Download Rapid Remission of Anorexia Nervosa and Unconscious

American Journal of Clinical Hypnosis
52:4, April 2010
Copyright © 2010 by the American Society of Clinical Hypnosis
Rapid Remission of Anorexia Nervosa and
Unconscious Communication
Bart J. Walsh
Portland, Oregon
Abstract
An alternate framework for thinking about anorexia treatment is presented
with a treatment approach that results in prompt remission of anorexia
symptoms. Prior treatment of eating disorders using hypnosis is
reviewed. A case example illustrating the method is followed by a
discussion. The process is described for teaching clients how to nullify
the anorexia symptom complex when it is reactivated.
Key words: Anorexia nervosa, eating disorder, unconscious
communication, ideomotor signaling, ego-states.
Address correspondences and reprint requests to:
Bart J. Walsh
1306 S.W. Bertha Blvd
Portland, Oregon 97219
Email: [email protected]
319
Anorexia Treatment
The treatment of eating disorders (ED) like anorexia nervosa (AN) and bulimia
nervosa (BN) pose significant challenges to both affected individuals and treatment providers.
Scientific investigation points to significant genetic and heritability factors linked to the ED
symptom complex (Bergen et al., 2003; Becanu et al., 2005; Bulik, 2006; Bulik, 2007; Bulik,
Sullivan & Kendler, 1998; Grice et al., 2002; Mercader et al., 2007; Ribases et al., 2003; Ribases
et al., 2004; Ribases et al., 2005; Devlin, et al., 2002; Gunstad et al., 2006; Frieling et al., 2007;
Frieling et al., 2008; Steiger et al., 2006; Javaras, Laird, Reichborn-Kjennerud, Bulik & Pope,
2008; Klump, Miller, Keel, McGue and Iacono, 2001; Kendler et al., 1991). These diseases are
systemic in their symptomatic expression and influence on thought, mood, perception and
behavior. Much of the AN and BN symptom complex demonstrates trance phenomena
(Edgette & Edgette, 1995) that include time distortion, hallucination, catalepsy, amnesia and
dissociation (Torem, 1986; Valdiserri & Kihlstrom, 1995a, 1995b; Vanderlinden & Vandereycken,
1990; Covino et al, 1994) with some indications that bulimics may be more hypnotizable than
anorexics (Pettinati et al, 1985; Sanders, 1986).
Behavioral management of the ED may keep a person healthy, but clients have
reported to this author that it often does little to resolve inner torment from this chronic
illness. Given the deep and comprehensive level of psychobiological functioning expressed
by the ED (Rotenberg, Taylor & Davis, 2004; Ribases et al., 2003; Mercader et al., 2007;
Kaplan, 2004; Klump, Bulik, Kaye, Treasure, & Tyson, 2009), deep levels of functioning must
be reached to effect more than behavioral change.
Documentation of ED treatment using hypnosis is largely anecdotal and without
supporting empirical research. Pierre Janet (1925) described hypnosis applied to “hysterical
anorexia” to inspire a woman’s eating by increasing focus on tactile and visceral sensations
(Baker & Nash, 1987). Reports since 1925 reflect direct and indirect suggestive approaches
as well as psychodynamic investigation aimed at resolving ED symptoms or uncovering
causal factors. Direct suggestion targeting sensitivity to hunger and fullness, body image
distortion and involuntary dissociative states was applied with noted benefit (Comani,1992;
Pettinati, Kogan, Margolis, Shrier, & Wade,1989). Enhanced self control and motivation
regarding bingeing and purging reportedly resulted from direct suggestion (Griffiths,1989;
Vanderlinden & Vandereycken, 1988, 1990). Ego enhancing suggestions, age regression,
and hypnotic dreaming reportedly targeted the underlying ED dynamics with some success
(Pettinati et al., 1989). Suggestions for increased enjoyment of food, coupled with amplified
hunger and food intake, reportedly bore positive results (Crasilneck & Hall, 1975; Kroger &
Fezler,1976). Thakur (1980) disclosed success with direct suggestions for healthier eating
habits, increased weight gain and realistic body image. Theissen (1993) indicated benefit by
hypnotically incorporating fairy tales with the eating disordered. Erickson (Erickson &
Rossi,1979) used indirect suggestion and paradoxical interventions to treat an anorectic girl.
Yapko (1986) employed indirect suggestion to address family enmeshment, delayed maturity,
self-esteem, and body image with an anorectic girl. Some noted hypnosis helpful in the
reduction of tension and resistance to treatment, management of ED symptoms, and
identification of affect in the eating disordered (Lynn, Rhue, Kvarl, & Mare, 1993;
Hornyak,1996). Gross (1984) outlined a hypnotic protocol for enhancing sensory awareness,
correcting distorted body image and increasing a sense of self control. Torem (1987,1989,
1992) employs ego-state therapy (Watkins & Watkins, 1997) combined with other modalities
intended to establish healthy eating patterns, resolve obsession with food, and relieve body
image distortion. Because trance provides a receptive context for corrective thought,
hypnosis finds merit as a useful adjunct to cognitive behavioral therapy (Beck, 1976; Ellis,
320
Walsh
1971) for ED treatment (Vanderlinden & Vandereycken,1990; Barabasz, 2000). This array of
anecdotal success lends confidence for examining the following novel approach.
A different framework for thinking about anorexia treatment
From the foundational contributions of the above-mentioned clinicians and
investigators and from the following scenario, a new way of thinking about unconscious work
with eating disorders evolved. An ideomotor signaling technique, while lacking empirical
support, can be employed as a type of metaphoric tool that allows clients to extend their own
efficacy regarding a problem. Upon using the metaphor or process of questioning an anorexic
girl’s unconscious using ideomotor signals (Cheek, 1994: Cheek & LeCron, 1968), this author
asked if the anorexia could be fully arrested. An affirmative response led to other questions
about when and under what conditions this arrest could happen. Inquiries ultimately seemed
to reveal a group of ego-states (Watkins & Watkins, 1997) fully invested in the ED. Trusting
the ED could be arrested, ego-states were informed of a pending shutdown of AN which would
result in no functional direction for these ego-states. New functions, posited as “jobs,” were
created and presented to the ego-states. When all AN contributing ego-states accepted new
jobs, the unconscious indicated AN could be arrested. The ensuing arrest resulted in rapid
remission of AN symptoms. Refining this approach and applying it to several dozen other
clients with similar outcomes resulted in a different way of thinking about ED treatment.
The perspective guiding much of what follows recognizes how unconscious
communication can appear to alter physiological experience (Spiegel & Moore,1997; Erickson
& Rossi, 1979; Rossi, 2002; Rossi, 1988; Saadat & Kain, 2007; Stewart & Thomas, 1995; O’Hanlon
& Hexum, 1990; Butler, Symons, Henderson, Shortliffe, & Spielgel, 2005), how ideomotor signals
are physical expressions of the unconscious (Cheek,1994; Cheek & LeCron,1968), how scientific
evidence implicates genetic contribution to much of the ED symptom complex, as cited above,
and how gene expression can be influenced by factors outside the individual (Owen, Treasure
& Collier, 2001; Kas, Van Elburg, Van Engeland & Adan, 2003; Siegfried, Berry, Hao, & Avraham,
2003; Schanberg, Ingledue, Lee, Hannun, & Bartolome, 2003; Weaver, Cervoni, Champagne, et
al., 2004; Bittman et al, 2005; Oberlander, Weinberg, Papsdorf, Grunau, Misri, & Devlin, 2008;
Dusek et al, 2008). How might a relatively simple sequence of ideomotor questioning disrupt
this disease process? The factors at play within the individual during this intervention are
unknown at this time and can only be conjectured.
Client reports and behavioral and collateral observational evidence derived from
24 AN cases, display consistent results. A deep level of AN functioning seems to be accessed
and arrested through a particular sequence of therapeutic communications imagined to be
with the client’s unconscious. This approach employs both ideomotor questioning (Cheek,
1994; Rossi & Cheek, 1988) and ego-state therapy (Watkins & Watkins, 1997). Because
application of the method described below seems to nullify the driving force fueling AN
symptoms, the client’s internal struggle involving thought, perception and behavior is reduced
significantly and therapeutic change is more easily facilitated. Symptom remission most
often occurs within four treatment sessions once the process described below has begun.
The case example cited met the diagnostic criteria of the Diagnostic and Statistical
Manual for Mental Disorders (DSM IV) (American Psychiatric Association, 2000) for anorexia
nervosa and was treated at a multi-disciplinary outpatient eating disorders clinic (Kartini)
serving youth up to 22 years old. This author contracts services to the clinic as one part of
a team offering medical and pharmaceutical management, physical therapy, yoga and
individual, family and group psychotherapy.
321
Anorexia Treatment
Intervention prerequisite
Because starvation significantly affects psychobiological functioning it is essential
that the AN patient be sufficiently re-fed before attempting an intervention like the one that
follows (Keys, 1950; Meehan et al., 2006; Choma et al., 1998). Re-feeding may occur with
supervised meals at home or in a clinical setting or using nasogastric tube feeding. Most
psychotherapeutic interventions will have little or no effect until the body has adequate nutrients
to restore the pre-morbid, baseline cognitive facility. The following method is best applied after
the affected individual has achieved at least ninety percent of estimated healthy weight.
Method
Initial Assessment
Following the development of rapport, assess the client’s motivation for change,
and identify the type of change that is desired. Does the client want to continue being
controlled by the ED? Proceed with this intervention only after the client convincingly
expresses a desire to fully manage the ED or to have more choice about the ED. Be aware that
some level of ambivalence will be common for most cases.
The Rating of Eating Disorder Severity (REDS-C) interview (Goldner, 2000; O’Toole,
2000; DeSocio, O’Toole, He, Koeller, Baird, & Lukach, 2008 ) is administered by the attending
pediatrician. This is a 16 item semi-structured interview designed to assess the severity of
eating disorder symptoms in children and adolescents. An adult version of this interview
(REDS) was originally developed by Elliot Goldner (2000) at the University of British Columbia.
Older adolescents and adults were the target age group for the original REDS.
In 2000, Julie O’Toole (2000) developed a child version of the REDS, with permission
from Elliot Goldner (personal communications, 1999). The REDS-C revision involved changing
the language to make items developmentally appropriate for children and adolescents, e.g. “school”
was used instead of “work.” Summation of ratings on the 16 symptom items yields a total child
symptom score ranging from 0 to 77. Summation of the 16 interviewer confidence ratings yields
a total confidence score ranging from 0 to 64. Most often the REDS-C is done at the beginning of
clinical treatment and at a six month interval. The REDS-C has proven to be a reliable indicator of
ED severity and predictor of relapse. Information about the REDS-C functional merits has been
prepared for publication and will soon be available (DeSocio et al., 2009).
Communication and rapport with the unconscious
Body language is a commonly recognized expression of the unconscious (Segerstrile
& Molner, 1997). Communication with the unconscious is effectively facilitated by developing
a specific, mutually agreed upon body language known as ideomotor (Latin roots: ideo=
idea/thought & motor = movement) or ideodynamic signaling (Cheek,1994; Rossi & Cheek,
1988; Cheek & LeCron, 1968). Clients are instructed to avoid conscious volition and allow
the unconscious to lift one finger to signal “yes” and a different finger to signal “no.”
Inform the client that the unconscious is there to help and is communicating all the
time through body language and that such language can be responsive to verbal questioning.
Ask the client to rest hands comfortably so all fingers are free to move. Suggest client focus
on something very positive or visualize the word “YES” as the unconscious apparently
decides which finger is most appropriate to lift up as a “yes” signal, allowing all the time
necessary to develop that signal. Scan the hands for any movement and take note of distinct
movement in a particular finger as a “yes” signal. As the “yes” finger rests, ask the client to
focus on something negative or visualize the word “NO.” A different finger on that same
322
Walsh
hand will lift up to signal “no.” Of course, when doing ideomotor questioning, all questions
must be geared for a “yes” or “no” response. It is best to keep questions simple. Some
individuals will initially require added time for information and experiences demonstrating
the function of the unconscious.
Ask the client to allow her (or his) unconscious to respond to questions through
the finger signals. Request the client’s unconscious to develop a deep comfort and calm.
Await a finger response to indicate this deep calm has occurred. After comfort is acceptably
established per client affirmation establish a physical anchor for comfort (Walsh, 1997) so
the same experience can be reestablished whenever desired. One option involves asking the
clients to touch two fingers together on the non-signaling hand and then asking if the client
will access the same experience whenever desired by simply touching those two fingers
together and requesting a comfortable experience. An unconscious “yes” response means
clients now have a comfort tool.
How can the clinician trust that finger signals are really coming from the
unconscious? Rossi (1986) and Cheek (Rossi & Cheek, 1988) have outlined methods for
distinguishing unconscious signaling from conscious manipulation. Ideomotor signals
sometimes will not develop in the alert client and trance induction may better facilitate this
process. For many, some level of trance develops as ideomotor questioning begins and this
can often make the client oblivious to finger movements. This procedure requires no formal
trance induction but, also, can be applied effectively after an induction.
Emotional stabilization
Apply the Goldfinger method (Walsh, 1997; Walsh, 2005) for a temporary clearing of
the emotional past. The Goldfinger method is a brief, non-invasive approach to clearing
accumulated emotion. After the client develops ideomotor finger signals, ask the unconscious
about the presence of any interfering emotion from the past. If the emotion is present, say
“Since you have been through all the experience of the past and you have whatever learning
can serve you well in the present, will that fear (anger, guilt etc.) now be released and resolved
in whatever way is best for you at this time?” Then say “When the resolution is complete and
you are free of that fear, the yes finger will lift up as a signal.” After the release, steps are taken
to ratify cognition, perception and behavior (Walsh, 1997). The cognitive ratification asks “Is
there a place in the past where you can put the various thoughts and perceptions that are no
longer appropriate in the present now that you have released those emotional burdens?” An
affirmative response is followed by “So that adjustment can now be made and a “yes” finger
lifting will indicate the adjustment is complete.” Ratifying perception and behavior is not
essential here because it is often consequential to the treatment that follows.
It is important to review the client’s tools for managing anxiety. Make certain the
client is familiar with and practiced at tools such as deep breathing, sensory focus, self-talk,
imagery manipulation or comfort tool application. It may be necessary to teach some of
these methods to the client.
If not already addressed, resolve or disconnect from any co-occurring depression
while integrating relevant information. Describe the network of experience that defines
depression and ask the unconscious if depression is operational in current experience. If a
“yes” response is given, ask if the depression will now be resolved or temporarily disconnected
from the current issue by providing the client an awareness of whatever is most important to
understand. Solicit a finger signal to indicate the resolution is complete. It is unlikely and
improbable that all emotional issues for a client are resolved after taking these steps. It is
323
Anorexia Treatment
possible, however, that clients indicate their willingness to continue because they have
made a sufficient, temporary disconnect from the problems in question to consider them
without fear.
Using the metaphor of opening a channel of communication with the unconscious
initially provides an avenue to expediently resolve potential obstacles to change, like
depression. Conditions including post-traumatic stress disorder and dissociative identity
disorder (American Psychiatric Association, 2000) will require more time during the emotional
stabilization phase to allow for the various contingencies these conditions may require.
Any individual who is sufficiently motivated to have greater management over AN can
benefit from this method, provided the person does not have a major psychiatric illness (e.g.,
schizophrenia). Responding to the idiosyncratic priorities of each individual ultimately
leads to the intended target for most.
Assess internal ED resources
Question the unconscious to determine how many ego-states are actively engaged in the
ED. This step is derived from ego-state therapy (Watkins & Watkins, 1997). To understand egostate theory and therapy, consider how an individual’s inner reality, that navigating fund of learning,
experience, knowledge, perception, belief and inclination, is being constructed piece by piece as the
body develops from infancy to adulthood. Through the growing up years, each new experience
becomes a piece of the foundation of inner reality. Some pieces of this foundation are held by
particular resources created for this purpose. John and Helen Watkins (1997) call these resources
“ego-states,” or parts of the greater self. These ego-states contribute to a fluid and responsive
interplay of resources useful in navigating through life. Helen Watkins (1993) summarizes ego-state
therapy as a psychodynamic approach in which techniques of family or group therapy are employed
to resolve conflicts between various “ego-states” that constitute a “family of self” within the
individual. Thus, the foundation of inner reality is not only seen as a network of perception,
emotion, thought and behavior tied to experience, but also as ego-states that hold, connect, or
express experience. The experiential functional flow and communication between these ego-states
and their respective purpose determines much about how a person functions.
For purposes of this script, the terms ego-states, parts and internal parts will be
used interchangeably with the same meaning. Typically most clients grasp the concept of
“parts” a bit easier than an elaboration on ego-states. When questioning the unconscious,
the term “parts” seems to require little explanation. Inquiries of the unconscious, using this
framework, often seems to reveal how one or more ego-states are invested in AN. Ask “Are
there parts of you currently involved in the functions of the eating disorder?” A “yes” finger
lifting would then prompt “Is there more than one part involved with the ED?” Continue
questioning until the number of ego-states functioning for the ED is determined.
Pending unemployment
Pose a ruse by implying to the ED parts that, because of current treatment, the ED
will soon become fully inactive. This, of course, means inner parts will have nothing to do.
Announce that there are actually some challenging and very satisfying jobs now available
that provide a great benefit to the entire system. Ask if ED parts would like new jobs before
they are completely without any purposeful focus. Creating new jobs for ED parts is a
delightful way to address idiosyncratic needs, developmental challenges, and management
of symptoms related or unrelated to the ED. Jobs are created to support client needs, goals
or potentials and typically enhance the full course of treatment.
324
Walsh
New jobs
Assume that the unconscious, and the various parts that compose it, typically
aspire for what is perceived to be in the best interest of the entire psychobiological system.
From this perspective, it is important to recognize that any neurobiological disorder like AN
or BN activates without conscious or unconscious intention. The disease may recruit or
create ego-states to express symptoms. If it is assumed that internal parts develop to serve
some function and continue to need a purpose or functional outlet, it is necessary to define
various invented “jobs” which are intended to be compatible with and beneficial to the
client. Jobs may be set up individually or for a group of parts. Introduce jobs to parts in a
permissive manner and contract for a start time. Encourage parts to be patient with themselves
(countering perfectionistic inclinations common to the AN client) as they explore effective
ways to understand and carry out new jobs. One group of parts, for example, may do a
“focus” job which involves helping the individual focus attention and eliminate distractions
whenever the individual says “I want to focus on X (desired focus) and nothing else for the
next hour (desired length of time).” Another group may take an “information processing” job
which involves organizing and categorizing new information coming into the system in a
way that makes it easily accessible.
Job supervision
Follow up with parts in subsequent sessions to see if they have followed through
with the agreement to start a job. Ask how the new job is going and if any parts need
additional help. If more assistance is needed for a job, solicit volunteer parts to help. Again,
this can be accomplished with the metaphor of communicating with the unconscious by
means of ideomotor questioning.
Turning off the ED
When all parts previously invested in the ED have new jobs, ask the unconscious
“Is it now possible to turn off the ED?” With a “yes” response, ask “Will the ED now be
turned off?” With an affirmative response, say “ When the ED is indeed off that ‘yes’ (or
‘no’) finger will lift up.” If the ED will not be turned off upon questioning, ask if there are
other parts contributing to the ED that have not been accounted for. Is there some other
adjustment that needs to take place before the ED can be turned off? Questioning the
unconscious will usually reveal what themes need attention.
Trigger-inoculation and ED residue
Ask the unconscious if adjustments can be made to clean up the detrimental residue
resulting from the previously active ED, i.e. perceptions, behaviors, habits, attitudes,
orientation etc. Offer specific examples of these undesirable elements when making the
request. Experience has shown how even after the functional disease process has been
halted with this procedure, it can be reactivated by a particular circumstance or experience.
The following approach can be applied to offset this possibility.
While the ED remains off, ask the unconscious “ Will you now be exposed to all
known triggering experiences that could possibly activate the eating disorder, as many times
as it takes to insulate you from the effect of those triggers?” Ask the “yes” finger to lift when
that experience is complete. Conduct this desensitization exercise at least three times in
different contexts. The various contexts may, for example, be different locations, varied
social settings, or times of year. Trigger-inoculation seems to significantly diminish the
325
Anorexia Treatment
previously detrimental conditioning of triggering events. Recruiting internal parts for a job
intended to nullify the effects of known triggers, or alter the perception of triggers, presents
a useful backup strategy. There is no way to know exactly what future experiences may
trigger the ED to be turned on, but these measures may reduce the likelihood and frequency
of that happening.
Adjust to change
AN remission is a major adjustment. Predict a period of “awkwardness” as clients
adjust to new experience. Some clients need to move through grief about losing an active
ED. This adjustment naturally invites planning for the future. Reflect with clients how they
now have charge of the ED instead of the reverse situation and help clients consider how
they will orient to future possibilities.
Self-treatment
Once the ED has been turned off, clients should rehearse how to go through the same
process on their own. Review how clients can continue to use the idea of communicating with
their unconscious and take steps to turn off the ED should it be turned on again. Review all the
signs indicating the ED has been activated and rehearse steps necessary to turn it off. Provide
a handout with instructions (Box 1) and lead clients to clearly understand the necessary steps
involved in making their own self-treatment should that ever become necessary.
Box 1: Turning Off ED
If you are experiencing ED thoughts, perceptions, behaviors or inclinations to any degree,
do the following:
1. Verify your ‘yes’ and no finger signals if you are not already clear what they are. Position
the hands so the fingers are all free to move and visible to you. Ask the unconscious to lift
the ‘yes’ finger as you focus on something positive. Then ask the unconscious to lift the
‘no’ finger as you think of something negative. Patiently await finger movements which may
be a lifting or a slow, jerky movement or a vibration.
2. Tell the unconscious you want to ask it some questions and have it respond through
those fingers.
3. Ask “Is the eating disorder currently turned on?” A “yes” response then raises the
question “Are there any parts of me currently active in the ED?”
A “no” response allows you to move to #4.
A ”yes” response prompts “Did this part or parts previously have a different job?” If so, then
ask the part(s) if it would like to return to that other job now, before the ED is completely
turned off. (All parts need and want a purpose or function). If necessary, create a new job
for that part(s) that assists you in some way. Get confirmation that the part(s) is engaged
in the non-ED job through a finger signal.
4. Ask “Will the ED now be completely turned off?” With a yes response, ask for the yes or
no finger to lift up when the ED is completely off.
326
Walsh
If you get a no response, ask “Is there some other adjustment needing to happen before
ED can be turned off?” With a yes response, ask “Will that adjustment now be made?”
With a yes response, ask for a finger signal when the adjustment is complete and then
start at the beginning of #4.
Another possibility with a no response involves asking “Is there something important I
need to understand before ED can be turned off?” With a yes response, ask “Will that
information now come to conscious awareness so I can benefit from understanding it?”
With a yes response, simply await that awareness and then go to the beginning of #4.
5. Once the ED is turned off, thank the unconscious and ask if it will help insulate you
in the future from whatever trigger(s) was responsible for turning ED back on recently.
Case Example
Dara is a 19 year old binge and purge type anorexic with a history of depression, self
harm, and suicidal ideation. She had undergone a combination of inpatient and outpatient
ED treatments since the age of sixteen. Dara’s most recent hospital admission followed a
prescription medication overdose suicide attempt . Dara arrived at the hospital with orthostatic
hypotension, bradycardia, amenorrhea, intractable vomiting, and food refusal. Once
sufficiently re-fed from a pre-hospitalization weight of 116 pounds for her 67 inch frame and
medically stabilized, she left the hospital and started the day treatment unit (DTU) with major
depression, anxiety and a powerful attachment to her ED. Medications were adjusted to a
selective serotonin re-uptake inhibitor and a low dose atypical mood stabilizer while
hospitalized. I began individual treatment with Dara upon her second week in the DTU.
We focused the first two sessions on stabilizing Dara’s mood. This involved
developing ideomotor finger signals, a comfort tool, soliciting help from the unconscious to
unload or avoid the emotional burdens of the past, and resolve depression. Anxiety was
high for this client and she learned tools to manage it.
Upon questioning the unconscious, as indicated by ideomotor responses, the
following interaction developed. Fifteen parts invested in the ED were identified. Five parts
took an “information processing” job involving the organization and categorization of new
information coming into the system. While doing ideomotor questioning Dara appeared to
have developed trance, as evidenced by eye flutter and closure, a slowing of breathing, and
a smoothing out of facial muscles. Trance facilitated the application of a reality lens
intervention (Walsh, 2008) in which Dara encountered a full length mirror with two pair of eye
glasses beside it. One set of glasses had ED lenses while the other had reality lenses which
allowed Dara to see her body realistically. She liked what she saw through the reality lenses.
Five parts took the job of applying the reality lenses full time. Three parts took a “restricting”
job which “guarantees the body will never get fat” as parts limit food type and quantity to
the prescribed healthy meal plan. Two parts took a job exercising assertiveness skills.
During the next session Dara explained how eating was much easier and she had less
anxiety. The unconscious agreed to turn off the ED and a finger signal confirmed this change.
Another adjustment to keep the ED off was solicited and confirmed. The next session found
the ED turned on and one part having abandoned its new job. Upon questioning, the part
found the “reality lens” job too difficult and agreed to help with the “restricting” job. The ED
327
Anorexia Treatment
was again turned off and Dara went through a trigger inoculation exercise. The following week
Dara reported managing triggers well and seriously thinking about future occupational plans.
All parts doing new jobs reported acceptable experiences. Dara went through the triggerinoculation exercise again. Dara presented no ED thoughts and a good body image.
Seven weeks later Dara had a very distressing experience involving a close friend’s
medical condition. This seemed to activate the ED with no inner parts actively involved. The
ED was turned off and stayed off until Dara became ill with the flu, lost some weight, and
recognized ED symptoms. The ED was turned off promptly.
Dara received a handout (Box 1) for self-management of AN. Upon initial ED
hospitalization Dara scored 51 on the REDS-C interview. She received a score of zero six
months later on the same test. At twelve months, Dara was maintaining a healthy weight of
125 pounds, a body mass index (BMI) of 19.1, a good body image, having regular menses and
continuing the same course of medication she started in the hospital.
Conclusion
Relapse
In most cases, when the ED gets triggered back on it does so within a week or two
after it is initially turned off. The trigger is usually some crisis, real or perceived. Clinicians
need to question the client’s unconscious to assess the ED state and determine if any parts
are actively contributing to the ED. If there are parts invested in the ED, find out how many
and ask if any are parts that abandoned new jobs. If parts have not been dealt with before,
offer a new job. If parts abandoned their new job, find out why. Once all AN parts have nonAN jobs, the AN can usually be turned off.
Sometimes there are no parts contributing to AN when it is turned on. The
unconscious may indicate something else needs to change before AN can be turned off.
This was the case with a client who needed to resolve depression before AN could be turned
off. For this client depression was a powerful AN trigger.
Personality style and developmental orientation tend to have significant influence on
relapse frequency and even a willingness to turn off the ED. When the ED is active, clients
often say “This is who I am.” This identification with the ED typically becomes “Now I can be
the real me without the ED” after ED ego-states engage new jobs and symptoms remit.
Intrapersonal and interpersonal support
Because other clinicians treat the clients seen by this author, successful treatment outcomes
cannot be credited solely to the intervention described here. Other clinicians teach, monitor and
rehearse client coping strategies, as well as reinforce healthy changes. AN symptoms have been
shown to abate quickly with this method, but these changes often rest upon a bed of useful
information and experience derived from the day treatment unit and parental cooperation in maintaining
a safe and healthy home environment. Symptom relief needs to be supported and reinforced by
various treatment providers and families.
This method can be an important part of treatment regimen which ideally adds facility and
expediency to the rest of the process. Diminishing the symptomatic force of AN seems to take the
physiological resistance out of AN treatment. When the symptom driver is off, regardless of how it is
deactivated, much of the client’s inner struggle is pacified. The client will still need to adopt new behaviors
around food, change old habits, and adjust to a new way of operating in the world. Adjusting to the
absence of a constant, dominating companion (AN) that touches every aspect of life is significant.
328
Walsh
The premise guiding this work is an assumption that ego-states are functioning at
the expressive level of the ED and that the functional force directing these ego-states can be
muted once all ED ego-states assume a different function. Extracting ego-states from the ED
role and muting the ED force then results in remission of the ED symptom complex. The
treatment intervention targets the entire symptom complex as opposed to focusing on single
symptoms or presumed underlying causal factors.
Following the application of this intervention, the overall course of treatment
depends greatly upon client personality style, client belief system, level of motivation for
change, and family dynamics. It is a step that accelerates the course of ED treatment and
gives the client an added sense of choice and control. Client reports, objective measurements,
testing and observations from clinical sources all support AN being inactive or non-expressive
in the clients who may be said to have “turned off” the ED. Something appears to be
changing when the unconscious agrees to turn off AN. Without knowing how the
unconscious turns off the symptom complex of AN, real experiential change is taking place
which allows full client management of AN.
Questioning the unconscious
While there is as yet no empirical evidence to support the unconscious
communication by ideomotor signaling theory, it is a potentially promising area with a rich
clinical history. Ideomotor signaling is used clinically as a medium to help promote change
as shown here as, perhaps, a metaphoric vehicle for therapy. It is also hoped that it may
provide among readers an understanding of this lens for further investigation. While greater
research is desperately needed to answer some of these questions, that research may have
to wait for improved means of measuring many of these variables and the impact they have
on one another.
References
American Psychiatric Association. (2000). Diagnostic and statistical manual of mental
disorders (4th ed.). Washington, DC: Author.
Baker, E.L., & Nash, M.R. (1987). Applications of hypnosis in the treatment of anorexia
nervosa. American Journal of Clinical Hypnosis, 29(3), 185-193.
Becanu, S.A, Bulik, C.M., Klump, K.L., Fichter, M.M., Halmi, K.A., Keel, P.K., et al. (2005).
Linkage analysis of anorexia and bulimia nervosa cohorts using selected behavioral
phenotypes as quantitative traits or covariates. American Journal of Medical
Genetics Part B: Neuropsychiatric Genetics, 139, 61-68.
Barbarasz, M. (2000). Hypnosis in the treatment of eating disorders. In L.M. Hornyak & J.P.
Green, Healing from within: The use of hypnosis in women’s health. Washington,
D.C.: American Psychological Association.
Beck,A.T. (1976). Cognitive Therapy and the Emotional Disorders. New York: Penguin Books.
Bergen, A., Van Den Bree, M., Yeager, M., Welch, R., Ganjei, K., Haque, K., Bacanu, S., et al.
(2003). Candidate genes for anorexia nervosa in the 1p33-36 linkage region: serotonin
1D and delta opioid receptors display significant association to anorexia nervosa.
Molecular Psychiatry, 8 (4), 397-406.
Bittman, B., Berk, L., Shannon, M., Westengard, J., Guegler, K.J. & Ruff, D. (2005). Recreational
music-making modulates the human stress response: A preliminary individualized
gene expression strategy. Medical Science Monitor, 11 (2), 31-40.
329
Anorexia Treatment
Bulik, C.M., Sullivan, P.F., Tozzi, F., Furberg, H., Lichtenstein, P., & Pederden, N.L. (2006),
Prevalence, heritability, and prospective risk factors for anorexia nervosa. Archives
of General. Psychiatry, 63, 305-312.
Bulik, C.M., Hebebrand, J., Keski-Rahkonen, A., Klump, K.L., Reichborn-Kjennerud, T.,
Mazzeo, S.E., & Wade, T.D. (2007). Genetic epidemiology, endophenotypes and
eating disorder classification. International Journal of Eating Disorders. 40(sup): s52-60.
Cheek, David B. (1994). Hypnosis: The Application of Ideomotor Techniques. Needham
Heights, Massachusetts: Allyn & Bacon.
Bulik, C.M., Sullivan, P.F., & Kendler, K.S. (1998). Heritability of binge-eating and broadlydefined bulimia nervosa. Biological Psychiatry, 44, 1210-1218.
Butler, L.D., Symons, B.K., Henderson, S.L., Shortliffe, L.D., & Spielgel, D. (2005). Hypnosis
reduces distress and duration of an invasive medical procedure for children.
Pediatrics, 115(1).
Cheek, D., & LeCron, L. (1968). Clinical Hypnotherapy. New York: Grune and Stratton.
Cheek, D. (1994). Hypnosis: The Application of Ideomotor Techniques. Boston: Allyn and Bacon.
Choma, C. W., Sforzo, G. A., Keller, B. A. (1998). Impact of rapid weight loss on cognitive
function in collegiate wrestlers. Medicine & Science in Sports & Exercise, 30(5), 746-749.
Comani, G.J. (1992). Hypnosis in the treatment of bulimia: a review of the literature. Australian
Journal of Clinical and Experimental Hypnosis, 20, 89-104.
Covino, N.A., Jimerson, D.C., Wolfe, B.E., Franko, D.L., Frankel, F.H. (1994). Hypnotizability,
dissociation and bulimia nervosa. Journal of Abnormal Psychology, 103, 455-459.
Crasilneck, H., Hall, J. (1975). Clinical Hypnosis. New York: Grune and Stratton
DeSocio, J.E., O’Toole, J.K., He, H., Koeller, P., Baird, S.A., & Lukach, M. (2008). The REDSC Rating of Eating Disordered Severity Interview for Children and Adolescents:
Clinical Usefulness and Comparison with the Modified EDI-2. Manuscript
submitted for publication.
Devlin, B., Bacanu, S-A., Klump, K.L., Berrettini, W., Bergen, A., Goldman, D., et al. (2002).
Linkage analysis of anorexia nervosa incorporating behavioral covariates. Human
Molecular Genetics, 11, 689-696.
Dusek, J., Hasan, H., Wohlhueter, A., Bhasin, M., Zerbini, L., Joseph, M., Benson, H., &
Libermann, T. (2008). Genomic counter-stress changes induced by by the relaxation
response. PLoS ONE, 3(7): e2576.
Edgette, John & Janet S. (1995). The handbook of hypnotic phenomena in psychotherapy.
New York: Brunner/Mazel.
Ellis,A. (1971). Growth Through Reason: Verbatim Cases in Rational-Emotive
Psychotherapy. Palo Alto: Science and Behavioral Books.
Erickson, M.H., & Rossi, E.L. (1979). Hypnotherapy: An Exploratory Casebook, New York:
Irvington.
Frieling, H., Bleich, S., Otten, J., Romer, K.D., Kormhuver, J., de Zwaan, M., Jacoby, G.E., et al.,
(2008). Epigenetic downregulation of atrial natriuretic peptide but not vasopressin
mRNA expression in females with eating disorders is related to impusivity.
Neuropharmacology, 2, January: advance online: doi:10.1038/sj.npp.1301662.
Frieling, H., Gozner, A., Romer, K.D., Lenz, B., Bonsch, D., Wihelm, J., Hillemacher, T., et al.
(2007). Global DNA hypomethylation and DNA hypermethylation of the alpha
synuclein promoter in females with anorexia nervosa. Molecular Psychiatry, 12, 229-230.
Goldner, E.M. (2000). The REDS rating of eating disorder severity. Unpublished instrument
and administration guidelines. Vancouver, British Columbia, Canada: Simon Fraser University.
330
Walsh
Grice, D.E., Halmi, K.A., Fichter, M.M., Strober, M., Woodside, D.B., Treasure, J.T., Kaplan,
A.S., et al. (2002), Evidence for a susceptibility gene for anorexia nervosa on
chromosome 1. American Journal of Human Genetics, 70 (3), 787-792.
Griffith, R.A. (1989). Hypnobehavioral treatment for bulimia nervosa: Preliminary findings.
Australian Journal of Clinical and Experimental Hypnosis, 17, 79-87.
Gross, M. (1984). Hypnosis in the therapy of anorexia nervosa. American Journal of
Clinical Hypnosis, 26, 175-181.
Gunstad,J., Schofield, P., Paul, R.H., Spitznagel, M.B., Cohen, R.A., Williams, L.M., Kohn,
M., Gordon, E. (2006). BDNF Val66Met polymorphism is associated with body
mass index in healthy adults. Neuropsychobiology, 53 (3), 153-156.
Hornyak, L.M. (1996). Hypnosis in the treatment of anorexia nervosa. In S.J. Lynn, I.
Kirsch, J.W. Rhue (Eds.), Casebook of Clinical Hypnosis (51-73), Washington,
D.C.: American Psychological Association.
Janet, P. (1925). Psychological Healing (Vol. 2). New York: Macmillan.
Javaras, K.N., Laird, N.M., Reichborn-Kjennerud, T., Bulik, C.M., Pope, H.G.J., Hudson, J.I.
(2008). Familiarity and heritability of binge eating disorder: Results of a case-control
family study and a twin study. International Journal of Eating Disorders, 41, 174-179.
Kaplan, A. (2004). Exploring the gene-environment nexus in anorexia, bulimia. Psychiatric
Times, 21 (9).
Kartini Clinic for Disordered Eating: Portland, Oregon.
Kas, M.J., VanElburg, A.A., VanEngeland, H. & Adan, R.H. (2003). Refinement of behavioral
traits in animals for the genetic dissection of eating disorders. European Journal
of Pharmacology, 480, 13-20.
Kendler, K.S., MacLean, C. Heale, M.C., Kessler, R.C., Heath, A.C., Eaves, L.J. (1991). The genetic
epidemiology of bulimia nervosa. American Journal of Psychiatry, 148, 1627-1635.
Keys, A. (1950). The biology of human starvation. Minneapolis, MN: University of
Minnesota Press.
Klump, K.L., Bulik, C.M., Kaye, W.H., Treasure, J., Tyson, E. (2009). Academy for eating
disorders position paper: Eating disorders are serious mental illnesses. International
Journal of Eating Disorders, 42(2), 97-103.
Klump, K.L., Culbert, K.M. (2007). Molecular genetic studies of eating disorders: Current
status and future directions. Current Directions Psychological Science, 16, 37-41.
Klump, K.L., Miller, K.B., Keel, P.K., McGue, M., Iacono, W.G. (2001). Genetic and
environmental influences on anorexia nervosa syndromes in a population-based
twin sample. Psychological Medicine, 31, 737-740.
Kroger, W.S., Fezler, W.D. (1976). Hypnosis and Behavior Modification Imagery
Conditioning. Philadelphia: Lippicott.
Lynn, S.J., Rhue, J.W., Kvarl, S., Mare, C. (1993). The treatment of anorexia nervosa: A
suggestive framework. Contemporary Hypnosis, 10(2), 73-80.
Meehan, K.G., Loeb, K.L., Roberto, C.A. & Attia, E. (2006). Mood change during weight
restoration in patients with anorexia nervosa. International Journal of Eating
Disorders, 39(7), 587-589.
Mercader, J. M., Ribasés, M., Gratacós, M., González, J.R., Bayés, M., de Cid, R., Badía, A.,
Fernández-Aranda,F., Estivill, X. (2007). Altered BDNF blood levels and gene
variability are associated to anorexia and bulimia. Genes, Brain and Behavior,6(8), 706-716.
331
Anorexia Treatment
Oberlander T.F. , Weinberg J., Papsdorf M., Grunau R, Misri S., & Devlin A.M. (2008).
Prenatal exposure to maternal depression, neonatal methylation of human
glucocorticoid receptor gene (NR3C1) and infant cortisol stress responses.
Epigenetics, 3 (2), 1-9.
O’Hanlon, W.H., & Hexum, A.L. (1990). An Uncommon Casebook: The Complete Clinical
Work of Milton H. Erickson. New York: W.W. Norton & Company.
O’Toole, J.K. (2000). The REDS-C rating of eating disorder severity interview for children.
Unpublished instrument and administration guidelines. Portland, Oregon: The Kartini Clinic.
Owen,J.B., Treasure, J.,& Collier, D.A. (2001). Animal Models- Disorders of Eating Behavior
and Body Composition. New York: Springer.
Pettinati, H.M., Horne, R.J. & Staats, J.M. (1985). Hypnotisability in patients with anorexia
nervosa and bulimia. Archives General Psychiatry, 42, 1014-1016.
Pettinati, H.M., Kogan. L.G., Margolis, C., Shrier, L., & Wade, J.H. (1989). Hypnosis,
hypnotisability, and the bulimic patients. In L.M. Hornyak & E.N. Baker (Eds),
Experiential Therapies for Eating Disorders. NY: Guilford Press.
Reichborn-Kjennerud, T., Bulik, C.M., Tambs, K., & Harris, J.R. (2004). Genetic and
environmental influences on Binge eating in the absence of compensatory behaviors:
A population-based twin study. International Journal of Eating Disorders, 36,
307-314.
Ribasés, M., Gratacòs, M., Fernández-Aranda, F., Bellodi, L., Boni, C., Anderluh, M.,
Cavallini, M.C., et al. (2004), Association of BDNF with anorexia, bulimia and age of onset
of weight loss in six European populations. Human Molecular Genetics, 13 (12), 1205-1212.
Ribasés, M., Gratacòs, M., Fernández-Aranda, F., Bellodi, L., Boni, C., Anderluh, M., Cavallini,
et at. (2005). Association of BDNF with restricting anorexia nervosa and minimum
body mass index: a family-based association study of eight European populations.
European Journal of Human Genetics, 13, 428–434.
Ribases, M., Gratacos, M., Armengol, L., de Cid, R.; Badia, A., Jimenez, L., Solano, R., et al.
(2003). Met66 in the brain-derived neurotrophic factor (BDNF) precursor is associated
with anorexia nervosa restrictive type. Molecular Psychiatry, 8, 745-751.
Rossi, E.L. (1986). The Psychobiology of Mind-Body Healing. New York: W.W. Norton.
Rossi, E.L., & Cheek, D.B. (1988). Mind-body therapy: Ideodynamic healing in hypnosis.
New York: W.W. Norton & Co.
Rotenberg, K.J., Taylor, D., & Davis, R. (2004). Selective mood-induced body image
disparagement and enhancement effects: Are they due to cognitive priming or
subjective mood? International Journal of Eating Disorders, 35 (3), 317 - 332.
Saadat, H., & Kain, Z.N. (2007). Hypnosis as a therapeutic tool in pediatrics. Pediatrics 120 (1), 179-181.
Sanders, S. (1986). The perceptual alteration scale: A scale measuring dissociation. America
Journal of Clinical Hypnosis, 29, 95-102.
Schanberg, S. M., Ingledue, V. F., Lee, J. Y., Hannun, Y. A., & Bartolome, J. V. (2003). PKC
Mediates Maternal Touch Regulation of Growth-Related Gene Expression in Infant
Rats. Neuropsychopharmacology. 28, 1026-1030.
Segerstrile, U., & Molner, P. (1997) Eds. Nonverbal Communication: Where Nature Meets
Culture. Mahwah, New Jersey: Lawrence Erlbaum Associates, Publishers.
Siegfried, Z., Berry, E.M., Hao, S. & Avraham, Y. (2003). Animal models in the investigation
of anorexia. Physiology and Behavior, 29, 39-45.
Spiegel, D., & Moore, R. (1997). Imagery and hypnosis in the treatment of cancer patients.
Oncology (Williston Park), 11, 1179-1189.
332
Walsh
Stein, M.K. (2007). New Directions and Challenges Ahead for Eating Disorders. Eating
Disorders Review, 18(4)
Steiger, H., Guavin, L., Joober, R., Israel, M., YingKin, M.K.Ng., Bruce, K.R., Richardson, J.,
Young, S.N., et al. (2006). Intrafamilial correspondences on platelet[H-] paroxetinebinding indices in bulimic probands and their unaffected first-degree relatives.
Neurophychopharmacology, 31, 1785-1792.
Stewart, A.C., & Thomas, S.E., (1995). Hypnotherapy as a treatment for atopic dermatitis in
adults and children. British Journal Dermatology, 132, 778-783.
Thakur, E. (1983). Treatment of anorexia nervosa with hypnotherapy. In H. Wain (Ed.),
Clinical Hypnosis in Medicine (446-493). Chicago: Yearbook.
Theissen, E. (1983). Using fairy tales during hypnotherapy in bulimia and other psychological
problems. Medical Hypnoanalysis, 4, 139-144.
Torem, M.S. (1986). Dissociative states presenting as an eating disorder. American Journal
of Clinical Hypnosis, 29, 137- 142.
Torem, M.S. (1987). Ego-state therapy for eating disorders. American Journal of Clinical
Hypnosis, 30, 94-103.
Torem, M.S. (1989). Ego-state hypnotherapy for dissociative eating disorders. Hypnos, 16, 52-63.
Torem, M.S. (1992). The use of hypnosis with eating disorders. Psychiatric Medicine, 10, 105-117.
Vanderlinden, J., & Vandereycken, W. (1988). The use of hypnotherapy in the treatment of
eating disorders. International Journal of Eating Disorders, 7, 673-679.
Vanderlinden, J., & Vandereycken, W. (1990). The use of hypnosis in the treatment of bulimia
nervosa. International Journal of Clinical and Experimental Hypnosis, 38, 101-111.
Valdiserri, S., & Kihlstrom, J.F. (1995a). Abnormal eating and dissociative experiences.
International Journal of Eating Disorders, 17(4), 373-380.
Valdiserri, S., & Kihlstrom, J.F. (1995b). Abnormal eating and dissociative experiences: A
further study of college women. International Journal of Eating Disorders, 18(2), 145-150.
Wade, T.D., Bulik, C.M., Neale, M., Kendler, K.S. (2000). Anorexia nervosa and major
depression: Shared genetic and environmental risk factors. American Journal of
Psychiatry, 157, 469-471.
Walsh, B.J. (1997). Goldfinger: A framework for resolving affect using ideomotor questioning.
American Journal of Clinical Hypnosis, 40(1), 349-359.
Walsh, B.J. (2005). Utilization Sobriety: A Substance Abuse Solution. Portland, Oregon:
Peaceful Pilgrim Press: 125-144.
Walsh, B.J. (2008). Hypnotic alteration of body image in the eating disordered. American
Journal of Clinical Hypnosis 50(4), 301-310.
Watkins, H.H. (1993). Ego-state therapy: An overview. American Journal of Clinical
Hypnosis, 35(4), 232-240.
Watkins, J. G.., & Watkins, H.H. (1997). Ego states: Theory and therapy. New York: W.W. Norton & Co.
Weaver, I.C.G., Cervoni, N.,, Champagne, F.A., Alessio, A.C.D., Sharma, S., Seckl, J.R., Dymov,
S., Szyf, M., & Meaney, M.J. (2004). Epigenetic programming by maternal behavior.
Nature Neuroscience, 7, 847 - 854.
Xu, B., Goulding, E.H., Zang, K., Cepoi, D., Cone, R.D., Jones, K.R., Tecott, L.H., & Reichardt,
L.F. (2003). Brain-derived neurotophic factor regulates energy balance downstream
of melanocortin-4 receptor. Nature Neuroscience, 6, 736-742.
Yapko, M.D. (1986). Hypnotic and strategic interventions in the treatment of anorexia
nervosa. American Journal of Clinical Hypnosis, 28, 224-232.
333