The Dopamine Narrative Begins: Just Say No to Dopamine Theft

Overview

Over the last several years, my husband Randy and I have been building up a set of concepts and models that collectively we call the Dopamine Narrative.

The goal is to craft and offer up to others a framework with which to live a better, more fulfilling, more loving life that acknowledges and works in loving partnership with human nature.

The Dopamine Narrative itself is a set of lenses and a toolbox with which to view the world, interpret underlying forces, make predictions, and relate to ourselves and others.  We constructed it bit by bit though the process of trying to debug various issues and anomalous observations about our feelings, our experiences and what we saw happening around us in the world.  It's been crafted over countless conversations between ourselves and others and through recognizing resonant ideas in books, podcasts, and other media.

It leans heavily on and borrows concepts from various writers and traditions, while rejecting much of the mainstream default narratives of the culture we inhabit.

It resonates with aspects of ancient faith traditions but does not require belief in or allegiance to any of them.

It resonates with the sort of scientific work typified by researchers like Jonathan Haidt, Robert Sapolsky, Bessel van der Kolk, and Oliver Sacks, but is not itself a scientific endeavor.

Please interpret the following as models and narratives offered up for your consideration, not as scientific claims.  Please feel free to ask in the comments for more specific stories of where particular aspects came from, but please do not demand journal references or use the lack of such references as a reason to reject and abuse the what we're trying to do here.

Expository Approach

I've struggled for years to figure out how to address the Dopamine Narrative in writing.  I love using it as a tool to spin particular conversations inspired by the active interest of particular individuals.  However, it has been hard to imagine how to communicate it to a nebulous audience of readers.

A particular challenge is that it built from a set of custom and/or likely unfamiliar concepts which build on each other and are not easy to compactly define.

My plan is to do a set of compact partial definitions here, just enough to respond to the motivating question:  Why do people sometimes seem to go out of their way to be be mean to each other and what can be done about it?

I recently wrote up a couple of extended comments on AskReddit threads asking versions of this question:

• What is a good way to be a better person?
• People who are mean to others regularly, why do you do it?

I think that addressing these questions through the lens of the Dopamine Narrative makes for a pretty good tour through the concepts and a pretty good example of how they can be used.

Concepts

Elephant and Rider

The idea is that the impetus for behavior like being mean to each other mostly comes from the limbic, social mammal part of ourselves, what the author Jonathan Haidt calls "the Elephant".  It does things like model an individual's status, ranking, and security of position within social groups.  It affects our feelings and behavior, but operates largely beneath the level of conscious awareness.

The other part in Haidt's model, "the Rider", is the part that handles the verbal, cognitive sorts of tasks and (unknown to it) in large part acts as the press secretary for the Elephant.

If you want to look at this concept in more detail, I'd recommend reading the first half of Jonathan Haidt's book The Righteous Mind.

Dopamine Level 

In our model, the Elephant maintains a moment-to-moment assessment of how well we're doing on its succeed-as-a-social-mammal agenda.  We call this parameter a person's "Dopamine Level".

It's not literally the amount of the neurotransmitter dopamine, but we believe that it is related -- dopamine is a major neurotransmitter used in parts of the limbic system involved in motivation and reward, and drugs that affect dopamine signaling (like Wellbutrin, L-Dopa, and cocaine) do seem to affect the feelings we associate with Dopamine Level.

Imagine how it feels when you get a major unexpected compliment, or succeed at some task that will impress your friends and family.  That's what the "High Dopamine" end of the scale feels like.

Now imagine how it feels when you've done something you figured was innocent and somebody jumps all over you for it and says you're a bad person.  That's what the "Low Dopamine" end of the scale feels like.

All sorts of interactions, perceptions, and thoughts affect Dopamine Level up and down.  The sorts of things that increase Dopamine Level include indicators of increased status or security within a group, such as receiving praise, positive attention, successfully helping someone, etc., as well as fulfilling more concrete social mammal needs, such as food and comfort.   The Elephant will perk up and dish up motivation and energy at the prospect of pursuing actions it deems to have a high degree of likelihood of such a positive outcome.

On the other hand, the sorts of things that decrease Dopamine Level include indicators of decreased status or security in the group, such as receiving signs of disapproval, derision, or rejection, as well as more concrete social mammal suckage like failing in efforts to find adequate food or shelter.  The Elephant will generally react with feelings of unease and resistance at the prospect of pursuing actions it deems to likely have such a bad outcome.

When you're feeling sufficiently High Dopamine, life is good.  If you slide (or worse, plummet) towards the Low Dopamine end, at some point you feel miserable enough that the Elephant will cast around with increasing desperation for ways to go back up to a tolerable level.

If you have a nice convenient wholesome Dopamine increasing action available, that's great.  Do that.

Unfortunately, there are other, less savory ways of increasing Dopamine that the Elephant will tend to grab for in such moments.

Dopamine Theft

One of these unsavory ways of increasing Dopamine is pulling a successful social dominance maneuver, like chewing out someone, calling them names, fault finding, intimidation, etc.  This is what we call "Dopamine Theft".

We call it Dopamine Theft because such actions, when successful, simultaneously increase the Dopamine Level of the attacker, and decrease the Dopamine Level of the victim.

When talking to the neighborhood kids, I describe this as "making yourself feel big by making someone else feel small."

If you're just here to understand the terms for another post, here is a good place to return.  The rest is an in depth discussion of Dopamine Theft.

Dopamine Theft Deep Dive

The Elephant is pretty savvy at predicting whether or not a given potential social dominance maneuver would be successful in a given environment with a given potential target.  It's not going to perk up for this strategy unless you're likely to both succeed at dominating the potential victim and receive social approval, or at least not receive disapproval, from whoever else is around.

This pattern is pretty clear when you watch group behavior of non-human social mammals, like dogs or baboons.  Something sucky happens to one animal in a group.  It starts looking around, then attacks or threatens or steals food from a lower ranking animal.  The attacker wanders off looking smug and satisfied with its ears and tail in the air.  The victim gets upset and either finds another even lower ranking member to abuse or slinks off with its ears and tail low to try to recover.

Robert Sapolsky, a neuroendocrinologist at Stanford who studied baboons in the wild for many years, talks about these sorts of interactions among his study group using the terminology "displacement aggression."  Chapter 4 of his book Behave: The Biology of Humans at Our Best and Worst is a good example of his work on this.

Humans tend to be less straightforward.  The Rider, which is what handles the conscious framing -- the words to think and say -- isn't likely be aware of this sort of thing going on under the hood.  Instead, it'll put together some kind of scenario like "that person is in the wrong; I'd better set them straight", or "what a little dweeb; I'd better put them in their place" that casts the instigator on the side of righteousness.

These sorts of thoughts flit through all the time.  What makes it Dopamine Theft is that when such a thought flits through:

1. The Elephant perks up and provides energy and motivation to do it but only in the case that the potential target is vulnerable to being dominated and any potential audience in the area would approve (or at least not disapprove), and
2. The tone and body language with which its delivered tear the target down rather than lovingly correct them.

It's certainly possible, and desirable, to work on instead acting on such thoughts in a constructive way that primarily focuses on preserving the welfare of the target while helping them improve.  Mr. Rogers and good kindergarten teachers provide models for what that could ideally look like.

It seems to me that in most contexts, at least in America, we tend to be too ready to accept the Rider's efforts at righteous framing, discount the tone and body language, and allow Dopamine Theft to be a successful strategy more often than we should.

There's typically some threshold above which we'll condemn aspects of such behavior as "verbal abuse" or "bullying", but we largely don't recognize the harm caused by giving lower intensity or sneakier Dopamine Theft.

Dopamine Theft, Social Pressure, and Reinforcement Learning

The biggest issue, I think, is that our culture is too accepting of dopamine theft directed from people higher in the pecking order towards those lower down. If the bystanders or, in the case of kids, the parents and other adults, would be more frequent and consistent about defending the target and giving the perpetrator sufficient social disapproval, then the option of dopamine theft would be negatively reinforced.

Instead, so long as people learn early on how to identify socially acceptable targets and justifications, and exist in an environment containing such socially acceptable targets, it's likely to be positively reinforced and turn into a habit.

According to my best understanding, this process involves the same pathways as addictive drugs -- reinforcement learning driven by dopamine release to the brain's reward centers.

These mechanisms, I believe, can lead to opportunities for likely-to-be-successful dopamine theft to feel tempting and motivating -- like an opportunity to use feels to an addicted drug user.  In the absence of internal or external restraint that would spoil the fun, acting on it generates a neurochemical reward and increases Dopamine Level -- like a hit would for the drug user.

Through this lens, the Golden Rule, Jesus' teachings in the gospels, the teachings of the Buddha, etc. can be seen as efforts by our ancestors to counteract these mechanisms and instill the internal and external constraints on both the individual and societal levels that would spoil the fun and negatively reinforce the pattern of dopamine theft.

Unfortunately, at our current cultural moment, that aspect mostly seems to have gotten lost. Instead, such traditional restraint mechanisms often get either ignored or co-opted to justify and exacerbate dopamine theft (Westboro Baptist Church's activities being an extreme example).

The Dopamine Theft model is an attempt to make a distinction between truly loving correction (like Mr. Rogers) and giving in to the inner baboon while our brain acts like a press secretary to make it seem righteous (like the stereotypical dopamine theft addicted asshole).

That distinction, plus striving towards the goal of recognizing and negatively reinforcing dopamine theft both within and externally, could potentially help move us in the right direction and reduce the meanness.  Jesus' behavior in the Gospels provides numerous examples of this, such how he intervened when a crowd tried to stone a woman for adultery.

Trying to ramp up calling out Dopamine Thieves by bystanders while failing to make that distinction risks further exacerbating the culture of Dopamine Theft.  Again, looking at you Westboro as the poster child for this risk.

Three corollaries of all this are:

1. That the responsibility for appropriate intervention to thwart attempted dopamine theft is highest on any bystanders who outrank the perpetrator or who at least have people in their corner who outrank the perpetrator and will plausibly come to their defense.  If a popular football star is trying to commit dopamine theft on a skinny outcast kid at recess, the Coach has a much better chance of successfully intervening than the victim's equally skinny and outcast friend, so his responsibility to step up and do so is greater.  However, in the likely case someone like the Coach isn't around or (worse),  is around and won't intervene,
2. That any defender would work so long as they can trust enough of the strangers around to back them, which is why it would make such a difference to have a sufficient cultural shift in this direction.
3. That the highest ranking members of any group are the ones who are most likely to get away with Dopamine Theft.  If you're typically the highest ranking person around, particularly while growing up, opportunities to commit Dopamine Theft and get social approval for doing so are high, and the chances of negative reinforcement are low.  You see this pattern over and over again: Harvey Weinstein taking sexual advantage of subordinates and getting away with it for decades, Donald Trump apparently getting away with anything he feels like doing, etc.
   
   At some level we understand this effect and portray it in our fiction: the behavior of John Lithgow's character in the movie Beatriz at Dinner, how often the football quarterback, son of the richest family in town, or corporate CEO are portrayed as entitled assholes, etc.   However, it seems to me like these situations are too often portrayed in terms of good and evil, hero and villain dichotomies, as "bad apples", and/or in terms of identity categories -- religious vs non-religious, this religion vs that one, this nationality vs that one, this race vs that one, etc. -- and too much underplay the dynamics of how reinforcement learning and Elephant/Rider effects play into it.
   
   We recognize that power corrupts, but don't seem to usefully understand or counterbalance the processes by which it happens, such as how social acceptance of top-down Dopamine Theft and toadying to power contribute to the problem.  This is something we really need to work on.

At a personal level, a good first step for moving in that direction is to practice watching for such interactions and learning to recognize Dopamine Theft.

I find it's actually easier to recognize if the participants are speaking a language I don't know.  That way I can hear the tone and observe the body language without being distracted by the meaning of the words.

Another harder step is to start to recognize that internal burst of enthusiasm at the idea of doing something like correcting someone as a sign that the Elephant might be trying for Dopamine Theft and overrule it.  A compact slogan could be "Just say no to Dopamine Theft".

Conclusion

I hope this is a useful starting point on understanding and employing the Dopamine Narrative.  I also hope that having this post to point to for defining the terms will help in being able to address other aspects and applications of this tool set.  If you have any questions or types of situation you're interested in exploring through the Dopamine Narrative lens, please let me know.

Thanks for reading.  :)

New potential A-Ha: niacin, SAM-e, and methylation SNPs

I recently stumbled into a new bit of obscure biochemistry and have been hopeful about its potential implications ever since.  I don't know yet if the effects will be sustainable, but the initial results are promising.  There've still been some ups and downs, but the ratio of up seems considerably higher with the new strategy than it has been for a while.  That could be all due to placebo effect, but I hope it's more than that!

First, I need to make a confession.  For months I've been spending a great deal of time hiding and either reading escapist fiction or listening to podcasts rather than confronting and engaging with the challenges of life.  With the generous support of my husband, colleagues, and friends, I have managed to do enough (I hope) to keep disaster at bay and (I hope) not totally burn all my bridges, but I certainly haven't been proud of the way things have been going.

The dominant sensation in all this is a distressingly jittery, heart racy, fight-or-flighty feeling when considering confronting even very minor challenges.  This doesn't happen 100% of the time.  Some of the time, without any discernible change in circumstances, I can consider and execute on quite significant challenges without that distressing feeling being there.  Sometimes those gaps can last for months, sometimes just for hours.

The maddening thing is that I haven't been able to figure out how to predict or engineer those gaps.  It's like sunshine in Pittsburgh: sometimes the clouds part and the sun shines through, but I don't know when it's going to happen, it can go away suddenly, and I mostly can neither predict nor control it.  Unfortunately, the last several months have been mostly clouds with only rare patches of sun.

I know that the feelings I describe are typically labeled anxiety and that there are whole industries built around approaches to treating it.  However, I spent years pursuing many of those approaches and have mostly lost faith in them being the answer here.  Only one thing, beta blockers, ever made a significant difference and it wasn't sustainable.  

From that experience, I learned 1) that blocking reception of epinephrine (aka adrenaline) can make that distressing jittery feeling go away, and 2) that I'm a beta receptor mutant and, probably because of that, am hypersensitive to epinephrine (details at Beta blockers: good idea or trap?).

The new bits of obscure biochemistry that brought me hope were learning that 1) epinephrine is broken down by the COMT and MAO enzymes, 2) that I've got slowish versions of both of these (heterozygous for COMT V158M and COMT H62H, and homozygous TT for MAO A R297R), and 3) that niacin is a cofactor that can increase the activity of COMT.

The idea that epinephrine hangs around too long due to underperforming breakdown enzymes and conspires with the mutant beta receptors to cause the distressing jittery sensations seemed like a promising new lead.  So, could additional niacin dosing help improve the breakdown efficiency and lead to less of that sort of feeling?

I first encountered this possibility here while reading about methylation SNPs at mthfr.net.  Dr. Lynch describes the use of ~50 mg of nicotinic acid (one of the two available supplement forms of niacin) to help a patient with anxiety caused by over-methylation.  He says: "Nicotinic acid is a cofactor for the COMT enzyme. This enzyme helps breakdown norepinephrine and epinephrine – and estrogen. These are all commonly elevated in those with anxiety. Since the COMT enzyme sped up, the breakdown of these occurred faster."

I went out and bought a bottle of nicotinic acid that same evening.  The closest I could find at the store was 500 mg, so I had to trim off 1/10 of a tablet to get the desired dosage.  Luckily my husband had bought a digital milligram scale for another project, so I could measure with enough precision to pull this off.

I took a dose that evening, and soon after felt noticeably more calm.  I fell right asleep, slept well, and woke with the jittery feeling still gone.  Twice during the next day I felt the jittery feeling starting, responded by taking another dose of the niacin, and felt the jittery feeling go away again.  I've taken it every day since then.  I usually take it once either in the morning when I get up or when I notice feeling jittery, and then at night before I go to bed.  It has consistently gotten rid of the jittery feeling pretty quickly.  The one night I forgot to take it before bed I woke up in the night with stress dreams, but have otherwise been sleeping quite well.

All this could certainly be placebo effect.  However, even if it is placebo it's the first ray of hope I've seen in a long time for being able to engineer gaps in the clouds and function well.  If it is a real effect, I am hopeful that this could lead to a more sustainable solution than the beta blockers.  I expect that achieving this goal will take continued effort.

The best sources I've found in trying to understand all this are an amazing 90 minute extravaganza on MTHFR and Methylation by Dr. Benjamin Lynch, ND of mthfr.net, and the results from feeding the raw data from 23andme into an analyzer at geneticgenie.org.  The heavy biochemistry diagrams begin at 33:08.  They show many of the interconnections where various genetic polymorphisms and variations on intake/supplementation can cause issues.

One of the big concerns is that niacin sponges up SAM-e, which is important for supporting methylation, producing melatonin, etc.  I know that methylation is an issue for me since I've also got an underperforming MTHFR version (heterozygous for C677T).  Knowing that and reading an article by Chris Kresser last year had led me to read up on the topic of methylation and add a methylated folate supplement back in early 2012, which had led to a significant and noticeable uptick in energy and oomph (the last a-ha before this one).  I definitely don't want to screw up methylation, glutathione production, etc.

The most obvious thing to try to keep things happy is to also supplement with SAM-e.  In the comments of the page where Dr. Lynch talks about niacin, he says:

One may look at dealing with MTHFR and COMT mutations together as ‘driving with one foot on the gas and one on the brake.’ 

It is common for those with COMT mutations to suffer anxiety, irritability while on methylfolate and/or methylcobalamin. These signs of irritability can be reduced by taking niacin, using less methylfolate and using less methylcobalamin – while at the same time supporting your liver via nutrients, diet and lifestyle changes.

I tried to buy some SAM-e the same night I got the niacin, but that store was sold out.  The second store I tried was also sold out, so I guess I'm not alone in suddenly being interested in SAM-e.  My husband eventually found some in stock at a local Walgreens.  I've been taking it each day since, usually one first thing in the morning.  I don't notice any dramatic reaction to the SAM-e, but I've been doing generally better on steadiness of energy and oomph since then.

I hadn't tried SAM-e before.  Many years ago in Seattle my husband did try SAM-e, but stopped after a few days because it made him agitated.  I noticed in Dr. Lynch's presentation that SAM-e is a co-factor in the conversion of norepinephrine to epinephrine.  My husband also turns out to have the lame versions of COMT and MAO, so I imagine SAM-e supplementation potentially contributing to increased epinephrine production could be consistent with his earlier experience, and potentially a concern for both of us.

It's clear from the diagrams that SAM-e and niacin work against each other in some ways: niacin sponges up SAM-e methylation capability, and SAM-e acts as a co-factor to encourage norepinephrine to epinephrine conversion while niacin counteracts that effect and acts to encourage epinephrine breakdown.   If I understand right, the trick is to use enough niacin to keep epinephrine down to where I don't feel jittery and enough SAM-e to keep methylation, melatonin, etc. happy.

There's no way other than experimentation to tell whether that potential happy zone exists and is practically attainable for someone with their particular mix of circumstances and mutations.  I think my current strategy is working for me, but it's too early to tell if it'll lead to a stable result or cause other problems.  Please wish us luck!

The Narrative Dimension of Health

I feel inspired today to write about something I'll call "The Narrative Dimension of Health". This is an important, yet mostly invisible, lurker in the room in discussions I encounter on health, illness, identity, and self-tracking.  Attempts to bring it more explicitly to the table would be easier if we had a better shorthand/search term for it. Otherwise it just takes too long to introduce the concept every time.

Humans are creatures of narrative.  Each experience, each interaction, each thought is both filtered through our currently active set of stories and potentially modifies those stories.  We are, for the most part, neither consciously aware of these stories nor actively involved in their curation, but they impact us anyway.  Many agents -- our parents, teachers, friends, partners, religious and civil authorities, marketers, media creators, etc.-- make intentional efforts to impose certain stories upon us.  Other influences are less intentional.  Some of it sticks, some of it doesn't.

Among this set of stories are the ones we tell ourselves about ourselves.  Again, some of this is influenced by intentional efforts to impose stories upon ourselves (such as "positive self talk"), but such attempts may or may not stick and much of it sneaks in via other routes.  The nature of the roles we play in these stories and the way that particular sensations and experiences feed into them have a big impact on us.

Some of these stories address how we relate to issues of "health" vs "illness", "normal" vs "abnormal".  So long as the combination of our current set of stories with our recent sensations, experiences, and personal interactions support us in casting ourselves in the role of "healthy" and "normal", things seem good and we may not think much about it.  What happens though when we start finding ourselves potentially cast in the "ill" or "abnormal" roles?

Identical sensations can have a very different impact depending on how they interact with our currently active set of stories, and which of these roles the result pushes us towards.  The best discussion I've seen of this is in "Upside of Irrationality" by Dan Ariely.  A quote he gives from from a WWII doctor named Henry Beecher sums it up well: "The amount of pain we end up experiencing is not only a function of the intensity of the wound, but it also depends on the context in which we experience the pain and the interpretation and meaning we ascribe to it."

So, what I mean by the narrative dimension of health are the interactions, for a given individual, between 1) their currently active set of stories, 2) the sensations they are experiencing, 3) the stories that various parties, such as doctors, family, etc., try to impose upon them, and 4) how these influences affect the role that they play in the stories they tell themselves about themselves.

The writings of Don Miguel Ruiz and Rachel Naomi Reman have particularly influenced my understanding of how the narrative dimension plays into our experience of life and health.  I read "The Mastery of Love" by Ruiz many years ago when things for me were about at their worst.  I read "Kitchen Table Wisdom" by Reman sometime later when I was starting to heal.  Then just a few days ago a friend in Brussels gave me the book "Teach Us To Sit Still" by Tim Parks, which is what finally inspired me to write this post.

What I'm trying to talk about is pretty much the area overlap between those three books, with maybe some Joseph Campbell thrown in.  They provide a much more nuanced and culturally grounded background than I can give. In "Kitchen Table Wisdom", Dr. Reman gives many vignettes of how this sort of thing has played out in her own life and the lives of other people she's known or treated.  She tells of her own journey both as a doctor, from medical school through the stages of her career, and as a patient, being diagnosed with Crohn's disease and going through the stages of coping with that.  She describes starting out somewhere between oblivious of and hostile to this narrative dimension both as a doctor and a patient, then increasingly understanding and appreciating the importance of it over time.

She teaches that our own narratives need to develop through telling our stories to each other, and points out that the natural opportunities to do so, such as sitting with others chatting around the kitchen table, seem to be mostly drying up in American culture.  She also has a lot to say about the culture of how doctors are trained in the US.  From what I can tell, this training largely tends towards devaluation of the narrative dimension of patients' experiences and treats it as a barrier to be overcome in order to achieve "patient compliance".

Yet, all our interactions with the medical system do impact us along the narrative dimension, whether we acknowledge it or not.  I would argue, and I think Dr. Reman would agree, that we would do better to be more explicit in our acknowledgement of those interactions.  Impacts of health-related experiences and pronouncements on the narrative dimension can be as significant and real as things that more directly and measurably affect the physical and biochemical dimensions, for good or for ill.

This issue is particularly relevant in situations where we find that we can no longer square the officially sanctioned go-to-the-doctor-and-do-what-he-says approach with our own experience of what's going on.  Do we meekly accept the roles that dead-end labels cast us in, despite the continued experience of illness-like suffering?  Or, do we keep looking for something else that resonates better with our stories, experiences, and sense of self?

The first half of "Teach Us To Sit Still" by Tim Parks is the most detailed first-hand account I've seen of someone becoming aware of this narrative dimension and then writing about their journey.  As he comes to realize, "Every illness is a narrative.  What matters is the version you tell yourself."  The version he tells himself changes over time, and he shares with the reader the ways in which those story shifts occurred.

Tim has been experiencing pelvic pain and increasingly frequent and disruptive nighttime trips to the bathroom, and finally decides to try to do something about it.  His friend Carlo is a urologist, so he starts there.  From talking to Carlo and the doctors Carlo refers him to, Tim expects that his problem is an enlarged prostate which could be treated by routine surgical procedure called TURP.  However, after going through the chain of diagnostic tests, the straightforward prostate story breaks down.  The doctor eventually tells him that he sees nothing dramatic and "If Signor Tim had no symptoms, I would say from these X-rays he was perfectly fine."

On the one hand, the normal-looking prostate is good news.  However, it leaves him adrift to explain or address his continued pain and urinary problems.  The doctors want him to do the TURP surgery anyway, but Tim is no longer convinced it would help with his symptoms.  The dominant stories plaguing him now are variations on the theme of it's-all-your-head.

Tim visits India for a conference and, while there, consults an Ayurvedic physician.  He asks the doctor if he thinks Tim's problems are entirely psychosomatic:

A slow smile spread across the doctor's face.  'That's not a word we have much use for, Mr. Parks.'   

I looked at him.   

'You only say psychosomatic', his wife explained, 'if you think that the body and the mind are ever separate.'  

It was a fair point."

The looming acceptance of the "psychosomatic" role had felt devastating in the context of the default set of stories that our culture feeds us about health and illness.  Until this point, the only defense Tim had had was a definitive diagnosis of something else more respectable.  The alternative story the Ayurvedic doctor and his wife offered resonated for Tim and made a big difference in getting past that hurdle.

A similar turning point happened in my own journey.  Just as the options offered by following the go-to-the-doctor-and-do-what-he-says approach through the tree of tests ordered and specialists consulted had clearly hit a wall, my primary care physican, Dr. Manoukian, went off the usual script.  He had a bit of training in Ayurvedic pulse analysis and noticed signs of what, in that system, was called "vata imbalance". He told me a bit about it and sent me off to learn about Ayurveda.

Even though it took a while of following that path before the physical sensations were much different, the immediate shift on the narrative plane was huge.  I went in resigned to accept the devastating "labeled as psychosomatic" role, and walked out hopeful about learning how to address vata imbalance.

Later on, after months of paying attention to what I ate preceding setbacks while following the vata balancing protocols, I became suspicious of nightshade (potato, tomato, peppers, eggplant, etc.).  Strictly avoiding them led to further improvements in my health, and to a new mission to build tools to help people going through similar situations--what I initially called "Human System Debugging."  Eventually that led to encountering others who had experienced similar sorts of transformations through self-tracking, and involvement in the Quantified Self (QS) movement.

This "narrative dimension of health" concept is very relevant to QS/self-tracking.  In this framework, what I think is going on for a lot of folks doing self-tracking is the following: they recognize and are bothered by some persistent discrepancy between their currently active set of stories and their sense of what they're actually experiencing.  Gathering data and reflecting on it allows them a new way to compare the expectations generated by their current stories to specific concrete instances they've recorded, potentially allowing them to generate and/or vet new stories that might work better.

In my case, adopting the Ayurvedic vata balancing story and the strategies that flowed from it led to better results than the earlier ideas.  However, I was still bothered by the persistent discrepancy between the setbacks I experienced after certain meals and what I would now expect.  The process of paying attention to and reflecting on such discrepancies eventually led to the new ideas about nightshade, and confirmed that efforts to strictly avoid them did seem to lead to even better results.

QS provides both 1) a social framework in which to engage in such explorations and feel like it's a normal, ok thing to be spending time on, and 2) other people who we can tell the various drafts of those stories to, and hear theirs from them.  This allows us to move closer to the role of an active agent in crafting our own narratives, and farther from the role of passive victim of whatever stories have been foisted onto us.

I hope this is helpful and resonates for some enough to enrich the discussion.  :)

Ruby, oAuth and BodyMedia

I am very pleased to bring to you today the very first Human System Debugging guest post!  

Miriam works with me at the CREATE Lab at CMU and is, among many other things, the guru I call on when I'm in over my head trying to do things in Ruby on Rails.  I am honored that she joined me in figuring out how to take this next big step in developing our ability to access data from self-quantification devices, and am very pleased that she chose to share this experience with the Human System Debugging community.

  -- Anne, Human System Debugger

Recently, Anne and I spent some time figuring out how to connect to BodyMedia's FIT Data API using the ruby-oauth gem. We ran into some confusing snafu's, so I figured I'd blog about it for posterity, in case someone out there runs into similar problems.

Here is BodyMedia's super-duper straightforward and uncomplicated explanatory diagram:



I'm going to walk you through how we navigated this graph.

Step 1

First you must sign up with BodyMedia and apply for a Consumer Key and Consumer Secret. Information on doing that can be found here.

Step 2

You can now use your key/secret pair to generate a Request Token:

Step 3

Now we must get the user's authorization. Using our API_KEY and API_SECRET, we can construct the following URL:


Following this link, we get to a page that looks like this:



Anne signed in with her BodyMedia credentials and we got redirected to localhost.

Step 4

Now we can exchange our Request Token for an Access Token, which we will use to make requests (yeah, that confused me)

Step 5

Finally, we can use the Access Token to make requests, like so:


Two important things to note here:

1. You have to pass a full URI to make your request and that the domain is different than the one you used to get your tokens
2. You must pass your API_Key in the GET, even though it is also being sent by the oauth gem in the header

These two points had us stuck for a while!

So there you have it. Hope someone out there can avoid a headache..

The Fallacy of Labels

Its been a long time since I have tried to post here, but I have been re-energized to do so after participating in the amazing Quantified Self Conference last weekend.  I've had all sorts of ideas I want to share, but didn't have a clear enough picture of who would care to have the confidence to put them down in blog posts.  Now that I have a concrete community in mind that I think would get it and care (those clustering around the idea of Quantified Self), here goes:

I think as a culture our thinking is badly tainted by what I call the "fallacy of labels."  This is the oversimplification that all things to which a given label has been applied are thereafter indistinguishable from one another and alike in all relevant ways.  This is particularly pernicious with nutrition studies, where the label "high fat" gets applied to a test diet of processed carbohydrates + varying amounts of margarine or crisco, yet hype around the study assumes that it somehow proves it's unhealthy to eat any type of fat.   In fact, "high fat" may not have been the most significant contributor to the damage seen in the test rats/monkeys/humans.  They might have gotten different results with different diet composition, such as whole foods with grass fed butter, despite that also falling under the same "high fat" label.  Peter Dobromylskyj's Hyperlipid and Stephen Guyenet's Whole Health Source blogs are particularly eloquent on this point.  

Just this morning I saw a twitter post from @bulletproofexec who I met at the QS conference making this pointing about another such study here:

Eating a high-fat diet during pregnancy increases the chance of stillbirth, according to new research at Oregon Health & Science University. The new data show eating a typical American diet, which is high in fat, decreases blood flow from the mother to the placenta, the temporary organ that nourishes the unborn fetus. Prior to this study, exactly how a fatty diet contributes to stillbirth was unclear. The findings are published in the June edition of the journal Endocrinology.

The study was conducted at the OHSU Oregon National Primate Research Center. Because the placental structure of the Japanese macaque is very similar to that in humans, cause and effect can be better established. The researchers hope their work will inform expectant moms and their physicians about the inherent dangers of a high-calorie, high-fat diet.

Nowhere in this article does it say what exactly what was in the diets they fed the monkeys.  Did the test diet differ from the control diet in trans-fats?  Fructose?  Wheat?  Linoleic Acid?  Any of those could be highly relevant, yet researchers may not even think about or control for such other possibilities if infected by the meme that the "high fat" label tells you everything that matters.  It may or may not even be possible to find such details in the paper itself (I haven't tried on this particular one, but Peter and Stephen are good at digging into that sort of thing).  

Another example is debates about whether the "SCD diet" works for "Crohns".  There are a variety of ways of eating and diverse people's biochemical situations to which those labels get applied but which are not equivalent.  As I understand it, "Crohns" relates to a person's immune/inflammatory system getting pissed off and taking it out on the lining of their guts.  There are a diversity of potential mechanisms which may be driving this process and really no good way to know which pathways might be significant players for a given individual.  There are also a diversity of ways in which the dietary changes a given individual makes when pursuing the strategy of "SCD diet" might play out beyond the ideological reasoning that went into designing it.  

For particular individuals in which there's a good match between the specific dietary inputs they choose after making the decision to follow the "SCD diet" and what their body needs at that point in time to be able to calm down on the inflammation/autoimmune processes and heal (call them "group A"), it can work incredibly well.  For others, despite similar labeling, maybe not (call them "group B").  If you're just randomly selecting individuals labeled "Crohns", you'll most likely you'll get a preponderance of group B in your sample and claim it doesn't work.  However, that doesn't mean that it wouldn't help people with the potential to be in group A.  There's no way to know which group a given person may fall in at a given point in time short of actually doing the experiment.

Secondly there's the question of sophistication and discipline of adherence.  Giving someone a half-assed summary of what the diet means isn't likely to work even if they have the potential to be in group A.  Most likely they will just make the minimal changes to sort of mostly adhere to their initial understanding of that summary for a limited time (this would particularly tend to be the case in study situations).  You've got to be pretty desperate and dedicated to do it strictly and constantly go back and question your current implementation.  It's also key to reach the point of discerning a difference before you lose your initial interest/zeal.  The feedback loop doesn't work until and unless you can experience the carrot of decreased suffering when you hit on a practice of eating that works for you, and the stick of continuing pain.  At that point your lower level limbic and motivational systems can kick in, and they're better at that sort of thing than your cortex.  That doesn't happen for everyone, and you particularly can't make it happen just by assigning someone randomly to a test group.  The people who do get to that point and see improvements often fall into another fallacy of labeling trap: assuming that everyone with their same diagnosis label would experience the same results if pointed at the same diet label, which is likely also not true.

Thirdly, the explicit claim about the mechanism of action for a given diet may not actually be what's responsible for helping any particular individual that it does help.  The SCD claims that it works by restricting the types carbohydrate which favor pathological strains of gut bacteria and increasing ingestion of certain specific strains of probiotic bacteria that can then outcompete the bad guys.  That may be true, though it's hard to tell for sure (I really really wish we had access to ways to quantify gut flora makeup over time!).  However, other parameters also tend to get altered when changing from typical standard American diet to strictly adhering to their protocol, and these may in fact be more significant to particular portions of group A folk.  Candidate factors include reduced consumption of processed/restaurant foods, more cooking at home from scratch, reduced antinutrients (gluten, lectins, phytates, etc. -- particularly relevant for undiagnosed celiac/wheat sensitive individuals), reduced chemical additives of various sorts, reduced nightshade (no potatoes), potentially improved omega 3/6 ratio and fat soluble vitamins (A/D/K2), increased freshness of ingredients (ayurveda would call it "prana") etc. etc.  It's hard to know to what extent any of those may/or may not be relevant to particular individuals, but they all potentially help.  Other diet philosophies, such as Paleo, Michael Pollan's Food Rules, Ayurvedic vata balancing diet, macrobiotics, Weston Price Foundation, etc. also share similar features and seem to help in similar ways for certain folks.

So, my take on it is that we really need to break free of labels and give people tools (both technological and cultural) to help track the specific details of their intake and wellness over time in enough detail that they can go back and reanalyze the observations through various lenses, try out various ideas, and iterate towards something that works for them.  One of the simplest, most powerful techniques to get started with this is photographing everything before you ingest it with a camera that does timestamping.  Various other ideas and efforts presented at the Quantified Self Conference, such as Quantified Doctor and BodyTrack are all about trying to foster social changes and tool development to make that dream a reality.  

It's like buying pants, if you have a 34 inch waist you wouldn't assume that all pants with "34 waist" written on them would be right for you.  Instead you try them on, look in the mirror, walk around the store in them, ask your friend if they make your butt look fat, and so on.  We understand that acquiring appropriate pants is a high-dimensional problem which is not fully captured by the waist size.  We know that other parameters -- leg length, waist/hip ratio, sense of style, context we want to wear them in, etc. --all factor in.  To get it right, we close the feedback loop of how they look, feel, and perform (to steal a phrase from Robb Wolf) on our particular body at this particular moment.  Why in the world do we act as if the impact of food (and other inputs) on wellness were of lower dimensionality and amenable to open-loop label based cookie cutter solutions?  

Beta blockers: good idea or trap?

For a few months in 2007 I worked very hard at bugging doctors to try to figure out what was going wrong. (A year later I tracked it to a problem with cholinesterase inhibitors, but I didn't know that then.) A neurologist I saw once (and only once) as part of this quest expressed that I was just being overly sensitive and suggested I try beta blockers.

When beta 1 receptors bind to epinephrine they make your heart beat harder and faster. This is what gives you that fluttery messed up feeling when you have to do something like get up and perform in front of a group of people. Beta blockers suppress, or at least attenuate, this effect. They're sometimes used (or abused, depending on your viewpoint) to control physiological symptoms of performance anxiety. This was the basis of his suggestion. Sounds like a good thing, right?

The problem is this: most neurons will adjust their gains and receptor densities to maintain a fairly constant level of input. This is a big part what goes on with things like drug tolerance. In this case, it means that while you're on beta blockers your beta receptors proliferate and ramp their gains to max trying desperately to get the signal level they expect. While the beta blocker levels are stable you feel fine, but when it goes down -- oh man...

I really wish they'd warned me about this when they suggested and/or prescribed the &%^$ things, but I learned this the hard way. I had to stop taking them for a while to do a test. The day after I stopped I felt jumpy, my heart rate was running ~130 just sitting still and ~160-180 if I tried to do anything, and I got really bad cardiac arrhythmia (multiple times per minute -- scary). This was not fun and so, so much worse than what had been happening to me before taking the beta blockers.

I tried to go without them after that, figuring these symptoms would fade and that I'd already paid the worst of the withdrawal symptoms waiting for the stupid test to happen. Months later, when these problems were still much worse than they'd been before and weren't getting any better I gave in and started taking them again. (BTW, the lovely interlude with the generic Ethex Toprol XL described in the last post happened at this point in the story.)

A few months after changing my diet to avoid cholinesterase inhibitors, I started having a different problem: the beta blockers were now too strong. The built up SGA had been keeping the epinephrine level artificially high. Once the level dropped enough, the beta blockers were making my blood pressure go so low I couldn't function.

I was already taking the minimum available dosage. Cutting them in half worked for a few weeks, but they couldn't be subdivided further without destroying the time release. (As described in the last post smooth time release is critical for this stuff.) The only option was go cold turkey and be miserably jumpy, heart racy, and arrhythmic until the beta receptors desensitized back to normal.

I couldn't find any useful info anywhere to help me understand how long that might take. The last experience stopping beta blockers was miserable and ultimately failed, but how much of that was caused by the hypersensitive beta receptors and how much by the high SGA levels?

It wasn't nearly as bad as I'd feared, implying that the SGA levels had been the dominant part of the problem last time. There was a little arryhthmia, but mild, and only for a few days. The jumpiness and heart racing faded slowly over a couple months.

Later, when I got the results back from 23andme, I discovered that I have mutant beta 1 receptors: GG on rs1801252. Only ~4% of the population have this genotype, and it's been associated with "low extroversion." I take that to mean that we suffer the fluttery feeling so bad that we mostly avoid having to be on stage in the first place. This may help explain why the beta blockers were so effective at such low doses.

So, the question is this: should I recommend the use of beta blockers to help counteract the effects of cholinesterase inhibitor sensitivity (CIS) during the detoxification process or not? It helped in the short term, but in the end felt like a trap. Also, I don't know how the mutant receptors play into this. How would this play out in people with CIS but with normal receptors? Sigh, need bigger sample size.

The more troubling thing is that ~millions of people are taking beta blockers for high blood pressure. It seems like everyone I talk to over the age of 60 is either taking them, or their spouses or friends are. Nobody warned them about receptor sensitization and withdrawal effects either. Yikes...

Generic drugs: I'm on to your tricks now

I've been thinking about writing this post for a long time, but was finally kicked into gear by LookyDaddy's recent post referring to the dangers of generic epilepsy drugs.

My first experience with this was about a year ago with Toprol XL. I'd been taking it for months with no problems. Then one refill the pills were clearly different. It turned out that Walgreens was now sourcing generic Toprol XL from a different manufacturer: Ethex instead of Sandoz. They didn't think this was worth mentioning. I only noticed because the size and shape changed.

Right away I started having trouble. During the course of the day I'd go through periods of incredibly low energy and blood pressure -- like, unable to move low -- and periods of jumpy heart racing.

Randy hypothesized that the release rate of the Ethex generic wasn't flat enough. During the low periods it was releasing the drug too fast: beta receptors too blocked, heart going too slow and weak. During the jumpy periods it was releasing too slow: receptors not blocked enough, heart going too fast and hard.

These problems went away within a few hours of getting the name brand. After that, we poked around on the web and found that lots of other people had the same problem with the Ethex generic.

More recently, I started experimenting with bupropion to try to deal with dopamine deficiency. Again they gave me a generic: Teva Budeprion XL. Again there was instability: high dopamine in the morning, sudden crash in the afternoon, ok in the evening after a nap. I thought at first that this was just startup edge effect, but it went on for weeks.

Again, these problems went away right after changing to the name brand. Again, lots of others had similar problems. We learned that two other people we know and care about were also getting screwed up by Teva Budeprion XL and got better when they stopped taking it. Ok, we thought, better put out a warning...

Now, I know this is all anecdotal and there's plenty of people on the net to complain about anything. However, consider this: the time release mechanisms in drugs are considered *inactive ingredients* and are therefore not regulated. They differ between brand name and generic, and even between generics from different manufacturers. The ones that are sophistocated enough to give reasonably flat release profiles are pricey. Generics have low profit margins. Seems like a good target for cost cutting.

Another problem with inactive ingredient substitutions is that they can be a problem for people with sensitivities. The one I have to watch out is potato starch (discussion of use in generics here). Pharmacists don't seem to have access to inactive ingredient information but will supply the phone number of the manufacturer.

I'm sure not all generics are bad, but after getting messed up by the last two in a row I no longer swallow the claim that they're "equivalent." If you're taking a generic, it may perhaps be a good idea to do an experiment:

• Get one refill, or a partial refill, of the name brand
• Watch yourself carefully for a few days while still on the generic, then compare how you do with the name brand
• If you can't notice a difference, go back to the generic with restored peace of mind
• If you notice a difference for the better, think about how much that quality of life improvement is worth to you compared to the cost differential

I know that for me it's well worth the $15 extra per month to be free of what the Ethex and Teva generics were doing to me.