STATE OF THE ART

PHARMACOLOGICAL INTERVENTION IN BINGE EATING DISORDER.

A NARRATIVE REVIEW

IULIA CÃLUGÃR1, ROXANA ªIPOª2*, ELENA PREDESCU2

1
Clinical Emergency Hospital for Children, Child and Adolescent Psychiatry Clinic, Cluj Napoca, Romania
2
Department of Neuroscience, Discipline of Psychiatry and Pediatric Psychiatry,” Iuliu Hatieganu” University
of Medicine and Pharmacy Cluj-Napoca, Romania and Clinical Emergency Hospital for Children, Child and
Adolescent Psychiatry Clinic, Cluj-Napoca, Romania

*Corresponding author email: sipos.roxana@umfcluj.ro

ABSTRACT
Binge eating disorder (BED) represents a common but problematic psychiatric condition. With
Lisdexamfetamine being the only approved drug for treatment, the current narrative review aims
to provide an update on more recent data regarding the pharmacological treatment of BED. The
primary focus of this review is represented by randomized clinical trials testing different drug
agents from diverse pharmacological classes. Drugs that potentiate noradrenergic and dopaminergic
transmission have a proven efficacy in the treatment of BED, while other mechanism of action such
as the opioid blockade have no or poor results. The ideal pharmacological intervention should take
into consideration the treatment of the psychopathological aspects of the disorder. The goals include
reducing impulsivity and compulsivity of the eating habits, improvement of the cognitive control,
as well as long-term, sustained weight-loss. The development of novel, effective pharmacological
therapy for BED will enable physicians to provide better care with a consequential significant
improvement of patients’ quality of life.
Keywords: schizophrenia, antipsychotics, cognitive symptoms, bipolar disorder, resistant
depression.

INTRODUCTION Findings of a recent systematic review

Binge-eating disorder (BED) was intro-
duced as a disease in the fourth edition of
the Diagnostic and statistical manual of
mental disorders (DSM-IV), being listed
as a distinct disease only in DSM-5. BED is
defined as recurrent episodes of consuming
large amounts of food in a relatively short
amount of time, accompanied by a lack of
control. These episodes are accompanied by
either rapidly eating, uncomfortable feelings
of fullness, eating large amounts when not
physically hungry or feelings of embarrass-
ment or guilt regarding their eating habits.
They are most frequently triggered by neg-
ative affect and are most likely happening
without anyone noticing [1, 2].
of the epidemiology of BED state its global
prevalence at 0,9% with a higher prevalence
for women – 1,4% than for men – 0,4% [3].
Furthermore, existing evidence has indicated
a rate of prevalence ranging from 1% to 5%
for adolescents. In particular, adolescent girls
showed a higher risk of BED than adolescent
boys, 1%-4% in comparison to 0%-1,2% [4].
Furthermore, BED represents the most com-
mon eating disorder subtype among youths,
although with transient forms for the adoles-
cent age group [5].
Classification and clinical characteris-
tics of binge eating disorder
The American Psychiatric Association
has defined the key diagnostic symptoms

26 Romanian Journal of Child and Adolescent Psychiatry

 Pharmacological intervention in Binge Eating Disorder. A narrative review
of BED under five criteria. The clinical fea-
tures consist in recurrent episodes with dif-
ferent levels of severity (at least once a week
for three months) of binge eating character-
ized by eating large amount of food in a dis-
crete amount of time associated with a lack
of controls [1]. The eleventh revision of the
International Classification of Diseases (ICD-
11) which was put into effect in 2022, has
proposed new guidelines in terms of feeding
and eating disorders diagnosis. Compared to
ICD-10, ICD-11’s new guidelines have been
indicated to outperform ICD-10 in distin-
guishing cases of eating disorders. Moreover,
the addition of the new category of BED has
been shown to improve diagnostic accuracy
and clinical utility [6]. As for the difference
between DSM-5 and ICD-11 in regards to the
diagnosis of BED, ICD-11 guideline scheme is
not as over-inclusive as the one from DSM-5
and it appears to identify less subthreshold
other or unspecified diagnosis [7].
Pathophysiology of binge eating
disorder
Multiple factors are involved in the devel-
opment of BE episodes such as enhanced
food craving, impulsivity and poor decision
making skills [8, 9], dietary restraint [10, 11],
negative affect and limited skills regarding
emotional regulation [12, 13], low self-es-
teem [14] and the interaction between pos-
itive, negative and permissive beliefs about
food and eating [15]. On a neurobiological
level, the most notable neurotransmitter
pathways involved in the pathophysiology
of eating disorders are the dopaminergic and
endogenous opioid pathways which are dys-
regulated in BED. Dopamine circuits play an
important role in overeating and food intake
which is mainly mediated by the mesocor-
ticolimbic circuits involved in motivated
behavior. This mesolimbic circuit involves
the dopamine neurons located in the ventral
tegmental area that send projections to the
ventral striatum which is related to cravings
Volume 9, Issues 1-2, January-June, 2021
[16-18]. Several genetic polymorphism have
been studied in association with BED such
as polymorphisms of the D2 [19-20], D3 and
D4 receptor genes, as well as other polymor-
phisms in the dopamine transporter genes
and COMT genes [21-24]. Furthermore, the
association between BED and dysregulated
dopamine circuits activity is supported by
several PET and fMRI studies [25-28] which
indicate altered measures of dopamine func-
tion in BED subjects. However, studies reveal
contradictory evidence regarding the hyper-
dopaminergic and hypodopaminergic states
associated with binge eating. It is however
possible that these states coexist at different
stages of binge eating or in different indi-
vidual genotypes [29]. The opioid system is
associated with appetite control and food-re-
lated stimuli processing via mu opioid
receptors from the ventral tegmental area.
Agonists of these receptors have been indi-
cated to increase the intake of high-energy
and high-sugar foods [30], while antagonists
reduce said intake [31]. Furthermore, these
pathways are interconnected, with inhibition
of opioid receptor possibly decreasing dopa-
mine release by disinhibiting GABAergic
interneurons from the ventral tegmental
area [32]. Serotonin function has also been
revealed as being dysregulated in BED. The
serotonin reuptake transporter (SERT) has
shown increased levels, binding in the pari-
eto occipital cortical regions in BED, with
associated decreased levels of ATP-binding
cassette (ABC) transporters and decreased
levels of SERT in the inferior temporal gyrus
and lateral orbitofrontal cortex [33].
Psychological interventions in binge
eating disorder
According to the NICE guidelines for eat-
ing disorders, psychotherapy is the first-line
treatment option for binge-eating disorder.
The target of psychological interventions in
binge are not aimed however at weight loss
and have a limited effect on body weight [34].
27
 CÃLUGÃR et al.
In cases where guided self-help is inef-
fective or contraindicated, cognitive behav-
ioral therapy (CBT) is recommended. CBT is
one of the most well-studied and effective
psychological interventions, focusing on
breaking the diet-binge pattern as well as
on the dysfunctional relationship between
self-esteem and body shape. Evidence sup-
port long term effects with diminished fre-
quency of BE episodes, normalization of eat-
ing patterns and improvement of negative
affect and impulsivity [35, 36]. However,
guided self-help CBT (CBTgsh) has proven
to be effective and low cost, being an appro-
priate intervention for uncomplicated BED,
but remains a slower-acting alternative com-
pared to face-to-face sessions of CBT [37].
Dialectic-Behavioral Therapy (DBT) repre-
sents another psychological intervention that
has been proven useful in the management of
BED. DBT can also be efficient when used as
a self-help option [38]. This kind of therapy
is based on emotion regulation and stress tol-
erance with positive results regarding food
and body shape concerns. However, it has
limited efficacy regarding weight loss, neg-
ative affect, or anxiety [39, 40]. Considering
the relationship between eating disor-
ders and poor interpersonal functioning,
Interpersonal Psychotherapy (IPT) focuses
on restructuring dysfunctional relational pat-
terns that trigger negative affect which in
turn determine eating impulsiveness [41, 42].
Other than being a cost-effective option, its
outcomes are stable and maintained in the
long term [43]. Having in mind that most
individual with BED have a higher body
mass index than the general population,
Behavioral Weight Loss (BWL) therapy can
be a potential alternative to specialist BED
treatment options. BWL focuses on reduc-
ing the caloric intake and increasing physical
activity. However, the results regarding the
impact on the frequency of BE episodes are
inconsistent, with both IPT and CBT being
superior management options for BED [44].
28
Alternative interventions in binge
eating disorder
Basic Body Awareness Therapy is a psy-
chomotor physiotherapy which has reported
positive results in regards to eating disorders
[45-47]. It addresses body image directly by
enhancing body awareness and quality of
movement. Existent studies on BBAT and
BED indicate possible positive outcomes
[48,49] but further research is needed in order
to establish its effectiveness in BED . Also, the
use of virtual reality has been proven to be a
promising therapeutic tool for patients who
suffer from eating disorders [50].
Deep Brain Stimulation (DBS), known to
influence the neuronal network by intracra-
nial electrode stimulation, is a well-tolerated
therapeutical option in Parkinson’s Disease
[51] with several studies indicating its appli-
cability in other diseases such as Tourette’s
syndrome [52], epilepsy [53], depression [54],
obesity and eating disorders [55-57]. DBS tar-
gets nucleus accumbens, a structure involved
in reward-seeking behavior, regulating the
dopamine levels. Further investigations into
the suitability of DBS in human subjects is
needed. However, preclinical studies on ani-
mal models indicate that DBS might become
a promising therapeutical alternative in the
management of BED and other eating disor-
ders [58-60].
Pharmacological treatment in binge
eating disorder
Lisdexamfetamine (LDX) is the only
approved drug in the treatment of BED. LDX
is a d-amphetamine prodrug that acts as a
competitive substrate for the dopamine and
noradrenaline reuptake transporters, caus-
ing a rapid surge of synaptic dopamine and
noradrenaline thus potentiating mesolimbic
dopaminergic neurotransmission [61, 62].
Findings of a 11-week, placebo-controlled
trial have illustrated the effect LDX exerts on
eating impulsiveness. Administration of 50
and 70 mg/day of LDX reduced binge eating
Romanian Journal of Child and Adolescent Psychiatry
 Pharmacological intervention in Binge Eating Disorder. A narrative review
days and revealed significant decreases in
the YBOCS-BE obsessional and compulsive
scales as well as in the Barratt Impulsiveness
Scale, version 11 (BIS- 11), Binge Eating Scale
(BES) and Three-Factor Eating Questionnaire
[TFEQ]. Although not efficient in reducing
the BE days, a dose of 30mg/day of LDX has
been indicated to determine weight loss [63].
A multinational, double-blind, pla-
cebo-controlled, randomized withdrawal
study including 418 participants diagnosed
with moderate to severe BED has assessed
LDX efficacy. Following a 12-week open
label phase consisting of dose optimization
(4 weeks) and dose maintenance (8 weeks),
275 LDX responders were randomized to
placebo (n = 138) or continued LDX treat-
ment (n = 137) during a 26-week withdrawal
phase. The risk of BE episodes relapse over 6
months was lower in participants in the LDX
group - 3.7% - than in those randomized to
placebo – 32.1% [64].
A newer randomized control trial (RCT)
provided insights into LDX effects on satiety
and reduced food-reward related respond-
ing, as well as improved cognitive control by
examining the behavioral and neural effects
of an acute dose of 50 mg of LDX (placebo
n=25 and LDX administration = 25). Findings
revealed reduced self-reported appetite rat-
ings, reduced eating rates, diminished bilat-
eral activity on fMRI scans when viewing
food pictures and sustained attention as well
as reduced impulsive responding [65].
Bupropion is a dual dopamine and
noradrenaline reuptake inhibitor indicated
in major depression disorder and smok-
ing cessation [66]. A RCT of sixty-one over-
weight and obese women with BED who
were randomly assigned bupropion treat-
ment (300 mg/d) or placebo for 8 weeks has
indicated positive results regarding weight
loss. However, administration of bupropion
did not improve binge eating, food crav-
ing, or associated eating disorder features
compared to placebo [67]. Association of
Volume 9, Issues 1-2, January-June, 2021
naltrexone and bupropion in a fixed dose
(50/300 mg) over 12 weeks did not show sta-
tistically different results from placebo, even
though significant reductions from baseline
in BE, depression and weight during treat-
ment were registered [68].
SSRIs are often used as first-line phar-
macotherapy for depression and numerous
other psychiatric disorders [69]. However,
existing evidence from trials that assess
SSRIs efficacy in BED are contradictory but
overall data indicates that they are ineffec-
tive in treating BED, although they showed
mild weight loss effect in some cases [70-
72]. This view is supported by recent results
of a RCT where 12-week administration of
Vortioxetine showed no efficacy in BED or
weight loss relative to placebo [73].
Phentermine is a catecholamine releas-
ing agent with a similar chemical structure
to d-amphetamine. Even though this agent
has not been studied in monotherapy in
BED, association with other agents indicated
promising results. Phentermine-topiramate
administration was evaluated with reported
BE features reduction and weight loss in
small-sized RCTs [74, 75]. However, further
investigation into this association of agents is
needed to evaluate outcomes in BED.
Mu opioid receptor antagonists are also
agents that have been studied in BED, con-
sidering the role they play in appetite con-
trol and food-related stimuli processing.
GSK1521498, an mu opioid receptor antago-
nist, has shown reduced attentional bias for
food cues on the visual dot probe task versus
placebo in a RCT consisting of overweight or
obese adults with BED randomized to either
placebo or 2 or 5 mg/d of GSK1521498 [76].
However, there is insufficient data on its
implications in BED, with other RCTs report-
ing contradictory results regarding the effi-
cacy in binge eating disorder [77,78]. Another
opioid antagonist, naltrexone, approved
for alcohol dependence and combined with
bupropion for obesity, has shown reduced
29
 CÃLUGÃR et al.
association between food-craving intensity
and reward-driven eating relative to placebo
on administration of 25 mg of naltrexone on
day 1 followed by 50 mg daily for 2 days [79].
Overall data indicate that opioid blockade as
a mechanism of action in BED pathophysiol-
ogy delivers either none or poor benefits in
BED.
CONCLUSIONS
Binge eating disorder has a complex
pathology, thus data on compounds that
show efficacy in this disorder are relatively
limited. By reviewing clinical trials of differ-
ent pharmacological agents with different
mechanisms of action, we revealed clinically
effective drugs, as well as agents that did not
indicate efficacy in BED. Further research is
needed to test the safety and efficacy of dif-
ferent drugs on the impulsivity and compul-
sivity implicated in BED’s pathophysiology.
Also, obtaining reduction of food intake and
sustained weight loss are an important goal
in BED management.
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