47
Bethesda, Maryland | September 19-21, 2013
SD 1.8; 70%mBMI SD 5) were randomly assigned to refeeding: 500kcal/
day (control group) or 1200kcal/ day (treatment group). Energy intake was
controlled by a meal plan which ensured similar macronutrient consumption
in both arms.
Results
A mean weight gain in the treatment group of 1.04kg
(1.0
SD) was greater than controls of 0.51kg (0.6SD) (95% CI 0.19, 1.57;
p=0.04). Hypophosphatemia was more common in the treatment group
(6/18)
than in control (1/18) (Odds Ratio 6.5, 95%CI 1.2, 100; p=0.04).
Heart rate and QTc dispersion improved equally in both refeeding groups.
Prior to refeeding 3 participants (2 control, 1 treatment) had QTc interval
prolongation (>440ms), after refeeding QTc prolongation resolved in 2
participants but worsened in 1, which was in the control group. Energy
intake or carbohydrate intake was not correlated with the nadir in
phosphate. However, the nadir of phosphate correlated with white blood
cell count (R
2
0.33,
CI 95% [0.6, 1.1], p = 0.004).
Conclusion
Refeeding
at 1200kcal elicits a greater weight gain but was associated with a higher
prevalence of hypophosphatemia, however refeeding hypophosphatemia
was not associated with energy intake but was associated with low white
blood cell count (<4.5 10
9
/
L). Nasogastric tube feeding did not increase
the incidence of hypophosphatemia. Future research may help to define
whether white blood counts may be a useful predictor of refeeding
hypophosphatemia.
F46
Predictors of Rapid Relapse in Bulimia Nervosa
Marion P Olmsted
1,2
,
Danielle MacDonald
3
,
Traci McFarlane
1,2
,
Kathryn
Trottier
1,2
,
Patricia Colton
1,2
1
Toronto General Hospital, Toronto, ON, Canada,
2
University of Toronto,
Toronto, ON, Canada,
3
Ryerson University, Toronto, ON, Canada
Relapse remains a significant problem following intensive day hospital
(
DH) treatment, with some patients relapsing within the first few months.
The purpose of the study was to identify predictors of relapse within the
first 6 months following DH treatment. The 86 participants were bingeing
or vomiting at least 8 times per month before DH and had a maximum of 2
episodes per month in the last month of DH and in the first month after DH.
Rapid relapse was defined as a mean of 8 or more episodes per month
for 3 months starting within 6 months of DH discharge. The rate of rapid
relapse was 27%. Stepwise Cox regression identified frequency of binge
episodes and body avoidance before treatment and slow response to DH
as predictors of relapse (X
2
= 19.43, df= 3, p <.0001). These 3 variables
accounted for 21% of the variance in rapid relapse. Tested variables
measured at the end of treatment were not significantly associated with
relapse. Although not included as a predictor, increase in BMI during DH
was significantly higher in patients who later relapsed (p <.02). Other
features such as depression and weight based self-esteem were not
significant predictors. Patients who relapsed soon after DH were more
symptomatic and engaged in less body avoidance before treatment, were
slow responders to treatment and gained more weight during DH. This
suggests that entrenchment in the illness including an intolerance of weight
gain augured a laboured and transient response to DH treatment.
F47
Toward an Integrative Model of Child and Adolescent Risk for Bulimic
Behaviors
Carolyn M Pearson, Elizabeth Riley, Heather A Davis, Gregory T Smith
University of Kentucky, Lexington, KY, USA
Considerable evidence has emerged indicating that early engagement
in bulimic behaviors, as well as risk for future disorders, results from
the emergence, across development, of multiple, mutually influencing
processes. Foe example: When children experience high levels of negative
affect, they are at increased risk for loss of control eating (Tanofsky-Kraff
et al., 2011). Individual differences in children’s likelihood of experiencing
negative affect predict subsequent depressive symptoms, which in turn
predict childhood loss of control binge eating (Pearson et al., 2013).
In addition, childhood elevations in negative urgency predict formation
of high-risk eating expectancies, which in turn predict childhood binge
eating (Pearson et al., 2012). Dieting behavior is common in children and
also predicts bulimic behaviors (Field et al., 1999). These personality
and behavioral processes operate in tandem with environmental factors,
including both maternal and societal modeling of the pursuit of thinness
and of eating when distressed (MacBrayer et al., 2001; Stice et al., 2002).
These risk factors transact with each other to increase responsiveness to
the genetic risk that emerges over the course of pubertal onset (Klump
et al., 2003). The result is a developmental cascade of risk (Masten &
Cicchetti, 2010): the cumulative consequences of the operations of the
various risk factors alter children’s developmental trajectories toward
increased engagement in bulimic behaviors.
F48
Examination of a Modified Dual Pathway Model of Disordered Eating
in Youth With Type 1 Diabetes
Claire Peterson
1
,
Deborah Young-Hyman
2
,
Sarah Fischer
3
1
University of Georgia, Athens, GA, USA,
2
Georgia Regents University,
Augusta, GA, USA,
3
George Mason University, Fairfax, VA, USA
Disordered eating behavior (DEB) may be more prevalent in adolescents
with type 1 diabetes (T1D) than their non-diabetic peers. However, current
risk models of DEB were tested in non-diabetic populations. Given that
youth with T1D the risk for health complications in this population, it is
important to consider variables that distinguish DEB from normative
eating behavior in the context of a diabetic care regimen. The current
study tests hypotheses from an integrated psychosocial and disease-
based model of risk for DEB in a sample of 101 diabetic youth (58 newly
diagnosed with T1D, and 43 transitioning to an insulin pump regimen)
ages 13-17. Participants completed the EDI-III, the Child Depression
Inventory, the Youth Risk Behavior Survey, and the Diabetes Treatment
and Satiety Scale (DTSS). Results revealed that for the entire sample
(
n=101), body image dissatisfaction (β=.35, p<.01), dietary restraint
(
β=.18, p<.05), and depression (β=.38, p<.01) accounted for significant
variance in DEB. In addition, the interaction between depression and body
image dissatisfaction (higher depressive symptoms, higher body image
dissatisfaction) explained unique variance in DEB (β=.40, p<.01). Finally,
we examined a model with pump transitioning adolescents (n=43) Results
indicated a significant interaction between depression and DTSS (higher
depression, higher hunger and satiety dysregulation) in predicting DEB (
β=1.82, p<.01). Results indicate that hunger and satiety dysregulation are
important in terms of explaining DEB in youth with T1D. Future studies
should assess hunger and satiety dysregulation in the context of DEB to
avoid overpathologizing this population.
F49
Binge Eating in Outpatients With Major Depressive Disorder
Lena C. Quilty
1,2
,
R. Michael Bagby
2,1
1
Centre for Addiction and Mental Health, Toronto, ON, Canada,
2
University
of Toronto, Toronto, ON, Canada
Introduction
:
Depressive difficulties are highly prevalent in clinical
settings; treatment response is invariably diminished in the presence of
co-occurring symptoms such as uncontrolled or excessive food intake.
The current investigation evaluated the association between binge eating
symptoms and depressive symptoms and cognitions in a treatment-
seeking sample.
Methods
:
A total of 104 participants (49 men, 55 women)
with a primary diagnosis of major depressive disorder were randomized to
receive 16 weeks of protocolized cognitive behavioural therapy (
n
=54) or
pharmacotherapy delivered according to CANMAT guidelines (
n
=50). Binge
eating symptoms were determined by the
Structured Clinical Interview
for DSM-IV, Axis I Disorders
.
Depression was assessed by the
Beck
Depression Inventory-II
and
Hamilton Depression Rating Scale
.
Cognition
was assessed by the
Automatic Thoughts Questionnaire, Dysfunctional
Attitudes Scale, Cognitive Errors Questionnaire,
and
Depression Change
Expectancy Scale
.
Results
:
Binge eating symptoms, uncontrolled eating
in particular, were both concurrently and longitudinally associated with
depression severity as well as several measures of cognition, including
negative automatic thoughts and expectancies.
Conclusions
:
Pre-
treatment binge eating symptoms demonstrated prognostic utility in
outpatient treatment for depression, not only in treatment outcome but also
in important therapeutic targets for cognitive behavioural therapy.
F50
Ethnic Identity and Thin-Ideal Media Endorsement in Female
Undergraduates
Liya M Rakhkovskaya
1
,
Cortney S Warren
2
1
University of Nevada, Las Vegas, Las Vegas, NV, USA,
2
University of
Nevada, Las Vegas, Las Vegas, NV, USA
Introduction:
Emerging research suggests that ethnic identity is negatively
correlated with eating pathology in US ethnic minority groups. However,
research examining the relationships between ethnic identity, sociocultural
attitudes towards appearance perpetuated by the media, and eating
pathology is sparse. Consequently, this study examined these relationships
in a sample of US college women.
Methods:
European American, African
American, Latina, and Asian American college women completed self-
report measures online. We examined mean levels of ethnic identity
and media endorsement by ethnic group; correlations between these
constructs; and whether ethnic identity influenced the strength of the
relationship between thin-ideal internalization and eating pathology.
Results
:
African Americans scored lowest on thin- and athletic-ideal media
endorsement, whereas European Americans scored lowest on ethnic
identity and highest on eating pathology. Regression analyses indicated
that thin-ideal internalization, ethnicity and BMI were unique predictors of
eating pathology. However, the relationship between media endorsement
and eating pathology was stronger for women with lower ethnic identity,
independent of participant ethnicity.
Conclusions
:
Ethnic identity may act
as a protective factor by moderating the relationship between thin-ideal
media internalization and eating pathology.
POSTER SESSION 2 ABSTRACTS
