Part Two: UCSD EDC2014 Review
Applying Neurobiological Research Findings to Inform the Treatment of Severe and Enduring Anorexia Nervosa
Following on from Part One, Drs. Stephanie Knatz and Laura Hill created a really well-tailored presentation and interactive assignment for us all as the mid-morning ice-breaker.
Dr. Knatz began the presentation by providing additional depth on the topic of temperament-based treatment. Current treatments for AN are all borrowed from other models of psychopathology and nothing exists that has been developed from the ground up with AN as the foundation shaping the treatment plans and outcomes.
The dominant framework for treatment today is essentially to take the current validated treatments (eg. CBT) and then fire it out to hopefully receptive neurobiological predilection within the AN patient—a top down approach.
Dr. Knatz explained that temperament-based treatment works from the bottom up where neurobiological mechanisms that generate personality and behavioural expression, that subsequently shape the onset and progression of AN, shape the targeted treatment approaches are developed and implemented.
The fundamental philosophy of temperament-based treatment is to help people develop constructive ways to cope with innate temperament.
They look to find ways to understand how the traits contribute to the onset and how best to use the innate temperament in proactive ways.
In the world of performance psychology in business, this approach is referred to as playing to your strengths. Originally developed by Marcus Billingham and Donald Clifton at Gallup Organization in 2001, the approach has been heavily marketed, by Gallup, with its product StrengthsFinder. Strengths-based development sits within the school of positive psychology. [1]
My brother works in the field of business psychology and neither he nor I is particularly enamoured with strengths-based development. The first problem is that nothing is ever unequivocally strength or a weakness. In reality, you have attributes, or traits, that may be useful in some circumstances and unhelpful in others. The second problem is that in real-world professional environments you will never get to use your attributes exclusively in ways that only reflect their strengths.
Let’s take my low vagal tone and high startle response (a neurobiological predisposition that I have) and elaborate on this point a bit further. From that neurobiological predisposition at birth, my temperament has been shaped to reinforce a cluster of highly sensitive personality traits. My temperament (emotional reflex) is vigilance. If you have a predilection for anxiety and are raised by anxious parents, well that’ll do it. Behaving somewhat like a sentinel meerkat has its strengths and weaknesses.
Lying awake in bed until 4 am ruminating is a definite weakness of a sentinel temperament. However this past Sunday afternoon while having a leisurely brunch, a commotion in the hallway of our apartment block drove me to be the first to call 911 (multiple calls followed from our building as I was speaking with the dispatcher). My husband thought it might be kids horsing around. The sounds alerted me to something being very amiss, although ask me to tell you what specifically and I’m at a loss. The commotion was actually our building manager wrestling someone who had broken into the building to the ground in the stairwell. The police arrived in record time and our building manager suffered only minor scrapes thankfully.
While it would be very cool to be asleep at 4 am and still identify a threat often faster than others, the reality is the trait won’t work like a switch.
That’s why I was heartened to see Dr. Knatz mention that their treatment approach includes compensating for traits that are not there. And this is a technique that has really good outcomes for those with fetal alcohol spectrum disorder (FASD). In FASD treatment it’s referred to as applying an external brain.
For patients with FASD, the traits that are weak, or absent, are executive functions. Dr. Sterling Clarren is a leading researcher and pediatrician in the field of studying teratogenic effects of alcohol on the developing brain, He first coined the term by mentioning that there is a need of an external brain for those with FASD. [2]
For those with FASD, parents and caregivers often act as the external brain to generate appropriate action where the patient’s internal ability to assess cause and effect is impaired. For those unfamiliar with FASD, people with the condition struggle to assess outcomes of behavioural choice ahead of making the choice, and they often also lack the ability to learn from having made a bad choice.
Young children with FASD will have very direct external brain direction provided by their caregivers and guardians. As they reach their teens, the external brain is enacted more through practiced and guided use of making lists. Regular check-ins with the guardians, along with likely more stringent chaperoning and control to protect them from peers that sense an opportunity to take advantage of them, are common external brain facets for the FASD teenager. In the absence of physical complications associated with the teratogenic effects of alcohol, most people with FASD (with appropriate support) appear to develop stronger executive function ability in their late 20s.
The traits that Dr. Knatz and her colleagues target for patients with AN are: anxiety, reward/punishment, set-shifting and interoceptive awareness. You’ll have seen and likely read numerous posts here on this site on anxiety and interoceptive awareness. Interoceptive awareness as a refresher is your sense of your internal physical state and this includes knowing you are hungry, tired, have a need to urinate, etc.
I also go into some detail on the reward/punishment (behavior activation and inhibition systems in the brain) mentioned in Part One.
But what is set-shifting?
There is cognitive, task and attention set-shifting. Optimal set-shifting allows for maximum flexibility for an individual in their environment.
Task and attention set-shifting difficulties can be all too easily triggered for those with attention deficits or hyperfocus challenges (attention deficit (hyperactivity) disorder for the former and autism spectrum disorder for the latter). For those with eating disorders, much of the task and attention set-shifting challenges will be exclusively driven by the fight/flight/freeze system being activated in the presence of food (as a misidentified threat to survival).
Either the patient is set-shifting wildly (distraction) to avoid focus on eating, or she is hyperfocused to the point that if the concentration or ‘correctness’ of the effort is broken in anyway, then it is impossible to continue eating. Address the anxiety, and much of the task and attention set-shifting will be ameliorated for those with eating disorders.
Cognitive set-shifting happens a tremendous amount in social situations.
Based on non-verbal and physical queues from others, you might identify that you are boring others and you may shift to another topic or ask a question as a way to try to put the others at ease and re-engage them in some way. If you are helping your daughter with some math homework and she continues to stare at you blankly, then you may grab a bunch of paperclips off the side of her desk and try to demonstrate the concept visually with paperclips. Those would be examples of cognitive set-shifts.
Cognitive set-shifting also is applied for entirely internal stimuli as well. If I am stuck in stop-and-go traffic and I’m getting frustrated about the fact that it’s going to make me late for a meeting, then I might choose to purposefully shift my mounting irritation towards calmer acceptance that being late is simply not going to be in my locus of control and I will handle the situation when I arrive at the meeting.
Cognitive set-shifting is the engine of cognitive behavioral therapy. For more concepts and techniques on developing greater cognitive set-shifting flexibility and strength, please review the following posts: Rebounding to Calm One and Two.
Dr. Knatz outlined the overall treatment structure as follows: psychoeducation, experiential learning, client coping strategies and carer management strategies.
Creating a strong foundation through psychoeducation is achieved didactically in this treatment approach. For a patient to understand not only how her temperament has useful and detrimental application depending on circumstances (as with my “sentinel meerkat” temperament), as well as to understand how the neurobiological predisposition to misidentify food as a threat is not her fault, frees the patient up to enter an experiential learning effort with curiosity and interest.
This treatment approach is directed at adolescents and young adults and they are almost always embedded within a family structure at the time of treatment. Therefore psychoeducational and experiential learning is occurring for the family as a whole. Helping carers and siblings to understand the condition is as important as having the patient understand it herself.
The client coping strategies (the term “client” is understandably more embedded within the US health care system as they are indeed all paying clients) will involve assessing when an attribute of temperament is reinforcing harmful behaviours and when it can be applied to leverage helpful behaviours. It will additionally involve many external-brain techniques (journaling, writing down reinforcement statements, lists, etc.) because the neurobiology is noisy and runs with too much interference (I’ll get into more detail on this when I talk about Dr. Laura Hills’ contribution to the seminar).
Carer management strategies include teaching carers to communicate effectively, respond to symptoms appropriately, reduce blame and increase empathy, and to be able to identify and manage burnout as well.
The presentation was a joint effort, where Dr. Knatz laid down all of the above information with lightning efficiency yet it was effortlessly well-paced, and then Dr. Laura Hill took us all through our own experiential learning event.
Dr. Hill has a truly infectious level of passion and her utter commitment to helping those with eating disorders is palpable. With a brief introduction to the hierarchy of thoughts to action we had an opportunity to create a simulation of what happens in the brains of those with eating disorders.
The areas of the brain that impact interoceptive awareness related to eating are the nucleus accumbens, the amygdala, the insula and the ventral tegumentum. When we speak of interoceptive awareness in relation to eating we are talking primarily about hunger and satiation. The combination of having a very noisy dorsal lateral pre-frontal cortex combined with an insula that is struggling to interpret interoceptive inputs (“Am I hungry?”) such that it either sends no message or weak messages that do not activate the nucleus accumbens to seek out and eat food was all cleverly mimicked with several variations on the telephone game.
I was next in line to the gentleman who was playing nucleus accumbens (often shortened to NAc or Acc). We held hands in a circle consisting of some 40 odd people. Various individuals around the large circle were assigned the roles of the other brain structures involved. The initial signal was sent out by the Acc as a hand squeeze. Each person in the chain was responsible for trying to mimic the strength and duration of the hand squeeze, as well as whether there were multiple hand squeezes or not.
Then the Acc had to assess whether the strength and duration of the hand squeeze he got back was as he had sent it out. Then Dr. Hill added a constantly firing Acc to the mix (multiple hand squeezes), varying the strength and duration, then a threesome of chatty individuals who had to somehow get the hand squeeze through all while carrying on a soft conversation then a loud conversation (mimicking the very noisy thought patterns of the dorsal lateral pre-frontal cortex someone with an eating disorder).
And then the Acc representatives from each circle were taken aside by Dr. Hill and given a sentence to be whispered all the way along the chain – the quintessential telephone game. The phrase, if I recall it correctly, was from a children’s song:
“Beans, beans, the magical fruit,
The more you eat, the more you toot.”
Naturally, hilarity ensued. I’ll leave that one to your imagination.
In addition to perhaps a very noisy dorsal lateral pre-frontal cortex and a weak, misfiring and confused insula, it appears as though the Acc itself may be wreaking havoc when it comes to how someone with an eating disorder finds herself struggling mightily in the presence of food. Dr. Hill did not touch on this directly, but in literature there is some evidence of this being the case.
The tight inter-relationship between the perseveration of both restriction and hyperactivity appears linked to the nucleus accumbens 5-HTR4-CART pathway. [3] What this means is that the apparent failure of homeostasis (staying energy balanced) in patients with eating disorders is a double-hit of a single molecular pathway that triggers both restriction of food intake and excessive expenditure of energy at the same time.
In some very recent literature, eight patients with intractable levels of AN, actually underwent ablation of the nucleus accumbens through stereotactic surgery. Basic vital signs, body mass index and menstruation were recovered one year after surgery. [4] Anterior capsulotomies have also shown up in the literature for treating severe OCD and one comorbid case of AN and OCD. In this surgery the connection from the orbitofrontal cortex and the thalamic nuclei is severed. [5],[6] There are also recent pilot-trial results from deep brain stimulation in treatment-refractory (difficult to treat/not responsive to treatment) AN. [7],[8] We should likely keep in mind that an eating disorder is a spectrum disorder, and while it is good to know that neurosurgery will likely provide life-saving value to those with severe and treatment-refractory cases of AN or AN with comorbid OCD, the risks associated with these surgeries and interventions are likely not suitable risks to take for the majority of patients attempting to get to remission from an eating disorder.
And so we return to the temperament-based treatment framework that offers non-invasive and powerful outcomes for the vast majority of those with eating disorders. Dr. Hill pointed out that the brain organizes itself from the cerebellum on up: actions, through feelings and on up to thoughts. Cognitive behavioural therapy (CBT) addresses thoughts and actions but misses out on the middle-man: feelings. Dialectical behavior therapy (which I have touched on recently in this EDI post: Dialectical Behaviour Therapy) addresses much more of the interconnectedness of actions through feelings and thoughts.
Although we focused on the reward and reinforcement role of the Acc, the threat identifying power of the amygdala is right in there in the looping challenge of maintaining energy balance for those with eating disorders.
Dr. Hill confirms that patients cannot eat mindfully and that they are largely eating blind because they are not receiving all the complex messages through the loops of the nucleus accumbens, the amygdala, the insula and the ventral tegumentum. Food must be prescribed. And her concluding message was that eating disorders should be seen more as a condition like diabetes rather than mental illness.
If you have the time it’ll be worth it to view her TEDTalk:
And for those in recovery grinding through these reviews of UCSD EDC2014, if your only takeaway is to remember that in Middle World you construct your reality moment by moment and it is not happening “out there”, but rather “in here” (in your brain), then you’ve given yourself a powerful foundation for reaching remission from an eating disorder.
Your personality as an adult no longer has to be that which enabled you to get through your childhood alive.
TD Hodges, DO Clifton, Strengths-based development in practice, Positive psychology in practice, pp. 256-268, 2003.
H Green, Fetal Alcohol Spectrum Disorders: understanding the effects of prenatal alcohol exposure and supporting students,Journal of School Health, Vol77(3), pp.103-108, 2007
A Jean, L Laurent, J Bockaert, Y Charnay, N Dusticier, A Nieoullon, M Barrot, R Neve, V Compan, The nucleus accumbens 5-HTR4-CART pathway ties anorexia to hyperactivity, Translational psychiatry Vol2(12), p.e203, 2012.
J Wang, Jing, C Chang, N Geng, X Wang, G Gao, Treatment of Intractable Anorexia Nervosa with Inactivation of the Nucleus Accumbens Using Stereotactic Surgery, Stereotactic and functional neurosurgery, Vol91(6), pp. 364-372, 2013.
J Barbier, L Gabriëls, K Van Laere, B Nuttin, Successful anterior capsulotomy in comorbid anorexia nervosa and obsessive-compulsive disorder: case report, Neurosurgery, Vol69(3), pp.E745-E745, 2011.
BE Oliver, J Gascón, AAparicio, E Ayats, R Rodriguez, JL Maestro de León, M García-Bach, PA Soler, Bilateral anterior capsulotomy for refractory obsessive-compulsive disorders, Stereotactic and functional neurosurgery, Vol81(1-4), pp.90-95, 2004.
H Wu, PJ Van Dyck-Lippens, R Santegoeds, K van Kuyck, L Gabriëls, G Lin, G Pan et al, Deep-brain stimulation for anorexia nervosa, World neurosurgery, Vol80(3), pp. S29-e1, 2013.
N Dipsman, DB Woodside, P Giacobbe, C Hamani, JC Carter, SJ Norwood, K Sutandar et al, Subcallosal cingulate deep brain stimulation for treatment-refractory anorexia nervosa: a phase 1 pilot trial, The Lancet, Vol381(9875), pp.1361-1370, 2013.
