Epistemic Spot Check: A Guide To Better Movement (Todd Hargrove)

Edit 7/20/17: See comments from the author about this review.  In particular, he believes I overstated his claims, sometimes by a lot.

 

This is part of an ongoing series assessing where the epistemic bar should be for self-help books.

Introduction

Thesis: increasing your physical capabilities is more often a matter of teaching your neurological system than it is anything to do with your body directly.  This includes things that really really look like they’re about physical constraints, like strength and flexibility.  You can treat injuries and pain and improve performance by working on the nervous system alone.  More surprising, treating these physical issues will have spillover effects, improving your mental and emotional health. A Guide To Better Movement provides both specific exercises for treating those issues and general principles that can be applied to any movement art or therapy.

The first chapter of this book failed spot checking pretty hard.  If I hadn’t had a very strong recommendation from a friend (“I didn’t take pain medication after two shoulder surgeries” strong), I would have tossed it aside.  But I’m glad I kept going, because it turned out to be quite valuable (this is what triggered that meta post on epistemic spot checking).  In accordance with the previous announcement on epistemic spot checking, I’m presenting the checks of chapter one (which failed, badly), and chapter six (which contains the best explanation of pain psychology I’ve ever seen), and a review of model quality.  I’m very eager for feedback on how this works for people.

Chapter 1: Intro (of the book)

Claim: “Although we might imagine we are lengthening muscle by stretching, it is more likely that increased range of motion is caused by changes in the nervous system’s tolerance to stretch, rather than actual length changes in muscles. ” (p. 5). 

Overstated, weak.  (PDF).  The paper’s claims to apply this up to 8 weeks, no further.  Additionally, the paper draws most (all?) of its data from two studies and it doesn’t give the sample size of either.

Claim:  “Research shows the forces required to deform mature connective tissue are probably impossible to create with hands, elbows or foam rollers.” (p. 5). 

Misleading. (Abstract).  Where by “research” the Hargrove means “mathematical model extrapolated from a single subject”.

Claim:  “in hockey players, strong adductors are far more protective against groin strain than flexible adductors, which offer no benefit” (p. 14).

Misleading. (Abstract) Sample size is small, and the study was of the relative strength of adductor to abductor, not absolute strength.

Claim: “Flexibility in the muscles of the posterior chain correlates with slower running and poor running economy.” (p. 14).

Accurate citation, weak study.  (Abstract) Sample size: 8.  Eight.  And it’s correlational.

[A number of interesting ideas whose citations are in books and thus inaccessible to me]

Claim:  “…most studies looking at measurable differences in posture between individuals find that such differences do not predict differences in chronic pain levels.”  (p. 31). 

Accurate citation.  (Abstract).  It’s a metastudy and I didn’t track down any of the 54 studies included, but the results are definitely quoted accurately.

 

Chapter 6: Pain

Claim: “Neuromatrix” approach to pain means the pattern of brain activity that create pain, and that pain is an output of brain activity, not an input (p93).

True, although the ability to correctly use definitions is not very impressive.

Claim: “If you think a particular stimulus will cause pain, then pain is more likely.  Cancer patients will feel more pain if they believe the pain heralds the return of cancer, rather than being a natural part of the healing process.” (p93).

Correctly cited, small sample size. (Source 1, source 2, TEDx Talk).

ClaimPsychological states associated with mood disorders (depression, anxiety, learned helplessness, etc) are associated with pain (p94).

True, (source), although it doesn’t look like the study is trying to establish causality.

ClaimMany pain-free people have the kinds of injuries doctors blame pain on (p95).

True, many sources, all with small sample sizes.  (source 1, source 2, source 3, source 4, source 5)

Claim: On taking some cure for pain, relief kicks in before the chemical has a chance to do any work (p98)

True.  His source for this was a little opaque but I’ve seen this fact validated many other places.

Claim: we know you can have pain without stimulus because you can have arm pain without an arm (p102).

True, phantom limb pain is well established.

Claim: some people feel a heart attack as arm pain because the nerves are very close to each other and the heart basically never hurts, so the brain “corrects” the signal to originating in the arm (p102).

First part: True.  Explanation: unsupported.  The explanation certainly makes sense, but he provides no citations and I can’t find any other source on it.

Claim: Inflammation lowers the firing threshold of nociceptors (aka sensitization) (p102).

True (source).

Claim: nociception is processed by the dorsal horn in the spine.  The dorsal horn can also become sensitized, firing with less stimulus than it otherwise would.  Constant activation is one of the things that increases sensitivity, which is one mechanism for chronic pain (p103).

True (source).

Claim: people with chronic pain often have poor “body maps”, meaning that their mental model of where they are in space is inaccurate and they have less resolution when assessing where a given sensation is coming from (p107).

Accurate citation (source).  This is a combination of literature review and reporting of novel results.  The novel results had a sample of five.

Claim: The hidden hand in the rubber hand illusion experiences a drop in temperature (p109).

Accurate citation, tiny sample size (source).  This paper, which is cited by the book’s citation, contains six experiments with sample sizes of fifteen or less.  I am torn between dismissing this because cool results with tiny sample sizes are usually bullshit, and accepting it because it is super cool.

Claim: “a hand that has been disowned through use of the rubber hand illusion will suffer more inflammation in response to a physical insult than a normal hand.” (p. 109).

Almost accurate citation (source).  The study was about histamine injection, not injury per se.   Insult technically covers both, but I would have preferred a more precise phrasing.  Also, sample size 34.

Claim: People with chronic back pain have trouble perceiving the outline of their back (p. 109). 

Accurate citation, sample size six (pdf).

Claim:  “Watching the movements in a mirror makes the movements less painful [for people with lower back pain].” (p. 111). Better Movement. Kindle Edition.

Accurate citation, small sample size (source).

Model Quality

Reminder: the model is that pain and exhaustion are a product of your brain processing a variety of information.  The prediction is that improving the quality of processing via the principles explained in the book can reduce pain and increase your physical capabilities.

Simplicity: Good.  This is not actually simple model, it requires a ton of explanation to a layman.  But most of its assumptions come from neurology as a whole; the leap from “more or less accepted facts about neurology” to this model is quite small.

Explanation Quality: Fantastic.  I’ve done some reading on pain psychology, much of which is consistent with Guide…, but Guide… has by far the best explanation I’ve read.

Explicit Predictions: Good, kept from greatness only by the fact that brains and bodies are both very complicated and there’s only so much even a very good model can do.

Useful Predictions: Okay. The testable prediction for the home-reader is that following the exercises in the back of the book, or going to a Feldenkrais class, will treat chronic pain, and increase flexibility and strength.  Since the book itself admits that a lot of things offer short term relief but don’t address the real problem, helping immediately doesn’t prove very much.

Acknowledging Limitations: low. (Note: author disputes this, and it’s entirely possible he did and I forgot).  GTBM doesn’t have the grandiose vision of some cure-all books, and repeatedly reminds you that your brain being involved doesn’t mean your brain is in control.  But there’s no sentence along the lines of “if this doesn’t work there’s a mechanical problem and you should see a doctor.”

Measurability: low.  This book expects you to put in a lot of time before seeing results, and does not make a specific prediction of the form they will come in.  Worse, I don’t think you can skip straight to the exercises.  If I hadn’t read the entire preceding book I wouldn’t have approached them in the correct spirit of attention and curiosity.

Hmmm, if I’d assigned a gestalt rating it would have been higher than what I now think is merited based on the subscores.  I deliberately wrote this mostly before trying the exercises, so I can’t give an effectiveness score.  If you do decide to try it, please let me know how it goes so I can further calibrate my reviews to actual effectiveness.

 

You might like this book if…

…you suffer from chronic pain or musculoskeletal issues, or find the mind-body connection fascinating.

This post supported by Patreon.

Dreamland: bad organic chemistry edition

I am in the middle of a post on Dreamland (Sam Quinones) and how it is so wrong, but honestly I don’t think I can wait that long so here’s an easily encapsulated teaser.

On page 39 Quinones says “Most drugs are easily reduced to water-soluble glucose…Alone in nature, the morphine molecule rebelled.”  I am reasonably certain that is horseshit.  Glucose contains three kinds of atoms- carbon, oxygen, and hydrogen.  The big three of organic chemicals.  Your body is incapable of atomic fusion, so the atoms it starts with are the atoms it ends up with, it can only rearrange them into different molecules.  Morphine is carbon, oxygen, hydrogen, and nitrogen, and that nitrogen has to go somewhere, so I guess technically you can’t reform it into just sugar.  But lots of other medications have non-big-3 atoms too (although, full disclosure, when I spot checked there was a lot less variety than I expected).

This valorization of morphine as the indigestible molecule is equally bizarre.  Morphine has a half-life of 2-3 hours (meaning that if you have N morphine in your body to start with, 2-3 hours later you will have N/2).  In fact that’s one of the things that makes it so addictive- you get a large spike, tied tightly it with the act of ingestion, and then it goes away quickly, without giving your body time to adjust.  Persistence is the opposite of morphine’s problem.

This is so unbelievably wrong I would normally assume the author meant something entirely different and I was misreading.  I’d love to check this, but the book cites no sources, and the online bibliography doesn’t discuss this particular factoid.  I am also angry at the book for being terrible in general, so it gets no charity here.

The Compassion Pain Scale

I never did do much with the kitten pain scale, because the pain meds’ effects were so striking there was no need for hour by hour monitoring.  But I’ve found another good marker.

When I first started at crisis chat I really really loved it, and would frequently stay hours past my scheduled shift.  I often left feeling energized*.  At some point that changed.  I put it down to a loss of novelty, or maybe nostalgia making me remember it as more fun than it was.  I kept going because it wasn’t about me having fun, it was about me helping people, but I was more conservative about the latest time I would start a new chat.

Then I got those really awesome pain meds in January, and suddenly I was staying late again.  But at some point it disappeared again.

One of the nice things about the meds is that they have a long lasting effecting.  They push the pain-tension cycle back, so I’m in less pain for days or even weeks after they wear off.  One of the bad things about one of them is that I hate being touched the next day.  That’s suboptimum on its own, but it scares me to think of what else it’s doing that I’m not noticing, so I try to go as long as possible without taking it.  I’m also very good at pushing away conscious knowledge of pain, even though it still effects me.  So I ended up going really way too long without taking the topical pain medication.

Finally I took it again, and what do you know, I stayed more than two hours past the end of my next chat shift.

It doesn’t surprise me that I’m better at chatting when I’m in less pain, but I am surprised by the way I’m better.  Ending chats is a tricky business.  You don’t want people to feel shoved out the door, but a good chunk of our target audience is having anxious ruminations.  The last two times I’ve been much better about recognizing when we’ve reached the end of the productive portion of the chat and wrapping it up.  A few people even seemed to take the nudge out as permission to relax.

*although not always.  Most days I had to call a child abuse report in were bad days

**Shift end times are a little fuzzy because of course you can’t leave in the middle of a chat.  If it’s 5 minutes before your shift ends, of course you don’t take a new chat unless you’re prepared to stay late.  But if it’s 30-45 minutes?  You’ll probably be done only a little after your stated end, but you never know which call is going to be a two hour active rescue.

Xylitol for sinusitis

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.

rabbit
Rabbits self-reported pain scores were ambiguous

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.

Pain, ADHD, and happiness

I jokingly referred to pain-induced ADD on Monday, but I’m becoming more and more convinced that is actually what was happening.  After prior surgeries I was too exhausted to notice anything, but this time I was energetic enough to experience the pain.  I mean, unless I tried to go outside or something.  That led to a really entertaining systems crash in the supermarket.  But if I stayed inside I was able to do things like get food and put away dishes without strain.  Contrast with when my pain meds sabotaged my cortisol production.  Intellectually I was there and able to do things like read and blog, but physically it was a struggle to make myself a smoothie.

After surgery I could not read or write or even enjoy a movie.  It was more than pain making everything 70% less fun, it was that everything was annoying and frustrating and no fun at all.  I couldn’t enter a state of flow or concentration or even relaxing for any length of time.  Except when I played video games or the piano.  Neither were fun, exactly, and I was still in pain, but they were at least distracting and rewarding.  Looking back, this explains a lot of my behavior when I was in constant pain last year, it just took being out of pain and then very sharply in a lot of pain to make the pattern obvious.

At first I thought this was  Harrison Bergeron type thing, where pain was sending out interrupts too often for me to get into a groove on anything.  But then I read this blog post (blogs were just about in my power) by Sara Constantin on dopamine, explaining Peter Redgrave’s hypothesis that the spike (phasic increase) of dopamine is not itself a reward (which is how pop journalism usually describes it) but a timestamp that lets you know what actions should get credit for the actual reward chemicals you are about to receive.  That would explain why humans and animals with broken dopamine systems do feel pleasure when eating but will nonetheless starve to death unless you put the food directly in their mouth.

Many of the drugs used to treat ADHD inhibit dopamine reuptake, which raises your tonic (baseline) dopamine levels.  Constantin hypothesizes that if the baseline is too low than stimuli that should be ignored suddenly are interpreted as important, leading to a lot of SQUIRREL.

[ I was going to make this a gif but putting unpausable moving pictures in a post on ADHD just seemed cruel]

If this is correct, it offers an explanation for why ADHDers are so drawn to things like videogames and sex:  the time gap between doing the correct thing and getting the chemical reward is so short they can still determine causality, even against the a background of SQUIRRELs.  This needn’t be purely about hedonism- if it was, something consistently pleasant would work.  I think it’s about having an internal locus of control and self-efficancy.  Humans are happiest they feel like they have the power to change their own circumstances and have an impact on the world.  It’s hard to feel those things if your attention is constantly being torn away from what you choose and you can’t (on a neural level) determine what made you feel the emotion you are currently feeling.  This is one reason the toll of ADHD shouldn’t be measured in lost productivity alone; even people with very successful coping mechanisms are being denied that internal locus of control, and that’s miserable.

Here’s my contribution: my description of being in pain sounds a lot like other people’s description of ADHD, right down to video games being rewarding without strictly being fun.  And as it turns out the basal ganglion, the area Redgrave believes is using dopamine to timestamp causes so they can be matched with effects, also releases dopamine in response to pain.  It seems entirely possible to me that high baseline levels of dopamine could diminish the effect of a spike.  Instead of everything being timestamped “good job”, nothing is, with similar results

But let’s make it even more interesting.  Several anti-depressants are also useful in treating chronic pain, and NSAIDS (usually mild pain killers) treat depression.  I had previously put this down to “pain is depressing”, “depression appears to be connected to inflammation in ways we don’t understand” and plain old “brains are squishy and they don’t make sense”, but if there was a causal link?  The symptoms of depression include fatigue, feelings of helplessness and lost of interest or enjoyment of previously liked activities, which sure sounds related.  Quick googling found a very tiny study showing a connection between low dopamine and suicide, and this fascinating study suggesting that inflammation reduced the basal ganglia’s production of dopamine, which would tie all of this up in a very pretty bow.  Something causes pain and/or inflammation (the two often go together), which long term causes inflammation in the basal ganglia, which causes depression and reduces your body’s natural analgesics.

Look body, if you were worried about us getting high off of pain, maybe you could have releases fewer happy chemicals in response to pain, instead of making it just as fun but also cause depression some time later.

This would also explain why ADHD medicines are promising in treating depression (source, source, and a large showing among my friends), and why ADHD and depression so often go together.*

I cannot stress enough how unqualified I am to make this hypothesis.  Lots of people know lots more on all of these things than me.  But it comes together to be an extremely plausible explanation for both the literature I’ve read and my personal experiences.

*There’s a lot of evidence that depressed parents correlate with ADHD kids, but it’s probably environmental.

Humans are complicated, children are even more complicated

[Had more dental surgery this week and am currently suffering from pain-induced ADD.  Expect less research and more wild speculation]

Consider pre-emptive testing for psychiatric or developmental issues in children.  If you’re too aggressive, you end up misdiagnosing a lot of perfectly normal deviations from the exact median as development issues in need of treatment.  Development is complicated, different systems come on line at different rates and in different orders in different kids, and they should be allowed to do that without being corralled into fitting a predetermined schedule .

But if you’re not aggressive enough, the kids develop coping mechanisms that hide the disability, making it harder to diagnose and treat.  Sometimes people treat this as solving the problem (especially for conditions that are often conflated with character flaws, like ADHD or some forms of depression), but they are wrong.  At best lack of treatment holds people back from their true potential, at worst it twists up their internal structure in ways that break at the worst possible time (usually grad school).  It’s a big problem with twice exceptional children, who have both brain-based deficiencies and a lot of raw intelligence, and I suspect for people with atypical presentations of their disabilities.  E.g. girls with ADHD or autism spectrum issues, boys with depression* or trauma from sexual abuse.**

Even perfectly accurate testing won’t fix this, because developmental asynchronies do not necessarily indicate a future problem, and treating them can prevent the issue from fixing itself.  The real issue is distinguishing natural, healthy leveling out from the development of costly compensation mechanisms, and we don’t know how to do that.

*Assuming the comomn adult male pattern of depression being expressed as anger holds true for boys as well.

**I think, couldn’t actually find data on this.