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.
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.
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
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.
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.
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.