We have now arrived at day two of the UCSD EDC2014 conference review. The morning was dedicated to integrative cognitive-affective therapy (ICAT) for bulimic symptoms with Drs. Stephen Wonderlich and Carol B. Peterson. I will handle this presentation in several blog posts because there is a lot to cover off.
ICAT has four phases. It was designed to try to address poor remission rates for bulimia nervosa (BN). A high estimate for remission of BN is 40% and dropouts and relapse rates are considerable.
Cognitive behavioral therapy (CBT) is superior to antidepressants and other psychological treatments. i However, CBT offers a limited view of emotional responding; has inadequate consideration of interpersonal factors; provides insufficient attention to therapist-client relationship; and creates an overemphasis on conscious controlled cognitive processing. ii Basically, the emotions are missing.
“The effectiveness of treatment and prevention improves when empirically-supported/causal maintenance factors of psychopathology or behavioral problems are targeted.” iii
When considering the mechanisms of the onset and reinforcement of eating disorders the causal and maintenance facets were as follows iv, v, vi, vii:
The theoretical and clinical underpinnings of ICAT include the intensive opening phase of CBT that encourages self-monitoring and disrupts dieting behaviors.
Behavioral activation therapy is incorporated to generate structured activity scheduling about food and eating. And motivational interviewing is included to help recognize ambivalence and the positive function of the disorder within the patient’s life.
Emotion-focused intervention features in ICAT to address cycles of binge/purge as an escape from negative emotions; applying restriction as a way to avoid negative emotion; and all the BN behaviors applied to address multiple emotions that occur in a given situation.
Self-discrepancy theory is integrated into ICAT: the actual, ideal, ought, and feared selves. There is structural analysis of social behavior interwoven into ICAT as well and it considers interpersonal patterns and relationship problems. Relapse prevention is the final necessary facet so that there is structured planning in place for addressing slip management.
Within the ICAT-BN model of onset there are significant self-discrepancy challenges. A cycle of self-criticism and self-control combine with negative emotional states so that both restricting and reactively eating are used to reduce negative emotion.
Compared with controls there is a marked lack of self-acceptance and self-protection for those with BN. The urgency of negative emotions leads to rash decision-making.
I will jump in here with an over-arching observation I believe is often lacking when researchers assess the emotional states and traits of those with BN— they overlook how an inability to successfully restrict actually generates a core anxiety and negative emotion in and of itself.
And while ICAT most assuredly incorporates the disruption of dieting behaviors at the outset of treatment, it’s my assessment that the program will rely too heavily on self-reported (inaccurate) average daily intake guidelines that are insufficient for rectifying pervasive and ongoing energy deficits for the patient.
In my estimation, remission rates are even worse for BN than for AN because in our diet-warped culture we fail to identify that BN patients are under eating relative to their energy requirements. Within all treatment modalities, ICAT included, the emphasis is on creating structure and developing increased distress tolerance as ways to stop the binge. But if you are hungry and have a serious energy deficit within your body, then we are continuing to roll out treatment modalities that still remain foodless when it comes to helping a patient reach remission from a restrictive eating disorder.
You will recall that many of the researchers who spoke at UCSD EDC2014 on family-based treatment pointed out that the dysfunction that can be seen within many families of those with a restrictive eating disorder is the result of what an eating disorder does to the family structure and not the cause of the condition’s activation.
And here we are doing the same thing that we did to generations of parents who were blamed for their children’s restrictive eating disorder; we confuse correlation with causation when it comes to the emotional dysregulation that can be readily measured in patients with BN.
That said, I do think that were ICAT to incorporate doubly-labeled water method trial data for re-feeding in addition to the accommodation of hyperphagia for the purpose of returning to an energy-balanced state, the entire treatment modality is an impeccably-designed and thoroughly-researched approach that could likely realize much better remission rates than it currently gets (in the absence of attending to re-feeding). I’ll get to the ICAT remission data in a later post on this topic.
Four Factor Deficits
Those with eating disorders displayed deficits in the following areas viii:
The ability to experience emotions with clarity, awareness and acceptance.
The ability to flexibly use adaptive strategies to regulate intensity and/or duration of an emotion.
The ability to resist impulses and engage in goal-directed behaviors when distraught.*
A willingness to experience emotional distress while pursuing meaningful activities (does not avoid emotion experiences or contexts.
*Again we need to keep in mind that resisting an impulse to hyperphagia (extreme eating) is assumed to be valid merely because patients with BN are usually of average or above-average weight. Basically, because most BN patients are distressed by a binge, and this distress aligns with cultural norms, it is taken on faith as having validity.
Essentially the addictions model is in full force and therefore food is treated as a drug to which the BN patient turns to alleviate emotional dysregulation. Treatment is focused on helping the patient sit with distress while not applying the presumed maladaptive response of eating food.
Instead, were the phobia model applied where a patient’s distress at eating was framed within the development of a misplaced fear response, then exposure and response prevention would be the go-to treatment modality to help a patient recalibrate distress at eating a large amount of food by identifying that the energy is needed for the body to return to a balanced state.
“…craving for food, preoccupation with eating and loss of control over food intake represent a natural psychobiological adaptation to sub-optimal weight and food deprivation. Compulsive eating is therefore best understood in terms of a conflict between a biologically derived drive for food and a culturally derived drive for thinness…the urge to eat is biologically adaptive, and recovery from compulsive eating depends upon relaxing restraint.”ix
The focus on the binge as the event that is the problem is patient directed and culturally confirmed. But the actual self-harming behaviors are restricting food intake relative to energy requirements and then applying compensatory behaviors in response to a binge (which is in effect a strong survival instinct against unremitting under eating).
If you consistently under eat, then how are you going to respond to interpersonal and or intrapersonal stressors? In other words, all this negative affect triggered by momentary self-discrepancy, self-criticism, self-neglect, self-control that is clearly part of the cycle of leading to a binge/purge event may be poorly regulated precisely because the individual is so under nourished.
The reason that the Snicker’s advertising campaign “You’re not you when you’re hungry” has stickiness— it’s more true than not.
However, we have to recognize that although the four factor deficits are likely not causative elements for the onset of BN, they are perseverating and reinforcing when it comes to BN behaviors. It won’t be enough to just attend to re-feeding so as to realize renewed energy balance within the body, if full remission is the desired end-state.
In the next post we will take an in depth look at the ICAT skills training and treatment program.
i Wilson, G. Terence. "Psychological treatment of eating disorders." Annu. Rev. Clin. Psychol. 1 (2005): 439-465.
ii Clark, David A. "Perceived limitations of standard cognitive therapy: A consideration of efforts to revise Beck's theory and therapy." Journal of Cognitive Psychotherapy 9.3 (1995): 153-172.
iii Strauman, Timothy J., and Kari A. Merrill. "The basic science/clinical science interface and treatment development." Clinical Psychology: Science and Practice 11.3 (2004): 263-266.
iv Fairburn, Christopher G., and Paul J. Harrison. "Eating disorders." The Lancet 361.9355 (2003): 407-416.
v Jacobi, Corinna, et al. "Coming to terms with risk factors for eating disorders: application of risk terminology and suggestions for a general taxonomy." Psychological bulletin 130.1 (2004): 19.
vi Stice, Eric. "Risk and maintenance factors for eating pathology: a meta-analytic review." Psychological bulletin 128.5 (2002): 825.
Batterink, Laura, Sonja Yokum, and Eric Stice. "Body mass correlates inversely with inhibitory control in response to food among adolescent girls: an fMRI study." Neuroimage 52.4 (2010): 1696-1703.
vii Stice, Eric, et al. "A preliminary trial of a prototype internet dissonance-based eating disorder prevention program for young women with body image concerns." Journal of consulting and clinical psychology 80.5 (2012): 907.
viii Lavender, Jason M., et al. "Dimensions of Emotion Dysregulation in Bulimia Nervosa." European Eating Disorders Review 22.3 (2014): 212-216.
ix Wardle, Jane. "Compulsive eating and dietary restraint." British Journal of Clinical Psychology 26.1 (1987): 47-55.