to be the exact same experiment, done 10 years earlier, with the exact same result. It’s nice to see something reproducible.
I’m taking on sinus inflammation because it’s a major contributor to my motion sickness, which is a major contributor to making commuting suck, and commuting is one of very few things that can actually depress your hedonic set point (psychologist talk for “make you miserable”). My doctor has suggested xylitol nasal spray, which she claims inhibits irritation in the sinus cavities. Quick googleing reveals it’s also considered useful for bacterial plagues on the teeth and in the arteries. Let’s dig in.
Xylitol’s main claim to fame is as a calorie-less sweetener in humans. The claim is that it kills (many but not all strains of) bacteria via the same mechanism: it can’t be converted into energy, so the bacteria starve to death. This has to be to be missing a step. Bacteria are surrounded by billions of molecules they can’t digest all the time, and they survive that. If xylitol is to have an affect it must not only be indigestible, but inhibit digestion of actual sugar. Off the top of my head there’s two ways that could happen. In the human body, sugar is moved around by the blood. If xylitol takes a sucrose molecule’s ticket to a particular area, there will be less sugar there for bacteria to eat. The downside of this is that you might starve out your own cells. Another option is that bacteria cells themselves become confused by xylitol. The ideal would be if xylitol fit into a sugar receptor but couldn’t be taken into the cell, so the receptor was blocked indefinitely. Or if it was taken in it could trigger a “yup, we got a sugar” reaction that caused the cell to take in sugar later, but I’m not sure why a bacteria would ever turn down calories.
I found a lot of studies on xylitol and dental use. Most of what I learned is that dental abstracts are more like teasers than summaries, not cluttering up the space with numbers or sometimes even conclusions. Overall there seems to be a mild consensus for xylitol mildly inhibiting cavities, although it’s certainly not a substitute for fluoride. Also I totally should have been chewing xylitol while I was recovering from surgery, since is almost certainly disrupts oral plaques, although I worry about what it would do to the intestinal biome.
What about sinuses? I found a lot of very small studies, but 5 studies of size n are not equivalent to one study of size 5n. You don’t know how many more studies of size n were done but not published.
This study and this one found decreases in medical severity (as measured by the SNOT-20 score. Yes that’s it’s real name), but not self-reported pain (as measured by the less well named VAS score). This study in rabbits was well controlled (if small) and found significant decreases in bacteria.
This study found that a nasal decongestant spray worked better than xylitol or saline spray, which worked about equally as well. Nontheless it’s conclusion was that [name brand of xylitol spray] was an effective treatment for nasal congestion. It also spelled spray with an ‘e’ . Twice.
One interpretation of these results is xylitol helps impedes infection but irritates the sinuses such that there’s no change in pain levels. Another is that people are really good at suppressing conscious knowledge of pain. My experience has been I’m really good at suppressing moment-to-moment awareness of pain but I do notice when asked (which is how I went weeks without treating my dental neuralgia, and then suddenly noticed I was at 8 on the pain scale), and that the pain has a great deal of effect on my behavior and happiness whether I acknowledge it or not. And if I keep using xylitol I need to change my brand to one that, when it buys positive press in a supposedly objective forum, spells its own name correctly.
I don’t even know where to start. This book was fun to read and I felt like I learned a lot. It covered both the specific facts of Robert Koch’s quest to prove germ theory and cure tuberculosis, and provided a good general sense of how science and medicine move forward and don’t.
A couple of specifically interesting points: doctors fought germ theory tooth and nail. They also rejected stethoscopes as technological interlopers to be disposed of because they threatened the doctors importance, while using so many leaches prosperous countries had to import them. The naive interpretation is “doctors are idiots, their reluctant to use quantified self data is proof they haven’t changed.” This is the first time I’ve seen any hint as to why they found germ theory so implausible. In the particular case of tuberculosis, everyone was exposed all the time, and it took the infection years to become symptomatic. Preventing any one exposure wouldn’t have had noticeable results. Another early-identified bacteria was Anthrax, which didn’t follow a typical exposure pattern either. The doctors still come out looking pretty bad for refusing to wash their hands between autopsies and childbirth, but marginally less than they might have.
I knew this already, but it was good to have a reminder that the first person to suggest the germ theory of disease, Ignez Summelweis, died in an insane asylum. This either means that people with truly visionary ideas can be broken when we reject them, or germ theory was so crazy it took a crazy person to see it. Goetz doesn’t mention it but according to my dad Summelweis was also an asshole, which I try to remind myself every time someone mean says something I disagree with.
Remember last week when I suggested using microchips to force people to finish their antibiotics? Several friends seriously questioned the effect of that, since they didn’t estimate the contribution of unfinished antibiotics to antibiotic resistance as very high. The Remedy says that the current protocol for drug resistant TB is to have a medic visit a patient every day for 6 -24 months to observe them taking their pills, because drug resistant TB is that big a problem and the pills are that unpleasant. So at least in that situation swallowable microchips would be an enormous improvement.
Apparently syphilis is always the [nationality] disease, where the nationality is not the speaker’s. French is the most popular, but far from the only
I’ve always found the methods section the most boring of any paper or textbook. I want to know what we learned, not how. But The Remedy (and to a lesser extent Neanderthal Man, which I reviewed last week) made it seem interesting. I’m still not terribly interested in microscopy, but it was deeply interesting to see how advances in technology enabled scientific advances. Using or inventing new technology is how you move the world forward. And when I thought about it, the modern field that most reminds me of the wide-open-ness of microbiology in the mid 1800s is programming. That is where I get the most sense of possibility. I still really care about translational health (in fact this book taught me that that is the word for what I am trying to do with this blog) and mental health, but I am feeling more and more like staying in programming would be the best way to accomplish that.
Yesterday I made an offhand remark that the Red Cross was so persistent in stalking me because I was O-. Here’s why that’s important:
Your red blood cells can have two different proteins on them (A or B), or both, or neither. If you receive a transfusion with red blood cells with a protein you don’t have, your immune system will mark it as a foreign invader and attack it. If you get too much of these cells, you will die. Parallel to this is another protein Rh factor, which you either have (Rh+) or you don’t (Rh-). A- means you have A proteins, but not B or Rh factor. If you are Rh- and receive Rh+ red blood cells, same problem.
O- red blood cells have no immune-triggering proteins on it, and so can be given to anyone. That makes O- blood extremely useful when you don’t have time to type a patient, or have limited carrying capacity. Moreover, O- red blood cells are the only type O- patients can accept. So O- is often the first to run out.
You might think this makes donations from AB+ people pointless, but that is not the case. Their red blood cells are of limited use, but their blood plasma (which is the part that contains the antigens that trigger attacks on foreign matter) contains no antigens to any blood type. Meanwhile everything looks like an invader to my O- plasma, and it will react accordingly. This also means you can only do whole blood donations between complete type matches. A B+ person can take my red blood cells, but would need plasma from someone else.
And that is why typed-matched blood is preferred and donations of all types are necessary.
Seattle is apparently not the only Effective Altruism group to talk about doing volunteering meetings, only to remember that the traits that make volunteering useful are almost antithetical to the traits that make it fun and doable to for a group on a drop-in basis. I am kind of hoping that blood donation can bridge that gap. So here’s my math on how effective donating blood is. The Red Cross estimates a single donation can save three people, but what they mean is “a single donation can go to three different people.” To get the actual value we need to see how many units of blood were donated and how many deaths they prevented.
The most recent data I could find was the 2011 National blood Collection and Utilization Survey Report (PDF), which couldn’t make it harder to do this kind of calculation if it tried. They were extremely loose with what “unit” referred to, so I’m going to stick with the whole and red blood cell transfusions, so my numbers are consistent. There were 15,721,000 units collected, of which 14,589,000 were deemed usable. 13,785,000 were used, of which 37,000 were directed to a specific patient, and 65,000 were self-donations, which are less effective for various reasons. The collections numbers don’t call out general vs. specific donations and the numbers are small, so I’ll just use the total number used. If some blood donations are also generating plasma and white cells in addition to the red blood cells counted here, that would only increase effectiveness.
A single donation is one pint. Health and Human Services fails to define what they mean by unit, but it appears to mean “whatever you get from one donation after some filtering“, so let’s assume it’s 1:1. The average recipient receives 2.75 units. If you assume each person who received a transplant would otherwise die (supported by this sourceless FAQ), that means each donation saves ~1/3 of a life (discounting for donations that are rejected). Using GiveWell’s $5,000/life number, that’s still equivalent to donating $1,667. That is overstating the case, because some portion of recipients (I can’t find out how many) have diseases like sickle cell anemia that require chronic transfusions, and the fair thing is to count their lifetime transfusion count, not their per treatment count. To get an upper bound I’ll use the Red Cross’s number that a car accident victim can use up to a 100 pints of blood, which means each donor saves 1% of that life, which is equivalent to $50 to an extremely effective charity.
But the question isn’t “what is the average value of donated blood?” but “what is the marginal value of your potential donation?” I can’t find any direct numbers for this, but we have the following evidence:
Very little blood is thrown out.
People are spending lots of time and money developing artificial blood substitutes. Despite this there are no generally accept substitutes for blood’s oxygen-carrying capacity.
The Red Cross spends a lot of time and money harassing people to donate. They called my parents’ house for years after my one donation (I’m O-).
Some blood is able to reach the “too old” state, but then used to ill effect, indicating lumpy supply or demand. Unless you can predict demand spikes you should use the average efficacy. If you can predict demand spikes, there are probably more effective things to do with that power.
So I’m just going to use the average effectiveness as the marginal effectiveness for now.
What are the costs to the donor of donating? The one time I donated it was high because I slept for the next two days. If you’re my friend Elena who went into shock after donating, it cost you days and several thousand dollars in ER visits. So it is probably not worth it for either of us to donate. But for a typical person with no side effects, it’s plausibly useful. If it’s replacing work time, then effectiveness depends on their hourly wage. Multiple websites list the time to donate as 60-90 minutes, which translates to a minimum psuedowage of $33/hour and a maximum of $1667. The average hourly American wage is $24/hour, although I would estimate the average wage of people earning to give as somewhat higher than that. So that’s extremely plausible on its face. But if the time isn’t coming out of work, and is made rewarding to the participant, blood donation is hugely effective. This suggestions that an event that induced people to donate without replacing work would be effective, more so if it could be made into a positive experience. So a blood donation event could be a huge win for an EA event.
[Side note: if you decide to do this yourself, I would recommend donating anywhere but the Red Cross if at all possible. I’m going to try for Bloodworks NW, because if I get enough people they will send a truck and we can make it an actual party]
When I started this blog I intended to leave programming for medicine fairly soon. After a long medical leave that let me recover from burnout, I realized that programming is actually a really valuable skill and before I throw it away and spend several years in school, I should see how far it can take me towards my goals. My goals are unchanged (mostly around nutrition and mental health, but with some bonus input from Effective Altruism), but maybe there’s a better way I can contribute.
Eventually this means founding or joining a company working on something I care about, but I’m still not capable of consistently working sufficient hours to work with other people. But I can play on my own projects with no coordination costs, so I started learning to program for android. Meanwhile on the health end, my nutritionist informs me there are states of hunger between “unpleasantly bloated” and “would shank an infant for juice” that are useful to experience, and that the first step to achieving that is tracking my hunger consciously. She meant with pen and paper, but I am an engineer, so I wanted something on my magic pocket computer to do it for me. I’m sure something exists on android that would do this, but I couldn’t find it, so I did the logical thing and started developing my own.
Thus was born the Hunger Tracker app. Here is my dream feature list for Hunger Tracker:
Alarm goes off at pre-set or random times (your choice), to shut it off you enter a number between 0 and 9, representing your fullness level.
Timestamp + fullness level data is dumped…somewhere, I don’t know. A google docs spreadsheet would work for me but there’s probably other services I should integrate with.
UI not actively offensive
Here’s what version 0.1 does
No alarm, user must manually call up app.
User enters number in ugly ass UI. Actually user can enter any arbitrary string, but don’t, it will break the retrieval.
User can retrieve first 10 numbers entered. Any further entries are skipped, if there are too few entries the last one is repeated.
It’s a debug build rather than a release build because Android Studio won’t produce a working release build and fixing that is not at the top of my priority list.
If you are interested, you can download version 0.1 here and install it the usual way for non-market apps. If you are spectacularly interested, you can check out the source code at github. Comments are extremely welcome
My next step is not actually features, but testing, which I will explain in the next entry.