Top Dog talks about some very interesting research into group dynamics. According to the studies they cite, working in dyads requires a very different set of skills than working in groups, to the point that techniques that are beneficial for one can be detrimental in the other. The most productive way to interact with a group is as a team: with each person taking a specialized role, which includes letting some people be more valuable than others. Dyads function best if both people are pretty equal. Treating a group of 5 as 4 individual dyads and managing the relationships as such is exhausting and slows down the group considerably.
My (new, good) sensory integration therapist’s current hypothesis is that the areas of the brain that coordinate between senses aren’t working properly in me. In particular, she thinks my vestibulo-ocular reflex (the system that automatically adjusts your eyes to compensate for movement) is weak. This seems plausible. I get motion sick easily and am constantly running into things, which indicates a proprioception/kinesthesia problem. But those are not the symptoms that drove me to seek treatment; my inability to filter out sound and especially conversation has a much larger impact on my life.
My first thought was “well, those are right next to each other and develop from similar precursors, it would make sense they’d fail together.” But she’s not suggesting physical damage*, but miswired connections in the processing apparatus. I say processing apparatus and not brain because the vestibular system has some extra-brain communication with the eyes, which is why the vestibulo-ocular reflex is so fast. Some of the neurons that listen to the vestibular (motion/spatial) system run alongside the neurons that listen to the cochlear (hearing) system, which is why they’re grouped to together as the vestibulocochlear nerve, but that wiki article suggested and everything else I read confirmed that the vestibular and cochlear nerves reported to different areas of the brain. It’s like having two roads run parallel to each other, but it’s impossible to jump from one to another and eventually branch to different locations. Both will be affected by a snowstorm in their shared area, but a traffic jam at the destination for one won’t affect the other.
My neurology is weak, so I’m not sure what snow storm could be an analogy for. “Pinched nerve” is a phrase that exists, or perhaps something in the fluid they both float in? Except the whole point of neurons is to be heavily insulated against outside effects. What about the destinations? Were they really so separate? That is a good question. The brain does not break down into discrete little units. It’s not quite true that everything connects to everything else, but it is true that tracking down everything affected by two particular sensory inputs and cross-referencing them is unlikely to be a good use of time.
Now, a digression. After writing down all the reasons The Fabric of Autism was stupid, I find myself reading it again. Even though it is wrong, it is bringing up facts in the right area, which spurs me to do more research. Faced with a dense, correct text it’s easy for my eyes to glaze over. DNBHelp seems to have a pretty good grasp on otology without my help. But given a light, fuzzy text with an occasional fact that I’m pretty sure is wrong or at least misleading but am unable to explain why, I will do lots of research so I can more accurately explain to it why it is wrong. This probably won’t scale for the amount of reading I’ll have to do for nursing school, but it’s helpful for now.
I read another two chapters last night. Mostly it was some nice, fuzzy work about the relationship between sensory input and safety, but there was a throwaway reference to the superior and inferior colliculus as the parts of the brain that process sensory input. I looked that up, and what do you know: the inferior colliculus is a processing center for integrating sensory input. It handles auditory and somatic senses. Somatic is a broad term, but it includes both proprioception and touch. It’s involved in both the startle reflex, which means assessing stimulus for danger potential, and that vestibulo-ocular reflex thing we’ve spent so much time on**. There is some evidence it’s responsible for filtering auditory signals, which is certainly weak in me.
The superior colliculus is just neat. Say some part of your brain wants to interact with a specific object in the world. E.g. you want to pick up that glass of water on the table. How do you translate your sensory input into something your motor system can use to calculate what movements are necessary? I don’t know, but apparently the superior colliculus does it. In humans the primary input is visual, but it also handles echolocation and magnetolocation in animals that have them.
After all that, I have a non-exhaustive list of sections of the brain that do sensory integration, one which I find awesome and others of which I glare at with suspicion. I still don’t have a good sense of what distinguishes a functioning system from a non-functioning one, and that is something I really want.
*Although it seems like something we should maybe check for</divp
**Interesting note: vestibulo-ocular reflex appears on the inferior colliculus wiki page, but the reverse is not true. This is probably because a lot of brain structures have their finger in the vestibulo-ocular pot, and we just don’t have time to list them all.
Quick Tip/Warning: Vibrating Toothbrushes
I’ve been using some form of electric toothbrush since I was 6. This was a well intentioned call on my parents part, because I have terrible teeth, and the vibrating toothbrushes are significantly better at cleaning out plaque. But it takes half an hour for a *normal* sensory system to calm down after that kind of stimulation (source: my OT, who didn’t say where she got that number from). Who knows how long it takes children, or people with sensory issues. That kind of stimulation right before bed is the worst possible thing for my sleep, and might explain why it’s always taken me forever to do so.
I’ve switched to no-vibration cleaning at night, and vibration cleaning in the morning, and I’m sleeping a lot better.
Book review: High Price
High Price is a really good book in ways that do not lend themselves to me writing a particularly good blog entry about it. It is about a boy who grew up in the Miami ghetto, observing the effects of poverty and drug use first hand, and grew up to be a tenured neuropsych professor at Columbia studying the neurology of drug use.
I think there’s a few reasons I’m having trouble saying anything interesting about it. One, it didn’t challenge any of my existing beliefs. I already believed that drug wars were racist, that drugs weren’t as dangerous as the government told us, that a lot of the problems blamed on drugs were actually poverty or toxic social structures or institutional racism. I also believed that academia is miserable to everyone and poor black men in particular. I knew that gentrifying yourself led to alienation from family. I’ve read about all of these in more detail elsewhere. Which brings us to point two: this is a survey book. It’s a very good survey book on a very important topic and I hope many people unfamiliar with the topic read it, but I’m not going to recommend it to any of my friends who already believe the things I listed above, or people with well researched opposition. It’s not going to change their mind.
Three, despite my previous statement that the book didn’t change my beliefs, the author clearly has much more data on everything he talked about than I do, and I don’t think I have anything of value to add to the discussion. More bluntly, I’m white, middle class, and have only an undergraduate degree: if I get air time on the topic of racism in academia, the correct thing for me to do is signal boost someone with a more informed opinion. *
Science wise, it’s pretty valid but not deep. He mostly gives his conclusions, not an in depth explanation of the experiments. On the other hand, he does a pretty good job explaining what makes the opposing research faulty, and I do love to see that.
So if you’re either looking for an introduction to this issue or share my very strange definition of light reading, I highly recommend this book. Otherwise, it is probably not for you.
*High Price spends less than a chapter on institutional racism. If you’re looking for information on that specifically, I’d recommend TressieMC
SAD and Inositol.
Over a month ago I mentioned I was treated for SIBO. If it helped the digestive issues, it was subtle. I am however pretty sure it gave me Seasonal Affective Disorder.
Let me give you some context. I grew up in Rochester, NY (165 sunny days/year). I went to college in Ithaca, NY (152 sunny days/year, but less snow than Rochester). I’ve lived for Seattle (152 sunny days/year) for almost 8 years. Winter weather might keep me indoors more, and I do need vitamin supplements year round, but that’s because wet socks are unpleasant and I’m bad at metabolism. I didn’t have any SAD symptoms leading up to starting treatment for SIBO, which happened to be the day after winter solstice.
The treatment for SIBO for me was two antibiotics, erythromycin and xifaxan. Two or three days after I started, I felt fine during the day, but as soon as the sun went down it felt like the world was ending. It felt Late as soon as it was dark, which was 4:30 PM at the time. As time went on, I got more and more emotionally distraught and depressed. Everything felt awful.
1.5 weeks in, I noticed this, upped my vitamin D and started using a sun lamp, and that helped. 2 weeks in the treatment naturally ended, and I felt better still. But not all the way better.
Finally, almost six weeks after I’d stopped antibiotics, I remembered a friend telling me about inositol, which is a carbohydrate used for intercellular communication. The conventional wisdom is that your body can naturally manufacture enough inositol from glucose that nutritional sources are irrelevant: however, there’s some evidence that it’s either made or affected by your intestinal flora.* I’d tried it when he suggested it and found it had no effect, but kept the bottle just in case. I gave it another shot, and felt better the next day. 2 weeks in, I feel like the SAD is completely gone.
Right on the web page, there’s a warning that Xifaxan can cause an overgrowth of Clostridium difficile. In the study my friend described but did not give me a proper citation for, he said the researchers had isolated six different bacteria that competed with C. difficile, one of which produced inositol. I cannot find this study, or even a news article, anywhere.
It’s hardly proven, but I have a strong hypothesis that the antibiotics screwed up my intestinal flora (which is, in fact, what they were supposed to do, we were just hoping to localize the effects to the small intestine), leading to an inositol deficiency, leading to SAD. In many ways my digestive system feels like it’s been bumped back to earlier stages of treatment (the HCl supplements and removing some food groups), which makes me think that some of the things I experienced were second order effects of changing intestinal flora, rather than my diet directly.
What does it mean to say a gene causes something?
When writing about the genetics of sensory processing sensitivity, I’ve tried to be careful to use the phrase “associated with” rather than “causes.” I do this because genes don’t directly code for anything. To a first approximation, genes either code for proteins or for regulation of when those protein coding genes are expressed.* Different alleles of the same gene code for different versions of the gene’s protein**.
Sometimes, the link between a change in the DNA and the phenotypic outcome is obvious. To return to perennial favorite sickle cell anemia: there are several different alleles that can cause sickle cell anemia (which appear to have arisen independently, adding even more weight to the hypothesis that the alleles are adaptive), but they all affect the hemoglobin protein. A change in one nucleotide leads to a single amino acid change in the protein. Under certain conditions, this leads red blood cells to take the characteristic sickle shape, which causes a pile up in the blood vessels, which causes oxygen deprivation. All of these things are easy to observe (comparatively) and easy to track the chain of causation. And even with that, it’s not quite fair to call it “the sickle cell allele”, because the same allele also codes for malaria resistance.
The genes associated with high sensitivity don’t do anything nearly so obvious.
DRD4 7R (the mutation associated with high sensory sensitivity, ADHD, greater susceptibility to maternal trauma, and nomadicism) occurs in the DRD4 gene, which produce dopamine receptor D4. It does not lead to an amino acid substitution: rather, there’s a string of amino acids that may be repeated somewhere between 2 and 11 times: the 7R allele codes for 7 of them. I am unable to find any evidence we know what this does to the tertiary (three dimensional) shape of the protein or even where the D4 receptor is typically found, much less how these mutations affect metabolism. There’s a lot of high level correlational studies about various mutations and various phenotypic pathologies, like schizophrenia and parkinsons, but there isn’t a nice neat chain of causation like we see in sickle cell.
The other gene I talked about, 5-HTTLPR, isn’t even a real gene. It’s a promoter region for SLC6A4, which codes for a protein that transports serotonin. That means that mutations in 5-HTTLPR can affect when, where, and how much serotonin transporter is produced, but not the amino acid sequence of the transporter.
What are the phenotypic consequences of slight variations in the expression of this gene? That’s a really good question. It could theoretically affect anything that is affected by serotonin, whose clients include “the digestive system” and “the central nervous system.” And if it’s affecting your digestive system, it could affect your nutrition. So pretty much anything, ever, could plausibly be affected by mutations in this area.
The DRD4 gene doesn’t code for parkinson’s disease. It codes for a protein. Any variation in that protein will have a multitude of consequences, one of which might be parksinson’s. There is no one gene for high sensitivity: there’s a number of genes that influence a number of traits, one of which may be sensory sensitivity. So please remember that if someone tells you gene foo codes for happiness, they are not your friend.
*There are exceptions, but they’re very complicated and don’t change what I’m about to say.
**This is a simplification. It’s possible to have two different DNA sequences code for identical proteins and yet lead to slightly different outcomes, because is slower or more error prone to transcribe.
If high sensitivity is so costly, why is it still around?
Evolution is often sold as a species/population converging on a single ideal solution for a population. This is incorrect. For one, the ideal solution in 2013 is not necessarily the ideal for 2014. Peter and Rosemary Grant demonstrated that ground finch weight and beak size varied from year to year, that this corresponded to shifts in food availability due to weather, and that the change was driven by genetics, not starvation. Beyond that, there is often more than one good strategy at a time. Wal-Mart and Rodeo Drive both technically sell clothes, but they’re not in competition. When you combine temporal variation with the existence of multiple viable strategies, you get population diversity.
What this means is that even if a gene is very, very bad, it’s probably there for a reason. At worst, it was a local optimum for a problem that no longer exists. See: sickle cell anemia. Sickle cell is a very nasty disease caused by a single gene. But being heterozygnous for the sickle-cell allele gives you some resistance to malaria. Which is useless if you live in the USA in the 2000s, but highly relevant if you’re in Africa now, and even more so Africa in the past. That is why the allele stuck around.
Moreover, the returns to a particular strategy depend on other people’s strategies. You’ll make more money selling cheap, mass-market clothes if there’s no Wal-Mart in your city. This is known as frequency dependent selection.
The moral of this story is: any time you see a genetic trait that looks negative but is widespread, look around. It’s almost certainly either linked to an advantage you aren’t seeing, or is advantageous under a different set of circumstances.
As we talked about previously, this appears to be the case for the trait known as sensory processing sensitivity . Belsky et al have an exhaustive synthesis of various ways high sensitivity has been shown to correlative with both unusually positive and unusually negative outcomes, depending on environment. You remember the DRD4 7R mutation, that was associated with ADHD and susceptibility to the individual’s mother’s trauma? More prevalent in nomadic and nomadic-descended populations than sedentary. And carriers do better than non-carriers when nomadic but worse when sedentary.
I tripped a little bit reading this, because something associated with ADHD and nomadicism seems like a novelty seeking gene, which is associated with extroversion. High sensitivity is highly correlated with introversion, and even the extroverts among them have very different brain patterns than low sensitivity extroverts. I got this from Quiet, which the library has unfortunately taken back so I can’t look up the specifics. I wonder if the extraverts were the ones who had good childhood environment. And it turns out this isn’t the only allele linked with both high sensitivity and ADHD. 5-HTTLPR short is too.
Quantifying the advantages of high sensitivity in humans is hard. Luckily, there’s a number of very good animal models. That’s a severe understatement. A more accurate statement would be “you can’t throw a rock without hitting a member of a species that demonstrates a shy-bold continuum.” This may mean we haven’t defined our terms well enough, but it could also mean that almost all species demonstrate frequency dependent selection in sensory sensitivity. The theme seems to be that higher sensitivity animals are more cautious, and thus get eaten less, but every once in a while a low sensitivity animal blunders its way into something amazing, like a new source of food, or founding a start up.
What we talk about when we talk about heritability
There’s some behavioral evolution stuff I want to talk about soon. This is great, because it’s what I studied in college and I will be able to contribute something beyond wikipedia synthesis. In order to really dig into this, I have to explain how we measure heritability.
“Heritability“, or h^2, is a very specific measurement in biology. It measures how much variation of a particular trait in a particular population is due to genetic variation, relative to the total variation. It is not a synonym for “genetically determined.” For example, having two arms is barely heritable, because there’s almost no variation in the number of arms people have. Of people that have less than two arms, most of them lost them to environmental accidents, not genetics. There’s no gene for “one arm”, although developmental accidents may have some genetic basis. Biological sex isn’t very heritable either. A person’s parents’ sex has very little predictive power on the person’s own sex. Despite this, number of arms and biological sex is very, very genetically determined
Additionally, a heritability measurement is only valid for the population it was measured in. In a population in which every individual has exact the same environment will demonstrate much higher heritability for every trait than a population with a varied environment.
Now here is the really weird thing: how sensitive a trait expression is to environmental variation can be influenced by genetics. High Sensitivity was originally discovered in people who were having severely maladaptive responses to normal stimuli, and was assumed to have a uniform negative effect on people who carried it. Newer research indicates that the effect is more complicated: Highly Sensitive People with really good environments do better that Low Sensitive People in those environments. HSPs in bad environments do worse that LSPs. Whatever genes cause the trait we call High Sensitivity make a person more sensitive to their environment. Ellis et al call this biological sensitivity to context.
Lee et al investigated a particular HSP- associated allele, DRD2 Taq1A, and found that mothers with the gene were harsher parents during a recession than mothers without the gene. Moreover, they found worsening economic conditions led to worse parenting in everyone, but the effect was more pronounced for mothers with the T allele as opposed to the CC allele. So a child’s outcome is being affected by their own genetically-driven response to their parents, their parents’ genetically-driven response to the environment, and the actual environment.
I thought what depressed me here was that highly sensitive parents are more likely to have highly sensitive children, which will magnify the negative effects of the recession on children. Then I read a study showing that maternal psychological trauma was associated with higher disorganization in infants, but only if they had a high-SPS associated allele.*
High Sensitivity is going to come up a lot, so remember that. But also remember that when journalists talk about heritability, they do not mean what they think they mean.
*The same mutation, DRD4 7-repeat polymorphism, is associated with ADHD.
Sensory input and economies.
Expanding on my metaphor from yesterday, let’s posit three different types of sensory inputs/equations: Trivial (sensory input that is not necessarily effortless to process, but not taxing), Unsolvable (puts you into overload), and Solvable (requires noticeable amounts of processing power). Unsolvable equations represent either completely new data, or complex combinations of problems that would be Trivial on their own, but combine in difficult ways.
More concretely: let’s say you have two sensations, A and B. Either one on its own is a Taxing problem, but together they’re Unsolvable. If you manage to move A into the Trivial category (by repeated exposure and processing), that moves A+B into Solvable. And when you have solved it, you have A, B, and A+B in the trivial category, which will come in handy when you see A+B+C later. In this way, very small differences in initial processing capabilities can compound into vastly different levels of ability. Going into overload isn’t just painful, it cuts you off from learning the things that could prevent it next time.
This suggests a huge payoff to investing problems that are right on the border between Trivial and Solvable. Not only do you move that one thing off your plate, and move some other problems from Unsolvable into Solvable, you create an environment where you can eventually solve the other components of that previously Unsolvable problem.
[The following paragraphs are free-association at best]
For some reason I’m reminded of Jane Jacob’s The Economy of Cities, in which she postulates that most economic growth follows the following pattern:
- I’m doing a thing.
- Hurray, I invented a slightly more efficient way to do that thing.
- Wait, I could use that new invention to do this other thing. There’s no demand for it yet because no one knows they want it, but there will be.
- Welp, I invited a whole new sector of the economy.
Tim Harford implicitly talked about this in Adapt. The best economics have several interlocking industries with moderate overlap. Similar enough that innovations in one can help enough, but dissimilar enough to cause them to approach problems in different ways. Adapt as a whole is about trying a lot of things quickly, with the expectation that most of them will fail. One important component of that is minimizing the cost of failure, and one important component of that is recognizing failure quickly. Which sounds like a sensory problem.
Like I said, this is free association. I know I’m on to something, but I’m not sure what yet.
I figured it out.
One thing that has frustrated me as I researched SPS has been that I couldn’t connect the macro with the micro. I know damn well what the macro pattern is (too much noise -> everything is terrible, and also I bump into walls a lot), and I’ve been learning about the micro pattern (auditory, visual, or touch stimulus leads to over-activation of certain areas of the brain), but how did overactivation lead to irritability? The Threads of Autism (which I’ve since finished) went on and on about teaching people to “organize” sensory input, but it only described the effects of this in macro language (people become more relaxed, more resilient, able to thrive under higher levels of stimulus), but not what that actually looked like in the brain. Much less why pronating and supinating my wrists in time with my breathing or tapping along my facial nerves was going to accomplish this.
I think I’ve figured it out. Before I tell you, I want to make it very clear that this is my own personal metaphor, and not something that’s been tested scientifically. I’m not even sure what it would mean to test it. But it makes sense to me.
Your/your body’s ultimate goal is to figure out what it should be doing at any given second, and especially if it should be running away from or trying to breed with something. In order to do that, it tries to work backwards from the sensory input to derive a model of what is actually happening*. It can then decide how it wants to respond to that thing that is happening. For example, if you’re wandering through the jungle and hear a twig snap, you would like to know if it’s a delicious herbivore, a hungry tiger, or a human being, and if so, is it from your tribe or the one you’re at war with. Past sensory experience is really helpful in this interpretation. For example, if you’ve heard lots of tigers walking in the jungle, you can pattern match the current sounds against the ones you remember and see how close they are.
But what if it were more basic than that? We think we just know when and where and how someone is touching us, or how we’re oriented in space, but that is actually something you have to learn. We don’t notice because it’s mostly done when when we’re very very young, and because it’s done in parts of our brain that we’re not consciously aware of. But human brains are actually very plastic, and we devote an extraordinary amount of time and energy to learning how to translate “nerve 43b is firing” to “something happened on my left ring finger.”
My metaphor is as follows: people with SPS either don’t have the same bank of experiences to pattern match against, or are worse at matching. So given the same amount of sensory input, it takes them a lot more energy to correctly model the source. It’s sort of like simplifying a mathematical equation. If you have something awful with lots of terms you can solve it by hand, but it’s error prone and time consuming. If you take that same equation and simplify it by removing terms that cancel and grouping like terms together, that same equation can be trivial.
I think the point of the sensory integration exercises is to build up either the database of experiences and/or your skill at simplifying equations. You can’t give a person every single experience, but you can teach them “this is what stimulus from the trigeminal nerve feels like deep inside your brain.” This makes it marginally easier to identify, or at least not freak out about, novel stimulus. It’s like teaching someone about a 3-4-5 triangle. They’ll not only recognize other 3-4-5 triangles faster, but eventually 6-8-10 and 4.5-6-7.5 as well.
When I started in computational biology, I was all about complex computer simulations. By my senior year of college, I’d learned to appreciate mathematical models. They left out details, but that was what let you see the general patterns. If I’m right, I’m about to undergo the same process for basic sensory data. And I know I can do it.