It’s long overdue that I transfer information to the Your Eatopia community on the conference I attended in San Diego hosted by the University of California San Diego Eating Disorders Center in October.
First of all, this series of blog posts on the conference are my filters and interpretations of the material presented and I won’t be providing a slide-deck replication of the sessions on offer. Given that all of the presenters are practicing researcher/clinicians, you will find all of their original trial results published in peer reviewed publications, if you would prefer to go to the source.
Secondly, the eating disorder research community seems distinct from many other research communities that I have worked around in the past. The researchers who presented at UCSD EDC2014 are all researchers and clinical practitioners. I suspect that maintaining close patient contact through clinical practice while undertaking complex research studies may be normative within the mental health arena, but many medical researchers are not exposed to the rigors of patient care. Possibly as a result of their ongoing embedded work as practitioners, the researchers presenting at UCSD EDC2014 all seemed far more humble and modest than many leading medical researchers I have met in years past.
Thirdly, by way of providing the punch line up front, no revolutionary or breakthrough treatments are available today for those with restrictive eating disorders. And, given how research funding necessitates a very narrow and iterative approach, it is highly unlikely that any future revolution or breakthrough will be forthcoming either.
Finally, I have a much more nuanced appreciation for why binge eating disorder (BED) was included in the DSM V as a distinct eating disorder and will impart that when I get to the accompanying presentation in this review. Many patients and clinicians are unaware of the underlying complexity regarding BED’s inclusion and this will very likely result in an increase in misdiagnosis, and improper treatment, of the condition in the population at large.
I am going to walk us through the presentations one by one and it will therefore be a multi-part blog series.
Innovative Treatment Approaches for Eating Disorders: Applying Cutting-Edge Research into Practical Clinical Skills
The intended goal of UCSD EDC2014 was to impart cutting-edge research to be applied in practical clinical skills. Innovative treatment? In the narrowest definition of “innovative”, the approaches in question certainly all introduced new methods of treatment. In the broadest sense however, these treatment approaches reflect an iterative progression that keep us all treading water.
The general consensus amongst both the researchers and practitioners with whom I had a chance to chat, is that our lack of progress in developing treatment approaches that actually generate solid remission rates is frustrating, disappointing but also tends to be why we are all in this field in the first place— driven to get a better handle on it because, quite literally, lives depend upon it.
Perhaps some elegant and simple solution eludes us, but most likely not. A restrictive eating disorder is expressed quite similarly to what is seen in an ecological trophic cascade. A trophic cascade is the waterfall effect of feeding and nutrition throughout an entire ecosphere when a top predator disappears.
Since wolves were reintroduced to Yellowstone Park in the US in 1995/6, scientists have had an unprecedented opportunity to watch the reversal of trophic cascade impacts. When a top predator is removed from an ecosystem, the impact of their absence is felt in unpredictable ways all throughout the food chain. A trophic cascade ends up mimicking more a flow of rushing water over rocks than a clean drop of water from the top of a cliff to the bottom.
The reintroduction of wolves has had direct reversal impacts for both elk population and aspen growth. However, there are innumerable ripple effect impacts from the presence of wolves that have also occurred: from the overall health of the elk, to the bear and raven populations, the increased variety of song birds, the decrease in coyote populations, the increase in small herbivore populations, and the increased biodiversity through the ecosystem as a whole.
As analogy, it is as if the top predator has been disappeared in the anthro-psycho-neuro-immuno-endocrinological (APNIE) living ecosystem of an individual with a restrictive eating disorder. And much of the study we undertake today centers on what we see in the living landscape after that disappearance, and I think it keeps us constantly confusing outcomes with underlying cause(s).
As a reminder, the researchers I reference are using the Diagnostic and Statistical Manual of Mental Disorder (DSM) classifications (it’s how the research money flows). As there is clinically confirmed data to suggest that symptom overlap and genetic underpinnings render those discreet classifications largely irrelevant, I do not delineate between anorexic and bulimic types and subtypes and use the overarching classification: restrictive eating disorder. For accuracy I will be using their terminology when I am quoting their talks. So when you see anorexia nervosa (AN) and bulimia nervosa (BN) or ARFID (avoidant/restrictive food intake disorder), it is merely because the speaker used those terms.
Just before I get into the talks in detail, I wanted to mention a very nice touch that the master of ceremonies applied when she introduced each speaker. Dr. Erin Parks had prepared an adjective to describe the essence of each speaker as part of her introductory comments. I wish I had had the presence of mind to write down each of those adjectives at the time, sadly I only recall a few now.
As I found that approach so appealing, I would like to offer up two adjectives as an overarching way to introduce all the UCSD EDC2014 speakers and organizers: grace and gracious.
Advancing Treatment for Eating Disorders
Walter Kaye, MD
Dr. Walter Kaye is one of those people who will inevitably look unchanged from ages 50 or so, through to 90 and beyond. It’s a rather pronounced trend I see in people who are really passionate about the work that they do— they simply don’t seem to age very much.
For those of you who have been around Your Eatopia for some time, you likely know all about Walter Kaye as I’ve quoted his and his colleagues’ papers and I reference his work constantly on the blog and forums. I must embarrassingly admit that I was actually too star-struck to speak to the man in person throughout the conference, but I at least took copious notes as he spoke.
Dr. Kaye is a fast- and critical-thinking individual and so his talk was thick with important points. The purpose of the conference was clearly delineated within his first few remarks: a targeted and practical knowledge transfer of evidence-based therapies and treatment advances to clinicians who support those with eating disorders.
Dr. Kaye voiced what each speaker throughout the conference also reiterated: current treatment outcomes for those with restrictive eating disorders are lackluster. He argues that eating disorder treatment cannot remain brainless—meaning that a focus on re-feeding alone will not realize any improvements in current remission rates.
Despite the proven efficacy of cognitive behavioral therapy (CBT) for restrictive eating disorders, he pointed out that the treatment modality isn’t commonly used. Part of the reason for its lack of widespread use is the dearth of practitioners able to offer this treatment modality.
He stated that “There are lots of ways to be anxious” and therefore brain-directed treatments are sorely needed.
What Dr. Kaye and his colleagues are developing is temperament-based treatment. They have essentially amassed clinical data to confirm that those with AN have distinct temperaments that persist in remission.
Temperament and Traits
So this will require a bit of a detour to talk about temperament. Temperament and personality traits have much overlap in psychology. There are various models for temperament and personality trait classification and typing in the scientific literature.
I’ve already discussed personality traits as they relate to restrictive eating disorders in the blog post Is there an eating disorder personality? By way of a refresher, the tenet that we are born with certain core personality traits that remain stable throughout our lives does not hold up too well over a lifetime.
The Big Five personality traits (openness, conscientiousness, extraversion, agreeableness and neuroticism) have test-retest correlations that decay as the time interval between assessments gets longer and there are vanishingly small coefficients obtained for agreeableness and neuroticism over a 40-year span.
As I mentioned in that blog post on personality and restrictive eating disorders, Drs. Caspi, Roberts and Shiner assessed the Big Five over a lifetime and found that domains of agreeableness, conscientiousness and emotional stability (reversed neuroticism) increase with age [A Caspi et al., 2005].
Not surprisingly, others have debunked the maturity principle (Caspi and colleagues’ longitudinal trend line to increased agreeableness, conscientiousness and emotional stability) in favor of la dolce vita impacts.
Drs. Richard Lucas and M. Brent Donnellan identified that the trend towards more agreeableness, openness, conscientiousness and less neuroticism up to age 60 or so, reverses after age 65. They call this la dolce vita effect (the good life effect)— you no longer likely go to work, socialize with people you don’t like and therefore you become less conscientious, agreeable and extraverted in old age [R Lucas, MB Donnellan, 2011].
Meanwhile, Dr. Colin G. DeYoung and his colleagues have been hard at work trying to correlate brain structures and neurotransmitter function with Big Five personality traits. In their work they have placed the Big Five traits into two distinct meta-traits: stability (emotional stability, agreeableness and conscientiousness) and plasticity (extraversion and openness) where the traits associated with stability are serotonin related and the traits associated with plasticity are dopamine driven. [CCG De Young et al., 2005]. DeYoung and his colleagues use the term “plasticity” to denote an exploratory tendency in behavior.
If this is starting to sound a bit like some medieval philosophical papal gathering discussing how many angels might dance on the head of pin, I'm with you.
These personality traits have heritability factors that are influenced by environmental input. As usual, it’s all about nature via nurture. Depending on the study you care to reference, the heritability factor for these traits is somewhere around 0.5— or a 50/50 split roughly between genetic predisposition followed by the environment, and time, shaping those traits and their expression.
The best way to describe temperament is that it is the underlying and long-standing type, strength and speed of response to emotional stimulus. We might even go so far as to call temperament the emotional reflexes seen pretty much from birth.
Drs. Albert Ellis and Michael Abrams in their book Personality Theories: Critical Perspectives described the difference between temperament researchers and trait researchers as follows: “…temperament researchers are concerned with the underlying processes of behavioral inclinations, whereas trait researchers examine the outcomes of these inclinations with particular regard to their origins.”[p. 423] In other words, temperament might be best viewed as some of the instinctive underpinnings of personality traits.
What are emotional reflexes? Well, there are plenty of models to choose from in this research area as well. But I prefer to start with my cats to illustrate the concept.
As you all likely know, I had three cats all of the same age and all adopted and unrelated to each other. They all lived to nice old ages (two of them to age 17 and one to 18). Their emotional reflexes were distinct and stable throughout their lives, with a variation I’ll get to in a moment. A loud noise outside and one would go to the window to investigate, the second would remain completely unreactive and the third would head for the nearest cupboard or dark space.
To a large extent our startle responses and our vagal tone (how quickly our parasympathetic nervous system can change in response to stimulus and return to baseline) differ from one individual to another; are identifiable at birth; and, although remediable, are largely stable throughout life.
How my three cats would each respond to various stimuli was fairly predictable. Their emotional reflexes were stable throughout the course of their lives. But interestingly, the one with the exaggerated startle response appeared to have high vagal tone (his parasympathetic nervous system shot back to baseline very quickly once he had removed himself from the startling stimulus in question). This return to baseline was noted by a vet when, as he tucked his head under my arm during an examination, the vet noted that it instantly had slowed his heart rate (she had the stethoscope on him at the time of that move to tuck under my arm).
The one who was always keen to investigate his surroundings (uninhibited response to the unfamiliar) likely had lower vagal tone as he remained aroused and focused, although confident, for elongated periods of time after the stimulus had passed. The non-reactor was unflappably calm in any unfamiliar circumstance, neither driven to investigate nor flee. However, given various illnesses that appeared in later life for him, his vagal tone likely did not surpass that of the one who was so easily spooked.
And the one who lived the longest was in fact the high-reactor. The complication of his later years however was that he developed neural degeneration that noticeably lowered his previously extremely high startle response.
Cats are all limbic system (the structures in the brain largely thought to direct emotion). They are a great study when it comes to uncomplicated emotional reflexes. But despite the fact that my cats were consistent in emotional reflexes, those reflexes shifted towards a neutral mid-line with two major environmental inputs: having human companions who could frame the stimulus such that it would reinforce appropriate reactivity; and the natural impacts of the human guardians being able to balance consistency and novelty to peak levels that supported each cat’s inherent temperament.
We always had a safe outdoor space for our uninhibited guy who could get easily bored; we always had a dark cupboard with familiar bedding readily accessible to our scaredy cat; and for our unflappable guy we had heated beds— he was an abandoned cat who had little interest in going outside unless it was stinking hot. He liked his creature comforts.
To a far more complex and multivariate level, parents and guardians either ease or exacerbate the emotional reflexes of their children by a) framing the stimulus and b) creating a space that balances consistency and novelty best suited to the child’s inherent temperament. And we also know that such reflexes are heavily influenced by peer group interactions for children and teens as well.
Temperament does not exist in isolation of reward, punishment and motivation. And now we walk on over to the world of Jeffrey Alan Gray and his biopsychological theory of personality.
Reinforcement Sensitivity Theory
Welcome to BAS, BIS and FFFS. And the use of acronyms will only get worse in this blog series I’m afraid. BAS is the behavioral activation system; BIS is the behavioral inhibition system; and FFFS is the fight/flight/freeze system.
To be clear, Dr. Kaye did not touch on this theory in his talk and I am using the model, as it is commonly used, but we do need to allow for the possibility that Dr. Kaye’s framing of temperament and reinforcement sensitivity might be completely different from what I am about to cover off. Nonetheless, I do believe it aligns well with the points he made regarding AN and temperament.
Dr. Kaye and his colleagues have confirmed that those with AN have low sensitivity to reward, high sensitivity to punishment, and a great drive for harm avoidance. Another way to describe those findings is that those with AN have strong behavioral inhibition systems in the brain and weak behavioral activation systems.
Gray’s model, originally developed in 1970, only had the fight and flight mechanisms attributed to the FFFS (FFS at that time). The model was updated in 2000 to include the freeze response as we know that freezing is a distinct threat response.
Gray’s current model posits that the FFFS resolves goal conflict between BAS (approach) and BIS (avoid). Although we can quibble on the details, in broad brush strokes the BAS system is the dopaminergic reward system, BIS is the serotonergic inhibition system, and the FFFS is the adrenergic conflict system.
Within this framework the FFFS is the seat of temperament, or emotional reflexes. The nature of how the FFFS resolves conflict between the BAS and BIS is both genetic predisposition and the result of ongoing lifetime inputs that attenuate or exacerbate its activation.
The Take Home Messages from Walter Kaye
Many of you with active restrictive eating disorders may find the conclusions offered in Dr. Kaye’s keynote presentation self-evident. But we must keep in mind that his audience comprised almost entirely clinical practitioners within the eating disorder field. It is fair to predict a wide swath of experience and skill within the audience and that means covering the basics is wise.
The FFFS found in AN patients is readily activated and its conflict resolution in the presence of emotional stimulus will attribute less value to possible rewards (BAS) when compared to possible punishment or risk (BIS).
Dr. Kaye confirmed that patients with AN have a measurable altered response to coding reward when compared to healthy controls. And this altered response persists in remission. They have difficulty valuating rewards; are oversensitive to risk, error and punishment; and this results in an anxious and inhibited temperament.
Now taking these conclusions into how I frame the condition, the FFFS has misidentified food as a threat and is activated in the presence of food. In healthy controls the FFFS would rarely be activated in the presence of food. The BAS would drive behavior, assuming the healthy control is energy deficient (hungry): approach the food and eat the food.
That’s not to say the FFFS might not be activated in a non-ED individual. If I’m out in the woods for days on end without food and I come across some red berries, you can be sure my FFFS system is going to be fired up. I may be very hungry, but eating possibly poisonous berries will not be the answer to my problem.
Another example is the FFFS is often activated when a non-ED person is exposed again to the same type of food that was eaten close to developing a gastrointestinal illness. However when this same situation occurs for an individual predisposed to develop a restrictive eating disorder, the activation is more powerful and more strongly sustained than for non-ED others.
And of course we know that one of several common ways in which a restrictive eating disorder is activated is through involuntary restriction of food (i.e. illness). In other words those with restrictive eating disorders sit on a powerful FFFS that has a predilection to use the BIS as the resolution of choice.
Another observation Dr. Kaye made in his closing remarks is that there would be evolutionary advantages to having those within the same species that are more likely to overestimate rewards and those more likely to overestimate risk. The former would have more opportunities for food and commensurately more risk of becoming someone else’s dinner, whereas the latter would have less opportunity for food and commensurately less opportunity for becoming someone else’s main course.
Why would temperament-based treatment be of value in helping patients achieve remission from a restrictive eating disorder? Well because many other treatment options (predominantly not science-based) are essentially brainless and therefore have much lower success rates for the achievement and maintenance of full remission.
When the focus is exclusively placed on weight restoration to a specific target weight and the perseveration of so-called healthy food choices and continued exercise regimes is encouraged (what I call “recover, but not too much”), then the entire recovery effort is playing to a BAS that is absolutely not “feelin’ it”.
To harken back to my original analogy regarding trophic cascades and those with restrictive eating disorders, it’s as if the BAS (as top predator within a trophic cascade) has been hunted to extinction.
There is simply not enough reward ingrained in approaching food for those with restrictive eating disorders. Remember that a restrictive eating disorder is activated, but then it is practiced as well. It’s the practice of avoidance to the misidentification of food as a threat that renders the entire BAS system a shadow of its former self. It doesn’t magically return to its former glory without conscientious application of approaching the food consistently enough and long enough to help strengthen the BAS.
These patients experience no conflict of approaching vs. avoiding food because the FFFS has reinforced patterns to activate avoidance to the point where any drive to approach has atrophied. Neurons that fire together wire together. These patients cannot “recover, but not too much” and achieve anything much more than harm reduction or, more commonly, relapse.
These patients have to learn to work with, and ultimately put pressure on (through purposeful practice and reinforcement), a temperament that has reinforced emotional reflexes to the point that it is crushing the individual’s very survival.
Up next on the Your Eatopia blog series review on UCSD EDC2014 will be Drs. Stephanie Katz and Laura Hill and their engaging and interactive presentation on Applying Neurobiological Research Findings to Inform the Treatment of Severe and Enduring Anorexia Nervosa.