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The two most clinically serious eating disorders are anorexia nervosa and bulimia nervosa. A drive for thinness and fear of fatness lead patients with anorexia nervosa either to restrict their food intake or binge-eat then purge (through self-induced vomiting and/or laxative abuse) to reduce their body weight to much less than the normal range. A drive for thinness leads patients with bulimia nervosa to binge-eat then purge but fail to reduce their body weight. Patients with eating disorders present with various gastrointestinal disturbances such as postprandial fullness, abdominal distention, abdominal pain, gastric distension, and early satiety, with altered esophageal motility sometimes seen in patients with anorexia nervosa. Other common conditions noted in patients with eating disorders are postprandial distress syndrome, superior mesenteric artery syndrome, irritable bowel syndrome, and functional constipation. Binge eating may cause acute gastric dilatation and gastric perforation, while self-induced vomiting can lead to dental caries, salivary gland enlargement, gastroesophageal reflux disease, and electrolyte imbalance. Laxative abuse can cause dehydration and electrolyte imbalance. Vomiting and/or laxative abuse can cause hypokalemia, which carries a risk of fatal arrhythmia. Careful assessment and intensive treatment of patients with eating disorders is needed because gastrointestinal symptoms/disorders can progress to a critical condition.
Gastrointestinal symptoms and disorders in patients with eating
Yasuhiro Sato
Shin Fukudo
Received: 13 August 2015 / Accepted: 7 October 2015
ÓJapanese Society of Gastroenterology 2015
Abstract The two most clinically serious eating disorders
are anorexia nervosa and bulimia nervosa. A drive for
thinness and fear of fatness lead patients with anorexia
nervosa either to restrict their food intake or binge-eat then
purge (through self-induced vomiting and/or laxative
abuse) to reduce their body weight to much less than the
normal range. A drive for thinness leads patients with
bulimia nervosa to binge-eat then purge but fail to reduce
their body weight. Patients with eating disorders present
with various gastrointestinal disturbances such as post-
prandial fullness, abdominal distention, abdominal pain,
gastric distension, and early satiety, with altered esopha-
geal motility sometimes seen in patients with anorexia
nervosa. Other common conditions noted in patients with
eating disorders are postprandial distress syndrome, supe-
rior mesenteric artery syndrome, irritable bowel syndrome,
and functional constipation. Binge eating may cause acute
gastric dilatation and gastric perforation, while self-in-
duced vomiting can lead to dental caries, salivary gland
enlargement, gastroesophageal reflux disease, and elec-
trolyte imbalance. Laxative abuse can cause dehydration
and electrolyte imbalance. Vomiting and/or laxative abuse
can cause hypokalemia, which carries a risk of fatal
arrhythmia. Careful assessment and intensive treatment of
patients with eating disorders is needed because gastroin-
testinal symptoms/disorders can progress to a critical
Keywords Eating disorder Anorexia nervosa Bulimia
nervosa Gastrointestinal symptom Gastrointestinal
Eating Disorders and Gastrointestinal (GI)
The Diagnostic Statistical Manual of Mental Disorders 5
Edition lists several disorders related to eating behaviors
[1]. The two most clinically serious eating disorders are
anorexia nervosa (AN) and bulimia nervosa (BN). Among
patients with AN, a drive for thinness and intense fear of
fatness leads them to engage in two types of energy-re-
stricting activities—restricting food intake, which is
referred to as AN of the restrictive type (ANR), and binge
eating followed by purging behavior, i.e., self-induced
vomiting and/or laxative abuse, which is referred to as AN
of the binge-purge type (ANBP). In addition, AN patients
perform excessive physical exercise. Together, these
activities result in bodyweight loss. Despite the loss of
weight, however, AN patients still consider themselves fat
(due to body image distortion) and refuse to acknowledge
their illness. AN commonly develops in young women,
with a prevalence rate in this population of 0.3 % [2]. The
mortality rate of AN is 5.1 % per decade [3], which is the
highest among mortality rates for stress-related disorders.
AN patients frequently present with associated psychiatric
disorders such as depression, obsessive–compulsive disor-
der, and personality disorder [4]. They also show several
types of cognitive dysfunction, including cognitive inflex-
ibility [57], impaired decision making [8,9], reward-
processing disturbance, and altered interoceptive aware-
ness [10]. In many cases, AN patients are resistant to
&Yasuhiro Sato
Department of Psychosomatic Medicine, Tohoku University
Hospital, Sendai, Japan
Department of Behavioral Medicine, Tohoku University
Graduate School of Medicine, Sendai, Japan
Clin J Gastroenterol
DOI 10.1007/s12328-015-0611-x
BN patients are also preoccupied with a drive for thin-
ness and engage in binge eating, purging, and exercise.
However, they cannot achieve a reduction in body weight
and remain at normal weight. As with AN, BN tends to
develop in adolescence and is prevalent in young women.
The prevalence rates for BN are 1 % in young women and
0.1 % in young men [2]. BN patients also show psychiatric
disorders and cognitive dysfunctions. A shift from AN to
BN or from BN to AN has been reported in some cases.
Complaints of GI symptoms are frequent among patient
with eating disorders. In a study by Salvioli et al. of
patients with eating disorders (39 with AN and 9 with BN),
96 % reported postprandial fullness, 90 % reported
abdominal distention, and more than half complained of
abdominal pain, gastric distension, early satiety, and nau-
sea [11]. In addition, Salvioli et al. found a significant
correlation between GI symptoms and hypochondriasis. In
other studies, AN patients tended to complain of early
satiety, post-prandial discomfort or recurrent vomiting
[12], severe constipation, and bowel obstruction [13], while
BN patients tended to experience bloating (74.4 %) and
flatulence (74.4 %), followed by constipation (62.8 %),
decreased appetite (51.2 %), abdominal pain (48.8 %),
borborygmi (48.8 %), and nausea (46.5 %) [14].
Common GI Symptoms/Disorders in Patients
with Eating Disorders
Esophageal symptoms and disorders
Although patients with eating disorders may report distur-
bances in swallowing, there is little evidence of esophagus
malfunction in AN [15]. Such esophageal symptoms without
evidence of structural abnormalities, referred to as functi onal
GI disorders (FGID) of the esophagus, include functional
dysphagia, globus, and functional heartburn, as defined by
the Rome III criteria [16] and co-occur with eating disorders
at rates of 6, 1, and 22 %, respectively (Fig. 1)[17].
To date, only a few studies have focused on esophageal
motor function in patients with eating disorders, despite the
clinical importance of evaluating such motor activity.
Stacher et al. found that 7 of 30 patients initially diagnosed
with AN had esophageal achalasia; one patient had diffuse
esophageal spasm, another had severe gastroesophageal
reflux disease with upper esophageal sphincter hyper-
tonicity, and 6 had nonpropulsive, repetitive, high-ampli-
tude, prolonged contractions of the lower segment of the
esophagus [18]. However, the very high prevalence of
esophageal motility disorders among the patients in that
study suggests referral bias [15]. Another study showed
that the basal pressure of the lower esophageal sphincter
was higher in ANR patients than in ANBP patients and
healthy controls, but still within the normal range [19] and
this difference disappeared after treatment. Another study
evaluating esophageal motility in 26 BN patients [20]
found normal motility in 18 patients, incomplete lower
esophageal sphincter relaxation in 4, vigorous achalasia in
2, and achalasia and diffuse esophageal spasm in one
patient each. In contrast, another study on patients with
bulimic eating disorders (8 with BN and 4 with mixed
features of AN and BN) revealed normal esophageal
motility in all 12 patients [21].
Slow gastric motility and functional dyspepsia
As mentioned earlier, patients with eating disorders fre-
quently report postprandial fullness, abdominal distention,
gastric distension, early satiety, and nausea [11]. Both AN
and BN patients have reported more severe postprandial
distress than healthy controls [22]. These symptoms may
be attributed to postprandial distress syndrome, a subtype
of functional dyspepsia. Functional dyspepsia, itself a type
of FGID, manifests as postprandial fullness, early satiation,
epigastric pain, or epigastric burning without any structural
disease [16]. In patients with eating disorders, one study
Fig. 1 Gastrointestinal disorders of patients with eating disorders
Clin J Gastroenterol
reported a prevalence rate of 45 % for postprandial distress
syndrome [17], and another study reported a prevelance
rate of 23 % for functional dyspepsia (Fig. 1)[23].
Slow gastric motility contributes to these gastric symp-
toms. AN patients have shown slow gastric emptying [12,
2428] in addition to gastric dysrhythmia, impaired antral
contractility, delayed emptying of solids, decreased post-
cibal blood levels of norepinephrine and neurotensin, and
impaired autonomic function [26]. Slow gastric emptying in
these patients was found to correlate with nausea, vomiting,
and gastric fullness [27], and has the potential to lead to
difficulties during re-feeding and weight restoration [29].
In BN patients, gastric relaxation after food intake was
significantly diminished [30], although gastric emptying
was normal [28,31]. Gastric compliance in BN showed no
difference from that in controls [32].
Several prokinetic agents have been tested for their
effects on delayed gastric emptying. Domperidone, a dopa-
mine D2-receptor selective antagonist used as a prokinetic
agent for the stomach, improved delayed gastric emptying in
AN patients [18,33]. Domperidone is available in Japan, but
not in the United States. Another prokinetic agent, cisapride,
a serotonin 5-HT4 agonist with weak 5-HT3 antagonistic
action, effectively enhanced gastric emptying in AN patients
[3436]. However, cisapride is not available in most coun-
tries because of the critical cardiac adverse effects of QT
prolongation and ventricular tachycardia. Metoclopramide is
another dopamine antagonist that proved useful for
improving gastric motility [25,37]. In contrast, the proki-
netic agent erythromycin, which is popularly used as an
antibiotic, was tested in BN patients but failed to achieve a
significant clinical response [31]. Other prokinetics such as
mosapride, itopride, and acotiamide are used in Japan, but
these drugs have not been specifically tested in patients with
eating disorders.
Superior mesenteric artery syndrome
Superior mesenteric artery (SMA) syndrome is the result of
compression of the third portion of the duodenum, which
lies between the aorta and the vertebral column posteriorly
and the superior mesenteric artery anteriorly (Fig. 1)[38].
In healthy individuals, the arch of the SMA is held away
from the aorta by the mesenteric pad of fat. Considerable
loss of mesenteric fat in conditions such as burns, pro-
longed bedrest, rapid growth in children without corre-
sponding weight gain, and AN, serves to reduce the
aortomesenteric angle [39]. Weight loss is regarded to be a
risk factor for SMA syndrome [40]. The symptoms of the
syndrome are appetite loss, abdominal pain, postprandial
distension, abdominal fullness, nausea, and vomiting [41].
Radiological methods are useful for diagnosing SMA
syndrome. Barium swallow radiography demonstrates an
extremely dilated stomach and restriction of contrast flow
past the third portion of the duodenum [42]. Computed
tomography (CT) reveals dilation of the stomach and
proximal duodenum in addition to severe narrowing of the
third portion of the duodenum (Fig. 1). Contrast-enhanced
CT reveals compression of the duodenum between the
SMA and aorta [42].
SMA syndrome has frequently been reported in AN
patients [39,4251]. Elbadaway presented four possible
explanations for the relationship between SMA syndrome
and AN [39]. First, acute or subacute SMA syndrome may
develop as a complication in AN patients. Second, chronic
SMA syndrome may simulate AN [52]. Third, chronic SMA
syndrome may complicate AN, in which case either syn-
drome may be diagnosed but probably not both. The fourth
possibility is that chronic SMA syndrome precipitates AN.
In a case report, Jordaan et al. pointed out that ‘Not
diagnosing SMA syndrome in a timely fashion may lead to
a delay in treatment, prolonged bowel obstruction, and an
increased risk of developing fear and avoidance of food’
[45]. In their female patient, although they noted interplay
between psychological and physical factors and arrived at a
diagnosis of ‘eating disorder not otherwise specified’, the
diagnosis according to DSM-5 criteria would be ‘restric-
tive/avoidant food intake disorder’.
In cases of total intestinal obstruction due to SMA
syndrome, decompression with nasogastric tube placement
and surgical consultation will probably be necessary [42].
Conservative treatments have been used with some
patients, including oral hypercaloric liquid feeding [52],
nasojejunal tube feeding [42,49], and total parenteral
nutrition [49], whereas other patients have been treated
surgically with duodenojejunostomy [39,43,45]. These
treatments sometime failed because the patients refused to
restore their body weight due to a psychopathological
desire for thinness.
BN patients rarely develop SMA syndrome because of
their normal body weight. Ikegaya et al. reported a fatal
case of BN in a woman who consumed enormous amounts
of solid food, where her distended stomach compressed the
SMA and pinched the duodenum, eventually leading to
fatal total intestinal obstruction [48].
Irritable bowel syndrome
Irritable bowel syndrome (IBS) is one of the most frequent
FGIDs. IBS patients have abdominal pain or discomfort
that is relieved with defecation, altered frequency of bowel
movement, and altered stool consistency [16]. Four sub-
types of IBS have been defined—with diarrhea (IBS-D),
with constipation (IBS-C), mixed (IBS-M), and unsubtyped
(IBS-U). Approximately 41–52 % of patients with eating
disorders have IBS [17,23,53], with 68.8 % of BN
Clin J Gastroenterol
patients diagnosed with IBS (Fig. 1)[54]. Although none
of these studies reported on the subtypes of IBS, IBS-C is
probably predominant given that IBS was weakly predicted
by laxative use (not abuse) in one study [17].
Constipation is one of the most common GI symptoms
among patients with eating disorders. Functional constipation
is an FGID with difficult, infrequent, and incomplete defe-
cation that does not fulfill the criteria for IBS [16], i.e.,
without abdominal pain or discomfort. On the basis of the
Rome II or Rome III criteria, 11–24 % of patients with eating
disorder are diagnosed with functional constipation [17,23,
53]. Constipation has been reported in 67–83 % of AN
patients [55,56] and 62.8 % of BN patients (Fig. 1)[14].
Constipation in AN is thought to be caused by reflex
hypofunctioning of the colon due to lack of food intake
[57] or by poor nutrition and hypokalemia due to purging
[29]. The possibility of constipation being caused by
antidepressant medication, particularly tricyclic antide-
pressants, should also be considered in such patients [29].
Low triiodothyronine (T3) syndrome, which is character-
ized by a markedly decreased T3 level, normal or sub-
normal thyroxine (T4) level, and normal basal thyrotropin
(TSH) level, is a persistent finding in AN [58]. It is thought
to be a beneficial response designed to ‘spare calories’ [59].
This hypothyroidism-like condition may also cause con-
stipation, in addition to dry skin, hypothermia, bradycardia,
hypotension, sluggish tendon reflexes, and pleural or
pericardial or peritoneal effusions [60].
An investigation using a radiopaque marker revealed
that whole-gut transit time was significantly longer in both
AN and BN patients than in controls [61]. In a study using
a radiopaque marker and anorectal manometry, 8 of 12 AN
patients (66.7 %) showed slow colonic transit times, while
5 (41.7 %) had significantly lower resting anal canal
pressures than healthy controls [56]. Colonic transit time
normalized in the 8 patients who completed a 4-week re-
feeding program. However, anorectal manometry did not
normalize in these patients. Therefore, pelvic floor dys-
function might be a characteristic trait of AN patients.
Although increased food intake and weight gain appear
to relieve constipation to some extent in AN patients, the
specific physiologic factors that bring about the improve-
ment in constipation have yet to be determined [62].
Rectal prolapse
Several case reports have documented the complication of
rectal prolapse in patients with eating disorders (Fig. 1)
[6367]. Predisposing risk factors for rectal prolapse
include history of pelvic surgery, obstetric trauma, elevated
intra-abdominal pressure, advanced age, and chronic con-
stipation [68]. Approximately 80–90 % of patients with
rectal prolapse are women [69]. Patients with rectal pro-
lapse exhibit a diminished anal canal pressure [70].
Therefore, patients with eating disorders are predisposed to
rectal prolapse.
Hepatic injury
Many AN patients show liver dysfunction (Fig. 1).
Although the liver dysfunction is mild and restores to
normalcy with nutritional recovery, some patients can
progress to severe hepatic failure that may eventually be
fatal [7173]. Excess accumulation of fat in the liver
causes elevation of liver enzymes in AN patients [74]. One
report suggests that oxidative stresses in hepatocytes could
be related to the pathogenesis of liver injury in AN patients
GI Symptoms Specific to Binge2Purge Behavior
Both ANBP patients and BN patients consume large
amounts of food and then discharge the food with self-
induced vomiting and/or laxative/diuretic abuse. These
behaviors can result in serious health problems.
Binge eating
In the United States, 2.0–3.8 % of female college students
have been reported to be bulimic [76]. In a study of 456
female nursing school and junior college students in Japan,
35 students (7.7 %) admitted to binge eating more than
once a week, 38 (8.3 %) to self-induced vomiting, and 21
(4.5 %) to using laxatives. The reported prevalence of
binge-eating behavior among women varies widely
depending on the sample population, ranging from 24 %
among adults from family practice clinics to 90 % among
college students [77].
Several case reports have been published on patients who
developed acute gastric dilatation due to excessive food
consumption (Fig. 2)[7880]. Acute gastric dilatation may
sometimes be life-threatening, as food compaction in the
stomach may obstruct gastric blood circulation, leading to
necrosis and perforation of the stomach wall (Fig. 2)[8184].
Self-induced vomiting
Many ANBP and BN patients vomit voluntarily after binge
eating. In fact, 8.06 % of ANBP patients and 29.50 % of
BN patients show Russell’s sign—the presence of lesions
such as calluses on the dorsal aspect of the hand as a
consequence of self-induced vomiting [85]. As the illness
Clin J Gastroenterol
progresses, many patients can vomit reflexively without
mechanical stimulation [86]. Patients with bulimic behav-
ior present with dysphagia and odynophagia, although their
esophageal motility is within normal range [21]. This may
be due to continuous acid exposure. Vomited acidic gastric
juice causes a number of problems such as dental caries,
salivary gland enlargement and inflammation, and gas-
troesophageal reflux disease (GERD) (Fig. 2).
Mallory–Weiss syndrome is a mucosal and submucosal
tear of the esophagus or stomach at or near the gastroe-
sophageal junction [87], and is typically indicated by non-
bloody vomiting followed by hematemesis. Although
ANBP and BN patients are considered susceptible to this
syndrome because they frequently vomit, there is no clear
data on the prevalence of the syndrome in eating disorder
patients in the English-language literature. Similarly, the
prevalence of another severe esophageal complication,
esophageal rupture (Boerhaave syndrome), is also
Kiss et al. performed esophagogastroduodenoscopy in
37 patients with long-standing BN and found the endo-
scopic appearance of the esophageal and gastric mucosa
was normal in 23 patients [88]. However, 8 patients
showed signs of mild esophagitis, which were not related to
the duration or severity of bulimic behavior or to symptoms
of gastroesophageal reflux. Two of these 8 patients had
sliding hiatal hernias. The remaining 6 patients had
superficial mucosal erythema in the stomach or duodenum
but did not exhibit actual erosions, ulcers, or bleeding. Kiss
et al. concluded that mucosal injury consequent to chronic,
self-induced vomiting in patients with BN is relatively
infrequent and limited. There is no similar report of
endoscopy findings in AN patients.
Esophageal achalasia is a dysmotility disorder of
unknown etiology, manifesting as dysphagia and vomiting.
In this condition, the vomitus is not acidic because the
swallowed food stops just above the esophagocardiac
junction. Achalasia has been mistaken for eating disorders,
particularly in young female AN patients [8995].
Electrolyte imbalance
Bulimic patients frequently present with electrolyte abnor-
malities, with hypokalemia occurring in 0–23.5 % of
patients, hypochloremia in 8.8–26.2 %, and elevated bicar-
bonate levels in 8.2–23.5 % [96]. Hypokalemia is the most
serious of these abnormalities since it can cause cardiac
arrhythmias, rhabdomyolysis, muscle weakness, hypoka-
lemic cardiomyopathy, and tetany [97]. As well as direct loss
of potassium from vomiting, the concomitant loss of chloride
ions and gastric acid leads to hypokalemic hypochloremic
metabolic alkalosis [97]. The treatment of marked hypoka-
lemic metabolic alkalosis requires volume repletion (with
intravenous normal saline) [86], and oral potassium chloride
is generally preferred for potassium repletion [86].
Oral symptoms
Oral lesions such as dental erosion, parotid gland swelling,
dental caries, and periodontal disease are frequently noted
in eating disorder patients with binge-purge behavior
(Fig. 2)[98]. In a university dental clinic, 9 of 400 patients
were females with BN [99]. Bulimic patients often report
increased sensitivity of the teeth to hot, cold, and acidic
substances, suggestive of damage to dental enamel [100].
Gentle brushing and use of a fluoride mouth rinse imme-
diately after purging may prevent caries [86]. Parotid gland
swelling is effectively treated with oral administration of
pilocarpine hydrochloride [101].
In one study, hyperamylasemia was found in 61 % of BN
patients and in 20 % of ANR patients (Fig. 2), with more
than three-quarters of BN patients showing a close positive
Fig. 2 Gastrointestinal-related binge-purge behavior by patients
with eating disorders. aDisorders induced by binge eating, bdisorders
induced by self-induced vomiting, cdisorders induced by laxative
Clin J Gastroenterol
correlation between the frequency of vomiting and total
serum amylase levels, and both frequency and type of
vomiting appearing to be associated with the extent of
salivary gland enlargement [102]. The hyperamylasemia in
patients with AN or BN is often caused by increased
salivary-type amylase activity [103]. In a study on the
amylase and isoamylase activity in 17 patients with eating
disorders, 6 showed elevated amylase activity, with 5 of the
6 having isolated increases in salivary isoamylase activity
[103]. Hyperamylasemia does not require any treatment.
Gastroesophageal reflux disease
GERD is a condition characterized by the reverse flow of
gastric contents through the esophagus and, in some cases,
into the pharynx [100]. In bulimic patients, spontaneous
reflux of acidic gastric contents into the lower esophagus
may occur due to laxity of the lower esophageal sphincter
after repeated vomiting [86]. Endoscopic investigations
revealed that 8 of 37 patients with bulimic behavior had
mild esophagitis (Fig. 2)[88]. Acid reflux has been
observed in BN patients evaluated by 24-h pH monitoring
and esophagography [104]. Proton-pump inhibitors are the
first-line therapy for GERD because of their efficacy,
safety, and cost-effectiveness [86].
Esophageal cancer
Long-term exposure to acidic gastric juice causes Barrett’s
esophagus, characterized by metaplasia from squamous to
columnar epithelium. Barrett’s esophagus is a precursor to
esophageal adenocarcinoma and increases carcinogenic
risk by 11-fold [105]. There have been several case reports
of patients with purging behavior who developed Barrett’s
esophagus [106], which then progressed to esophageal
cancer [107,108]. Other reports have described BN
patients who developed esophageal cancer in the absence
of Barrett esophagus [109,110]. In a large cohort study of
3,617 patients with a history of hospitalization for eating
disorder, 7 were found to have esophageal cancer [111].
The standardized incidence ratio of patients with eating
disorders to the general population was 6.1 in that study.
Thus, patients hospitalized previously with eating disorders
are thought to be at increased risk of developing esopha-
geal cancer. All the patients with esophageal cancer in the
abovementioned study had squamous cell carcinomas
although adenocarcinoma would be more in line with
expectations. Therefore, the involvement of confounding
factors, including alcohol, smoking, and nutritional defi-
ciency, appears to be a more plausible explanation than
acidic damage. Further extensive research is needed to
elucidate the relationship between self-induced vomiting,
Barrett esophagus, and esophageal cancer.
Laxative abuse
Laxative abuse is another common purging behavior in
patients with eating disorders. One study indicated that
36.5 % and 7.9 % of patients with eating disorders reported
laxative abuse and enema abuse, respectively [112].
Patients believe that laxatives help to remove the calories
in food and keep them thin. However, in fact, only
10–12 % of ingested calories are lost as a result of laxative
use because laxatives have little effect on the small intes-
tine where caloric absorption primarily occurs [86].
Chronic watery diarrhea (Fig. 2) caused by laxative
abuse leads to dehydration and electrolyte imbalance.
Laxative abuse results in the loss of potassium and bicar-
bonate via the stool, resulting in hypokalemia and non-
anion gap metabolic acidosis [97]. The development of
hypokalemia may be marked by generalized muscle
weakness, lassitude, skeletal muscle paralysis, rhabdomy-
olysis with renal impairment, and nerve palsies [113].
More severe hypokalemia can result in cardiac arrhyth-
mias, with an increased risk of sudden death. Expulsion of
water via stool causes dehydration, leading to hypotension,
tachycardia, postural dizziness, and syncope [113].
Melanosis coli, or pseudomelanosis coli, refers to dark-
ening of the colonic mucosa as a result of chronic use of
laxatives, especially anthraquinone derivatives (Fig. 2)
[114]. No correlation between colorectal cancer and mela-
nosis coli or laxative use has been noted [115]. The condi-
tion can resolve gradually after laxative withdrawal [114].
So-called ‘cathartic colon’ is a loss of normal colonic
peristalsis because of long-term habituation to stimulant
laxatives. However, the cathartic colon is not induced by
currently available laxatives even when used over long
periods or in excessive doses [116]. Cathartic colon must
not be mistaken for laxative abuse.
Patients’ erroneous beliefs about the normal number and
frequency of bowel movements are usually obstacles in the
treatment of laxative abuse, so educating them on normal
bowel physiology is an essential first step in treatment
[113]. Patients with eating disorders have been reported to
have increased anxiety levels with laxative withdrawal
[117]. Body weight gain due to constipation and edema due
to fluid retention may contribute to their increasing anxiety,
and close supervision is required during this time to ensure
that withdrawal is successful [113].
Patients with eating disorders present with various GI
symptoms/disorders, some of which are critical. Therefore,
careful assessment and intensive treatment is needed. Data
on the prevalence of GI symptoms/disorders in patients
Clin J Gastroenterol
with eating disorders have been mainly obtained from
small-scale studies. As such, comprehensive and extensive
surveys on GI symptoms/disorders are necessary among
patients with eating disorders to elucidate the actual nature
of these intractable disorders and facilitate the development
of innovative treatment strategies. Few clinical trials have
been conducted on therapeutic measures for GI symptoms/
disorders in patients with eating disorder patients, and to
achieve better treatment outcomes, large randomized con-
trol trials are warranted.
Compliance with ethical standards
Conflict of Interest: Yasuhiro Sato and Shin Fukudo declare that
they have no conflict of interest.
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... The patient's diagnosis of panic disorder is typical. Eating disorders are frequently seen in association with other psychiatric illnesses, especially mood and anxiety disorders [2,3]. ...
... Denial of the seriousness of a medical condition is consistent with an eating disorder. Patients with eating disorders often exhibit cognitive dysfunction, including impaired decision making [3]. ...
... This may explain why our patient waited to come to the ED and why she left AMA. Additionally, eating disorders may lead to secondary effects on GI motility, specifically gastric emptying [3]. ...
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Introduction Gastric perforation with necrosis is rare following acute gastric dilation (AGD) and can be fatal. We present a case of a patient with AGD due to a binge-eating episode who left the emergency department (ED) against medical advice (AMA) only to return with gastric perforation and necrosis requiring total splenectomy and partial gastrectomy. Case A 28-year-old female without a remarkable past medical history presented to the ED with diffuse abdominal pain and obstipation after a three-day “food crawl.” On admission, a computerized tomography (CT) scan revealed a markedly dilated stomach from the diaphragm to the pelvis with severe mass effect. The therapeutic plan at the time was gastric decompression via a nasogastric tube. The following day, the patient reported feeling better and left AMA only to return the same evening with worsening symptoms and peritoneal signs. The patient was then emergently taken to the operating room (OR). In the OR, laparotomy revealed frank spillage of partially digested food and necrosis along the greater curvature of the stomach that extended to the spleen. Damage control surgery was performed, which required a total splenectomy and a partial gastrectomy. The patient was admitted to the intensive care unit (ICU) and subsequently underwent five more trips to the OR due to severe edema that delayed the primary closure of the fascia. Once the patient was transferred out of the ICU, she was evaluated by psychiatry and diagnosed with a binge-eating disorder. Conclusion This case demonstrates the severity of acute gastric dilation and its potentially lethal consequences. In some cases, such as this one, the patient may present with mild symptoms and not comprehend the gravity of the situation. Therefore, it is important for clinicians to recognize this condition as a true emergency and perform immediate decompression and evaluation for surgery.
... Several studies suggest that gastrointestinal disorders are common in patients with AN, contributing to increased anxiety, decreasing quality of life, and worsening of treatment outcomes (119,120) . In fact, gastrointestinal symptoms are very common, and involve different anatomical regions, such as the esophagus, stomach, and intestine. ...
... Sometimes patients can suffer from delayed gastric emptying, constipation, or visceral hypersensitivity. This symptomatic picture could result in poor compliance and reduced outcomes (119,120) . ...
Anorexia nervosa (AN) is characterised by the restriction of energy intake in relation to energy needs and a significantly lowered body weight than normally expected, coupled with an intense fear of gaining weight. Treatment of AN is currently based on psychological and refeeding approaches, but their efficacy remains limited, since 40% of patients after ten years of medical care, still present symptoms of AN. The intestine hosts a large community of microorganisms, called the “microbiota”, which live in symbiosis with the human host. The gut microbiota of a healthy human is dominated by bacteria from two phyla: Firmicutes and majorly Bacteroidetes . However, the proportion in their representation differs on an individual basis and depends on many external factors, such as medical treatment, geographical location, and hereditary, immunological and lifestyle factors. Drastic changes in dietary intake may profoundly impact the composition of the gut microbiota, and the resulting dysbiosis may play a part in the onset and/or maintenance of comorbidities associated with AN, such as gastrointestinal disorders, anxiety, and depression, as well as appetite dysregulation. Furthermore, studies have reported the presence of atypical intestinal microbial composition in patients with AN compared to healthy normal-weight controls. This review addresses the current knowledge about the role of the gut microbiota in the pathogenesis and treatment of AN. The review also focuses on the bidirectional interaction between the gastrointestinal tract and the central nervous system (microbiota-gut-brain axis), considering the potential use of the gut microbiota manipulation in the prevention and treatment of AN.
... erefore, it is important for both the patients and the dental team to be aware of such possible negative consequences of oral hygiene practices in relation to acidic challenges such as from SIV. In addition, a more detailed practice of these behaviors and the duration of these events over time, often extending over years, is equally important since the negative impact on oral health is to a large extent cumulative [2][3][4][5][6]15]. ...
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Background: Self-induced vomiting (SIV) is often present in patients with eating disorders (ED) and potentially damaging for oral health. Related behaviors, such as binge eating and oral hygiene habits, may equally increase the risk for dental damage. This study aimed to investigate behaviors and habits in patients with ED and SIV in relation to oral health. Methods: All patients enlisting for treatment in an ED clinic for 1 year were offered to take part in the study. Fifty-four of 65 patients were accepted to participate, and a questionnaire included questions on dietary and oral hygiene habits was included. A subgroup consisting of only those 17 ED patients who reported SIV during the previous six months comprised the sample for this study and received additional questions related to other compensatory behaviors and oral hygiene habits in relation to oral health. Results: Binge eating before SIV was common (14/17 patients). Time point for SIV after binge eating and the procedures performed after vomiting varied. Tooth brushing after vomiting was common (7/17). Food and drinks during binge eating included mainly items rich in calories (sugar/fat) or acid. All 17 patients believed that vomiting could damage their teeth, but only one of them had informed the dentist about having an ED. A number of oral symptoms were reported. Ten patients considered their oral health to be good/fairly good, while the remaining seven patients reported their oral health as not so good/bad/very bad. Information on how ED could affect their teeth was commonly received from the media. Conclusions: The dental team should be made aware of the likely detrimental effects of binge eating and vomiting on oral health in patients with eating disorders. The team should also be aware of the cyclical nature of the disease and the similarities and diversities that exist within this group of ED patients. Since ED patients hide their disease from the dental team, this stresses the importance of open and trustful communication between patients and health workers. An organized collaboration between ED clinics and dental professionals is suggested as well as a development of avenues for information about ED and oral health.
... Gastric symptoms in patients with eating disorders who are admitted to the hospital for refeeding are quite common; postprandial fullness, early satiety, abdominal distension, epigastric pain, and dyspepsia are frequently reported complaints [3]. These symptoms are likely secondary to slow gastric emptying, impaired autonomic function, diminished cytokinin release, and dysrhythmic antral contractility [4,5]. ...
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Gastric perforation in patients with anorexia nervosa is a rare entity associated with high morbidity and mortality [Norris in Int J Eat Disord 49:216–237, 2016]. In cases reported in the literature, the perforation was often preceded by a binge episode, and the subsequent clinical presentation was rapid and acutely deteriorating with a fatality rate as high as 80% [Norris in Int J Eat Disord 49:216–237, 2016, Pitre in J Med Case Rep 15:61, 2021]. We present a case of gastric perforation in the context of restrictive anorexia nervosa unique both for the absence of a premorbid binge episode as well as delayed clinical manifestations of medical distress, leading to abdominal compartment syndrome. Level IV Evidence obtained from multiple time series analysis such as case studies.
Background: Hypermobile Ehlers-Danlos Syndrome (hEDS) and the hypermobility spectrum disorders (HSD) can be challenging to diagnose and manage. Gastrointestinal symptoms and disorders of gut-brain interaction are common in this cohort and multifactorial in origin. Aims: The primary aim of this review is to arm the gastroenterologist with a clinically useful understanding of HSD/hEDS, by exploring the association of gastrointestinal disorders with HSD/hEDS, highlighting current pathophysiological understanding and providing a pragmatic approach to managing these patients. Methods: Literature relevant to the gastrointestinal system and hypermobile Ehlers-Danlos Syndrome was systematically searched, critically-appraised and summarized. Results: Diagnosis is based upon clinical criteria and a genetic basis is yet to be defined. The prevalence of many gut symptoms, including abdominal pain (69% vs 27%, p<0.0001), postprandial fullness (34% vs 16%, p=0.01), constipation (73% vs 16%, p<0.001) and diarrhea (47% vs 9%, p<0.001) are significantly higher in HSD/hEDS compared with non-HSD/hEDS individuals. Disorders of gut-brain interaction are also common, particularly functional dyspepsia. The pathophysiology of gut symptoms is poorly understood but may involve effects of connective tissue laxity and its functional consequences, and the influence of autonomic dysfunction, medication and comorbid mental health disorders. Awareness is the key to early diagnosis. Management is limited in evidence-base but ideally should include an integrated multidisciplinary approach. Conclusions: HSD/hEDS is a multisystemic disorder in which gastrointestinal symptoms, particularly related to disorders of gut-brain interaction are common. Deficiencies in knowledge regarding the pathophysiological processes limit evidence-based interventions and remain important areas for future research.
Objective: We estimated the prevalence of diagnosed eating disorders, overall and by select demographics, among commercially insured individuals identified as transgender in a national claims database. Methods: From the 2018 IBM® MarketScan® Commercial Database, there were 10,415 people identifiable as transgender based on International Classification of Disease (ICD-10) codes and procedure codes, specific to gender-affirming care, from inpatient and outpatient claims. Eating disorders were identified from ICD-10 codes and included anorexia nervosa, bulimia nervosa, binge eating disorder, eating disorder not otherwise specified, avoidant restrictive feeding and intake disorder, and other specified feeding and eating disorders. We estimated the prevalence of specific eating disorders diagnoses by selecting patient characteristics. Results: Of individuals receiving some form of gender-affirming care, 2.43% (95% confidence interval: 2.14%-2.74%) were diagnosed with an eating disorder: 0.84% anorexia nervosa, 0.36% bulimia nervosa, 0.36% binge eating disorder, 0.15% avoidant restrictive feeding and intake disorder, 0.41% other specified feeding and eating disorders, and 1.37% with an unspecified eating disorder. Among transgender-identifiable patients aged 12-15 years, 5.60% had an eating disorder diagnosis, whereas 0.52% had an eating disorder diagnosis in patients aged 45-64 years. Discussion: In patients identifiable as transgender, with receipt of gender-affirming care, the prevalence of diagnosed eating disorders was low compared to extant self-reported data for eating disorder diagnosis in transgender individuals. Among this population, eating disorders were highest in adolescents and young adults. Clinically verified prevalence estimates for eating disorder diagnosis in transgender people with a history of gender-affirming care warrant further investigation. Public significance: The present study aims to provide clinically validated, contemporary prevalence estimates for diagnosed eating disorders among a medically affirmed population of transgender adults and children in the United States. We report low prevalence of having any eating disorder relative to prevalence estimates reported in prior literature without clinical validation. These findings may be explained by access to affirming care and medical care generally.
Özet Düşük vücut ağırlığı, bozulmuş beden algısı ve kilo alma korkusu ile karakterize psikiyatrik bir bozukluk olan anoreksiya nervozanın etiyopatogenezi tam olarak bilinmemektedir. Literatürde yer alan çalışmalar anoreksiya nervosalı hastalarda beslenme rehabilitasyonunun ve yeniden ağırlık kazanımının intestinal disbiyoz yönetiminde yeterince etkin olmadığını göstermektedir, ancak çalışmaların sonuçları karmaşıktır. Bu derlemede intestinal mikrobiyotanın anoreksiya nervosa patofizyolojisindeki olası rolü, anoreksiya nervosalı hastalarda intestinal disbiyoza ilişkin özellikler ve intestinal mikrobiyota yönetiminde olası tedavi yaklaşımları hakkında bilgi verilmesi amaçlanmıştır.
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Anorexia nervosa is a psychiatric disorder characterized by severe low body weight, impaired self-body image, and intense fear of gaining weight, however its etiopathogenesis is not fully known. Some studies show that nutritional rehabilitation and corresponding weight restoration are not effective enough in the management of intestinal dysbiosis in patients with anorexia nervosa, but results are inconclusive. This work aims to review the existing studies to provide information about the possible role of intestinal microbiota in the pathophysiology of anorexia nervosa, characteristics of intestinal dysbiosis in patients with anorexia nervosa, and possible treatment approaches in the management of intestinal microbiota.
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Purpose of Review Abnormal interoception has been consistently observed across eating disorders despite limited inclusion in diagnostic conceptualization. Using the alimentary tract as well as recent developments in interoceptive neuroscience and predictive processing as a guide, the current review summarizes evidence of gastrointestinal interoceptive dysfunction in eating disorders. Recent Findings Eating is a complex process that begins well before and ends well after food consumption. Abnormal prediction and prediction-error signals may occur at any stage, resulting in aberrant gastrointestinal interoception and dysregulated gut sensations in eating disorders. Several interoceptive technologies have recently become available that can be paired with computational modeling and clinical interventions to yield new insights into eating disorder pathophysiology. Summary Illuminating the neurobiology of gastrointestinal interoception in eating disorders requires a new generation of studies combining experimental probes of gut physiology with computational modeling. The application of such techniques within clinical trials frameworks may yield new tools and treatments with transdiagnostic relevance.
Hirschsprung disease (HD) is a congenital disease which occurs in about 1 in 5000 births and is most commonly diagnosed shortly after birth. True incidence of HD in adulthood is unknown, because the illness is often undiagnosed or misdiagnosed in the adult population. A variety of nonspecific gastrointestinal complains (constipation, abdominal discomfort, and abdominal pain), which can be characteristic for HD, also commonly occur in eating disorders (ED). This chapter will discuss the symptomatic overlap between the two conditions across the lifespan and will present some clinical considerations promoting their thorough diagnosis and treatment.
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To investigate the predictive value of low freeT3 for long-term mortality in chronic hemodialysis (HD) patients and explore a possible causative role of chronic inflammation. One hundred fourteen HD patients (84 males) consecutively entered the study and were assessed for thyroid function and two established markers of inflammation, high sensitivity C-reactive protein (hsCRP) and interleukin-6 (IL-6). Monthly blood samples were obtained from all patients for three consecutive months during the observation period for evaluation of thyroid function and measurement of inflammatory markers. The patients were then divided in two groups based on the cut-off value of 1.8 pg/mL for mean plasma freeT3, and were prospectively studied for a mean of 50.3 ± 30.8 mo regarding cumulative survival. The prognostic power of low serum fT3 levels for mortality was assessed using the Kaplan-Meier method and univariate and multivariate regression analysis. Kaplan-Meier survival curve showed a negative predictive power for low freeT3. In Cox regression analysis low freeT3 remained a significant predictor of mortality after adjustment for age, diabetes mellitus, hypertension, hsCRP, serum creatinine and albumin. Regarding the possible association with inflammation, freeT3 was correlated with hsCRP, but not IL-6, and only at the first month of the study. In chronic hemodialysis patients, low plasma freeT3 is a significant predictor of all-cause mortality. Further studies are required to identify the underlying mechanisms of this association.
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Background It has been suggested that the risk of oesophageal adenocarcinoma might be increased in patients with a history of eating disorders due to acidic damage to oesophageal mucosa caused by self-induced vomiting practiced as a method of weight control. Eating disorders have also been associated with risk factors for squamous cell carcinoma of the oesophagus, including alcohol use disorders, as well as smoking and nutritional deficiencies, which have been associated with both main sub-types of oesophageal cancer. There have been several case reports of oesophageal cancer (both main sub-types) arising in patients with a history of eating disorders. Methods We used linked records of hospitalisation, cancer registration and mortality in Scotland spanning 1981–2012 to investigate the risk of oesophageal cancer among patients with a prior history of hospitalisation with eating disorder. The cohort was restricted to patients aged ≥10 years and <60 years at the date of first admission with eating disorder. Disregarding the first year of follow-up, we calculated indirectly standardised incidence ratios using the general population as the reference group to generate expected numbers of cases (based on age-, sex-, socio-economic deprivation category-, and calendar period-specific rates of disease). Results After exclusions, the cohort consisted of 3617 individuals contributing 52,455 person-years at risk. The median duration of follow-up was 13.9 years. Seven oesophageal cancers were identified, as compared with 1.14 expected, yielding a standardised incidence ratio of 6.1 (95% confidence interval: 2.5–12.6). All were squamous cell carcinomas arising in females with a prior history of anorexia nervosa. Conclusions Patients hospitalised previously with eating disorders are at increased risk of developing oesophageal cancer. Confounding by established risk factors (alcohol, smoking, and nutritional deficiency) seems a more likely explanation than acidic damage through self-induced vomiting because none of the incident cases of oesophageal cancer were adenocarcinomas, and because the study cohort had higher than background rates of hospitalisation with alcohol-related conditions and chronic obstructive pulmonary disease.
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Anorexia nervosa (AN) tends to be a chronic and deadly disorder with no proven treatments that reverse core symptoms in adults. New insight into neurobiological mechanisms that contribute to symptoms may support development of more effective interventions. We describe the development of a temperament-based treatment for AN on the basis of empirically supported models. It uses a systemized approach and takes into consideration an understanding of how neurobiological mechanisms are expressed through behaviour and personality and contribute to specific AN symptomatology. This model integrates the development of AN-focused constructive coping strategies with carer-focused strategies to manage temperament traits that contribute to AN symptomatology. This intervention is consistent with the recent Novel Interventions for Mental Disorders initiative mandating that treatment trials follow an experimental medicine approach by identifying underlying mechanisms that are directly targeted by the intervention to influence symptoms. Copyright © 2014 John Wiley & Sons, Ltd and Eating Disorders Association.
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Anorexia nervosa is one of a few mental health diagnoses that affects every organ system. Patients with AN often present with multiple secondary effects of starvation at the time of first assessment, including gastrointestinal (GI) complaints. In extreme cases, severe GI complications such as rectal prolapse may be encountered as a consequence of the illness although formal studies investigating the frequency of such occurrences are lacking. We present the case of a 16 year old female previously diagnosed with anorexia nervosa that developed a rectal prolapse as a consequence of her disease as well as a detailed literature review investigating the frequency and prevalence of such occurrences in this population.
Purpose: The purpose of this article is to thoroughly review the medical complications associated with bulimia nervosa and their evidenced-based or typical treatments. Methods: A thorough review of medical literature to cull pertinent and best articles which guide the diagnosis and treatment of the medical complications of bulimia nervosa was performed. Results: There are many different medical complications of bulimia nervosa which are caused by the mode and frequency of purging. Some are fluid and electrolyte alterations from the utilized mode of purging and some are due to the local damaging effects of purging behaviors on those body sites. Conclusion: Bulimia nervosa is a serious mental health disorder which has many medical complications associated with it. Most are reversible with treatment.
Anorexia nervosa is a complex psychiatric disorder with significant morbidity and mortality. It is important for gastroenterologists to be aware of the physiological effects and potential complications of anorexia nervosa, as they are frequently involved in treating patients with this disorder. We review the classic, GI, and neuroendocrinological features of anorexia nervosa. We also discuss gender differences and treatment options in anorexia nervosa. Further studies of GI physiology and pharmacology are needed to determine whether any disturbances may be amenable to therapeutic intervention. Future treatments directed at improving GI sensorimotor function and neurohormonal abnormalities in patients with anorexia nervosa may impact their nutritional rehabilitation and may have important health economic implications as patients avoid hospitalization and are restored to full activities in society. The current team approach, which incorporates psychiatrists, psychologists, nutritionists, pediatricians, internists, and gastroenterologists in the treatment of patients with anorexia nervosa, will continue to be essential.
Objective Rectal prolapse is a complication of AN that may be more common than previously recorded experience would suggest. Method In this report we document, for the first time, the association of anoxia nervosa (AN) and rectal prolapse in a series of three patients seen in the past three years. An extensive review of the literature using Medline over the period from 1966 to Jan 2000 failed to reveal any previous example of this association. Results and Conclusion The finding could have significant health care implications if confirmed. It would suggest that patients with either the psychiatric or surgical problem may not be receiving the appropriate complementary referrals: psychiatrist to surgeon and vice versa. The importance of recognition of this association in anorectic patients is the availability of effective surgical therapy.
To compare the prevalence of Functional gastrointestinal disorders (FGIDs) using ROME III and ROME II and to describe predictors of FGIDs among eating disorder (ED) patients. Two similar cohorts of female ED inpatients, aged 17-50 years, with no organic gastrointestinal or systemic disorders, completed either the ROME III (n = 100) or the ROME II (n = 160) questionnaire on admission for ED treatment. The two ROME cohorts were compared on continuous demographic variables (e.g., age, BMI) using Student's t-tests, and on categorical variables (e.g., ED diagnosis) using χ (2)-tests. The relationship between ED diagnostic subtypes and FGID categories was explored using χ (2)-tests. Age, BMI, and psychological and behavioural predictors of the common (prevalence greater than 20%) ROME III FGIDs were tested using logistic regression analyses. The criteria for at least one FGID were fulfilled by 83% of the ROME III cohort, and 94% of the ROME II cohort. There were no significant differences in age, BMI, lowest ever BMI, ED diagnostic subtypes or ED-related quality of life (QOL) scores between ROME II and ROME III cohorts. The most prevalent FGIDs using ROME III were postprandial distress syndrome (PDS) (45%) and irritable bowel syndrome (IBS) (41%), followed by unspecified functional bowel disorders (U-FBD) (24%), and functional heartburn (FH) (22%). There was a 29% or 46% increase (depending on presence or absence of cyclic vomiting) in functional gastroduodenal disorders because of the introduction of PDS in ROME III compared to ROME II. There was a 35% decrease in functional bowel disorders (FBD) in Rome III (excluding U-FBD) compared to ROME II. The most significant predictor of PDS was starvation (P = 0.008). The predictor of FH (P = 0.021) and U-FBD (P = 0.007) was somatisation, and of IBS laxative use (P = 0.025). Age and BMI were not significant predictors. The addition of the 6-mo duration of symptoms requirement for a diagnosis in ROME III added precision to many FGIDs. ROME III confers higher precision in diagnosing FGIDs but self-induced vomiting should be excluded from the diagnosis of cyclic vomiting. Psychological factors appear to be more influential in ROME II than ROME III.
Barrett's esophagus (BE) is a metaplastic lesion that may result from long-lasting gastroesophageal reflux and it is an established precursor of esophageal adenocarcinoma. There are reports of an increased prevalence of BE, and eventually esophageal adenocarcinoma, in patients with eating disorders characterized by purging behaviors like those with bulimia nervosa (BN). Among patients with eating disorders, those affected by anorexia nervosa binging purging subtype (ANBP), are behaviorally very similar to those with BN, but to our knowledge there are no data in literature about BE in patients with ANBP. We present the case of a 37-year-old female with a 20-year history of ANBP in comorbidity with bipolar disorder, who developed a BE requiring multi-specialistic intervention. © 2014 Wiley Periodicals, Inc. (Int J Eat Disord 2014).