Review

Eating disorders in adolescents with chronic gastrointestinal

and endocrine diseases
Jonathan T Avila, KT Park, Neville H Golden

Eating disorders are one of the most common chronic conditions in adolescents. The clinical symptoms can mimic Lancet Child Adolesc Health 2019
those of other chronic diseases including gastrointestinal and endocrine disorders. However, an eating disorder can Published Online
coexist with another chronic disease, making the diagnosis and management of both conditions challenging. This January 9, 2019
http://dx.doi.org/10.1016/
Review describes what is known about eating disorders in adolescents with chronic gastrointestinal and endocrine
S2352-4642(18)30386-9
diseases, focusing on coeliac disease, inflammatory bowel disease, diabetes, and thyroid disorders. The prevalence
Department of Pediatrics,
and onset of each condition during adolescence is discussed, followed by a description of the associations among Division of Adolescent
the conditions and eating disorders. We also discuss management challenges posed by the coexistence of the Medicine (J T Avila MD,
two conditions. When both diseases coexist, a multidisciplinary approach is often needed to address the additional Prof N H Golden MD) and
Department of Pediatrics,
complexities posed.
Division of Gastroenterology
(K T Park MD), Lucile Packard
Introduction interleukin-6 in patients with anorexia nervosa. These Children’s Hospital, Stanford
Eating disorders are prevalent in adolescents and young cytokines are known to play a role in regulation of both University School of Medicine,
Palo Alto, CA, USA
adults aged from 12 to 25 years. More than 90% of patients mood and appetite. Furthermore, auto­antibodies against
Correspondence to:
with eating disorders present before the age of 25 years. neuro-peptides involved in appetite regulation and the
Prof Neville H Golden,
Some other chronic medical conditions, including coeliac stress response have been identified in patients with Department of Pediatrics,
disease, inflam­matory bowel disease, diabetes, and thyroid Division of Adolescent Medicine,
disease, can also begin during adolescence and need to be Lucile Packard Children’s
dis­tinguished from an eating disorder when evaluating Key messages Hospital, Stanford University
School of Medicine, Palo Alto,
an adolescent for weight loss, vomiting, abdominal dis­ • Signs and symptoms of eating disorders can mimic those CA 94304, USA
comfort, dizziness, or menstrual dysfunction. However, of chronic gastrointestinal and endocrine diseases. ngolden@stanford.edu
emerging evidence shows that eating disorders and However, these diseases can also coexist.
chronic diseases can coexist1 and might even share • The approach to adolescents with an eating disorder and
common genetic susceptibilities,2,3 suggesting common a chronic gastrointestinal or endocrine disease should be
molecular pathways. Adolescents with chronic illness are multidisciplinary given the complexities in management
at high risk for engaging in unhealthy weight control of these conditions.
behaviours.4 Medications such as corticosteroids, used to • Adolescents with an eating disorder presenting with
treat some chronic medical conditions, can cause weight unexplained abdominal pain should be evaluated for
gain and body image dissatisfaction that can lead to coeliac disease and inflammatory bowel disease.
disordered eating. Diabetes and coeliac disease require • An elevated ESR or a low serum albumin concentration
attention to dietary intake for appropriate treatment, but should raise suspicion of inflammatory bowel disease.
preoccupation with dietary intake can become excessively • An eating disorder is one of the most common
restrictive, leading to weight loss and a fully developed comorbidities in patients with insulin-dependent
eating disorder. Finally, some medications such as thyroid diabetes. Intentional insulin omission is a common
hormone and insulin, used to treat certain chronic behaviour for weight manipulation, resulting in elevated
diseases, can be misused by an adolescent trying to lose glycated haemoglobin and other complications of
weight, making treatment of the chronic condition more persistent hyperglycaemia, including diabetic
challenging. ketoacidosis.
Evidence is emerging of links between eating disorders • Low triiodothyronine euthyroid sick syndrome is the most
and several autoimmune diseases with different genetic common thyroid function test abnormality seen in
backgrounds. Such diseases include coeliac disease, patients with malnutrition, and resolves with nutritional
inflammatory bowel disease, diabetes, and thyroid rehabilitation.
disorders,1,5,6 suggesting a possible role of autoimmunity • Surreptitious levothyroxine use (thyroiditis factitia)
in eating disorders. Evidence is also growing implicating might be seen in adolescents with an eating disorder who
changes in the microbiome and gut–brain interactions in have access to levothyroxine medication. Although their
the cause and course of anorexia nervosa.7 It has been thyroid function tests would be consistent with
postulated that exposure to microbes can result in hyperthyroidism, the absence of a goiter, a decreased
autoantibodies that could crossreact with neurons, radioactive iodine uptake, low thyroglobulin
possibly mediated via cytokines, and can play a role in concentrations, and high faecal thyroxine concentrations
the patho­ genesis of some neuropsychiatric illnesses.8 help to distinguish this condition from true hyperthyroid
A meta-analysis from 20189 found elevations in the pro­­­­­­­­ pathology.
inflammatory cytokines tumour necrosis factor-α and

www.thelancet.com/child-adolescent Published online January 9, 2019 http://dx.doi.org/10.1016/S2352-4642(18)30386-9 1

 Review

Bodyweight Fear of Negative feelings Dietary restriction Binge eating Purging

weight gain about shape or
weight
Anorexia nervosa, Decreased Yes Yes Yes No No
restrictive type
Anorexia nervosa, binge Decreased Yes Yes Yes Yes Yes
eating or purging type
Atypical anorexia nervosa Normal or increased Yes Yes Yes Sometimes Sometimes
Bulimia nervosa Normal or increased Yes Yes Sometimes Yes Yes
Binge eating disorder Normal or increased No Yes No Yes No
Avoidant restrictive food Decreased No No Yes No No
intake disorder
Rumination disorder Normal or decreased No No No No No
Pica Normal or decreased No No No No No

Table 1: Key clinical features of eating disorders per fifth edition of the Diagnostic and Statistical Manual of Mental Disorders criteria22

both anorexia nervosa and bulimia nervosa.10 Recent
interest in the gut–brain axis has led to the discovery of
changes in the composition and diversity of the gut
microbiome (dysbiosis) in both anorexia nervosa11–15 and
in inflam­matory bowel disease.16 Such alterations can
cause down­stream depletion of short chain fatty acids,
especially butyrate, which acts not only as a physical
barrier of protection along the intestinal mucosa but also
as a biochemical regulator of T-cell function. This
regulation is integral for correct recognition of self and
non-self in humans.17 Such a mechanism could explain
the coexistence of eating disorders with not only
gastrointestinal diseases but also diabetes18 and thyroid
disorders.19,20 We did the search according to PRISMA
guidelines.21
Diagnostic criteria for eating disorders
In 2013, the diagnostic criteria for eating disorders in the
fourth edition of the Diagnostic and Statistical Manual of
Mental Disorders were revised to improve clinical utility
of the diagnostic categories. Before the revision, the
majority of children and adolescents presenting to
clinical eating disorder programmes did not meet
diagnostic criteria for either anorexia nervosa or bulimia
nervosa, and were assigned the diagnosis of eating
disorder not otherwise specified.22,23 With the fifth edition
of the Diagnostic and Statistical Manual of Mental
Disorders (DSM-5),24 diagnostic criteria for anorexia
nervosa and bulimia nervosa are less stringent, and new
diagnostic categories have been introduced, including
avoidant restrictive food intake disorder and atypical
anorexia nervosa (table 1). Furthermore, eating disorder
not otherwise specified was eliminated as a diagnostic
category. As a result of application of the DSM-5 criteria,
there have been modest increases in the number of
children, adolescents, and young adults meeting criteria
for anorexia nervosa and bulimia nervosa.25,26
The key features of anorexia nervosa are persistent low
bodyweight, marked fear of weight gain, and disturbance
in the way that body image is experienced. Although the
specific cutoff for low bodyweight has been removed,
guidance suggests that a body-mass index less than the
fifth percentile for age indicates a low bodyweight. In
DSM-5, amenorrhoea has been removed as one of the
required diagnostic criteria for anorexia nervosa because
it does not apply to male patients, to female patients
before menarche, or to some female adolescents on
hormonal contraception. Atypical ano­ rexia nervosa
describes patients who meet all criteria for anorexia
nervosa, but despite substantial weight loss, their weight
is within or above the normal range.
Key features of bulimia nervosa are recurrent episodes
of binge eating and the use of inappropriate compensatory
behaviours such as self-induced vomiting, excessive
exercise, periods of starvation, or the use of laxatives,
diuretics, or diet pills to prevent weight gain. A binge is
defined as the consumption of an objectively large
amount of food in a discrete period of time, accompanied
by a subjective sense of loss of control over eating during
the episode. Patients with bulimia nervosa are usually of
normal bodyweight. Patients who binge but do not
engage in inappropriate compensatory behaviours are
assigned the diagnosis of binge eating disorder.
Avoidant restrictive food intake disorder describes
individuals who avoid some foods because of taste,
texture, colour, smell, or fear of vomiting, with their
reduced dietary intake leading to weight loss, failure to
gain weight, or interruption of growth. No fear of weight
gain and no body image concerns are present. In clinical
samples, between 5% and 23% of patients referred to
specialised adolescent eating disorder programmes meet
criteria for avoidant restrictive food intake disorder.25,27,28
Compared with patients with anorexia nervosa or bulimia
nervosa, adolescents with avoidant restrictive food intake
disorder are more likely to be younger and male.27,28
In DSM-5, rumination disorder and pica are included
under the broad category of feeding and eating disorders.
Rumination disorder describes the repeated regurgitation
of recently eaten food over a period of at least 1 month.
The regurgitated food might be re-chewed, re-swallowed,

2 www.thelancet.com/child-adolescent Published online January 9, 2019 http://dx.doi.org/10.1016/S2352-4642(18)30386-9


or spat out. The behaviour is not better explained
by gastrointestinal disease and does not occur during
an episode of anorexia nervosa, bulimia nervosa, or
avoidant restrictive food intake disorder. Although these
symptoms occur most commonly in infants and children
with intellectual disabilities, they can occur in children
and adolescents of normal intelligence.
Pica describes the ingestion of one or more non-
nutritive, non-food substances (such as hair, paper, paint,
among others) on a persistent basis for at least 1 month.
Pica can be observed with other medical and psychiatric
conditions such as developmental delay, autism spectrum
disorder, and schizophrenia, but is only given a separate
diagnosis if the symptoms are serious enough to warrant
additional clinical attention.
Epidemiology of eating disorders
Eating disorders typically arise during adolescence29 and
occur in all racial and ethnic groups. The highest
prevalence is in adolescent females. Approximately
5–15% of patients diagnosed with an eating disorder are
male, with a 9:1 female-to-male preponderance.30 The
proportion of male patients is higher in individuals
presenting under the age of 13 years, with a female-to-
male ratio closer to 6:1.31–33
The lifetime prevalence of anorexia nervosa, bulimia
nervosa, and binge eating disorder is estimated to be
0∙9%, 1∙5%, and 3∙5%, respectively for female individuals
and 0∙3%, 0∙5%, and 2∙0%, respectively for male
individuals.34 A large Dutch community cohort study26
found a lifetime diagnosis of any eating disorder in 5∙7%
of adolescent females and 1∙2% of adolescent males.
Mean age at onset was 15∙1 years (SD 2∙8) for anorexia
nervosa, and 16∙0 years (1∙9) for bulimia nervosa.26 In the
UK, there has been a modest increase in the incidence of
eating disorders from 2000 to 2009, with the highest
incidence in adolescent females aged 15–19 years.35 A
study from Denmark revealed that over the observation
period from 1995 to 2010, the most frequent age group at
first diagnosis of anorexia nervosa decreased from
16–19 years in 1995 to 12–15 years in 2010.36
Population-based estimates of the prevalence of avoidant
restrictive food intake disorder are not known, but
adolescents with avoidant restrictive food intake disorder
account for 12–23% of patients referred to specialised
adolescent eating disorder programmes.25,27,28,37 Adolescents
with avoidant restrictive food intake disorder differ from
individuals with other types of eating disorders. They are
more likely to be males, to be a younger age, and to have a
longer duration of illness.27,28,37,38 Similar to avoidant
restrictive food intake disorder, population-based estimates
of prevalence of atypical anorexia nervosa are not known.
Patients with atypical anorexia nervosa account for
approximately 30% of patients referred to specialised
adolescent eating disorder programmes28,39 and 25–50% of
all patients hospitalised on adolescent eating disorder
units.40,41 A study from Melbourne, Australia40 found that
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Review
the number of patients with atypical anorexia nervosa
requiring hospitalisation for medical instability grew five
times from 2005–10.
Specific eating disorders and chronic diseases
Coeliac disease
Coeliac disease is an immune-mediated enteropathy
triggered by gluten ingestion resulting in small bowel
inflammation and chronic nutrient malabsorption.
Approximately three million people in the USA
(paediatric prevalence of 1–13 per 1000) have coeliac
disease,42,43 the majority of whom are undiagnosed or
untreated.44 As the vast majority of patients with coeliac
disease have silent or subtle signs and symptoms,
characteristic poor weight gain and failure to thrive in an
adolescent or young adult might be the initial
presentation. Undiagnosed and untreated coeliac disease
can lead to substantial com­plications, including chronic
nutritional deficiencies, progressive bone loss and
derangements, increased risk of early osteoporosis and
non-traumatic fractures of hip and vertebrae, and
intestinal lymphoma. Given these concerns, it is
important to consider serological screening for coeliac
disease in any adolescent and young adult being
considered for diagnosis of an eating disorder. The
standard screening for coeliac disease involves a one-
time serological test for IgA antibodies to tissue trans­
glutaminase and total IgA. The combination of high
levels of tissue transglutaminase IgA with a normal IgA
while ingesting at least 3–10 g of gluten daily is both
highly sensitive and specific (>95%) for coeliac disease.45
Patients with a positive serological test often require
duodenal mucosal biopsy confirmation per American
consensus guidelines.
A 2015 population-based study5 described the
significant association between coeliac disease and
anorexia nervosa, both before and after the diagnosis of
coeliac disease. The investigators found the hazard ratio
for later development of anorexia nervosa in individuals
with biopsy-supported coeliac disease to be 1∙46 (95% CI
1∙08–1∙98), and a previous diagnosis of anorexia nervosa
was also associ­ ated with coeliac disease (odds ratio
[OR] 2∙18, 95% CI 1∙45–3∙29).5 In the same study, the
bidirectional association of the two diseases could imply
a shared genetic susceptibility or an incremental risk of
developing either anorexia nervosa or coeliac disease if
the other condition is present. The clinical implication of
this study is that misdiagnosis or delayed treatment of
coeliac disease can occur during the peak age of onset of
an eating disorder. Undiagnosed or misdiagnosed coeliac
disease and eating disorders can be devastating during a
particularly vulnerable period of growth and develop­
ment. It is important to note that both coeliac disease
and anorexia nervosa can present with non-specific
gastrointestinal discomfort, disordered defecation (either
constipation or diarrhoea), intestinal bloating, and failure
to thrive.
 Review
Recommended screening laboratory tests
Complete blood count
ESR
Serum chemistry panel
Liver function tests, albumin
Thyroid function tests (thyroid stimulating hormone, free thyroxine, triiodothyronine)
Urinalysis
25-hydroxyvitamin D
If amenorrhoea test for luteinising hormone, follicle stimulating hormone, oestradiol
If suspicious of gastrointestinal disease test for coeliac screen, stool calprotectin
If goiter on exam test for thyroid peroxidase antibodies, thyroid-stimulating immunoglobulins,
and antithyroglobulin antibodies
Expected findings in anorexia nervosa Findings suggestive of other gastrointestinal or
Complete blood count endocrinological chronic diseases
White blood cells: normal or decreased Complete blood count
Haemoglobin: normal or decreased White blood cells: can be increased in untreated
Platelets: normal or decreased coeliac disease or inflammatory bowel disease,
can also be normal; normal in thyroid disease
Decreased ESR and diabetes
Haemoglobin: decreased in inflammatory bowel
Chemistry panel disease and coeliac disease
Na+, K+, Mg, or P: normal or decreased Platelets: increased in inflammatory bowel disease
Transaminases: normal or increased and inflammatory conditions
Other laboratory tests Increased ESR in inflammatory bowel disease and
Thyroid function tests: decreased triiodothyronine other inflammatory conditions
Urinalysis: normal or increased ketones
(starvation) Chemistry panel
25-hydroxyvitamin D: often decreased Decreased Na+ and increased K+ in adrenal
insufficiency; increased glucose in diabetes
Albumin is decreased in inflammatory bowel
disease or chronic kidney disease
Other laboratory tests
Increased triiodothyronine in Graves’ disease
Urinalysis: increased glucose and sometimes
increased ketones in diabetes
Figure 1: Recommended laboratory tests in adolescents and young adults with weight loss, and expected
findings in anorexia nervosa and in other chronic gastrointestinal or endocrinological medical diseases
Inflammatory bowel disease
Inflammatory bowel diseases, consisting of Crohn’s
disease and ulcerative colitis, are chronic inflammatory
disorders of the gastrointestinal tract that are most
commonly diagnosed between adolescence and young
adulthood. Although it is common to have haematochezia
as one of the initial presenting signs of inflammatory
bowel disease, especially in ulcerative colitis, some
phenotypes of inflammatory bowel disease are more
indolent in disease progression.
An elevated ESR or a low serum albumin level in an
adolescent suspected of having anorexia nervosa, should
raise suspicion of inflammatory bowel disease (figure 1).
Similar to the subtle clinical progression of undiagnosed
coeliac disease, the indolent nature of some inflammatory
bowel disease presentations make co-occurrence with an
eating disorder in the adolescent and young adult cohorts
more probable. The clinician caring for suspected or
diagnosed patients with an eating disorder should be
mindful of the stool calprotectin screening test, which has
a more than 90% sensitivity for underlying inflam­matory
4 www.thelancet.com/child-adolescent Published online January 9, 2019 http://dx.doi.org/10.1016/S2352-4642(18)30386-9
bowel disease with quantitative calprotectin levels more
than 50 μg/g.46 Calprotectin, a calcium-containing protein
that makes up 60% of the cytosolic protein of neutrophils
and monocytes, is released during acute and chronic
inflammation.47 Having a low threshold for testing stool
calprotectin before treatment of an eating disorder is
advised as reliance on polymeric formula supplementation
in patients with anorexia nervosa to achieve daily caloric
needs can concomitantly treat undiagnosed small bowel
Crohn’s disease. Exclusive enteral therapy with use of
polymeric formulas has been shown to have a treatment
effect similar to corticosteroids during treatment
induction.48
The diagnosis of inflammatory bowel disease is made on
the basis of a combination of history, physical, and
laboratory findings, oesophagogastroduodenoscopy and
ileocolonoscopy with histology, and imaging of the small
bowel.49 Crohn’s disease of the duodenum, jejunum, and
ileum can be elusive to diagnose because of the relapsing
and remitting nature of the inflammation and the difficulty
of obtaining histopathology in the small intestine. It is not
uncommon for patients with isolated small bowel Crohn’s
disease to have negative results in endoscopic and
colonoscopic investigations. A referral to an inflammatory
bowel disease specialist and a targeted evaluation of the
small bowel are often necessary with use of advanced
endoscopic techniques (ie, enteroscopy or wireless capsule
endoscopy) or highly sensitive radiological imaging
(ie, magnetic resonance enterography).
In a large Finnish cohort6 of patients with anorexia
nervosa, bulimia nervosa, and binge eating disorder,
increased prevalence of gastrointestinal disease was largely
explained by Crohn’s disease (0∙6% in patients vs 0∙2% in
controls, OR 3∙1, 95% CI 1∙5–6∙3), and not by coeliac
disease (OR 1∙4, 0∙7–3∙1), or ulcerative colitis (OR 1∙6,
0∙7–3∙2). This increased prevalence of gastrointestinal
disease was significantly increased in patients with
anorexia nervosa, but not in individuals with bulimia
nervosa or binge eating disorder.6
In contrast to coeliac disease, bidirectionality of asso­
ciation between inflammatory bowel disease and eating
disorders has not been shown. However, given the
emerging relationship between dysbiotic gut microbiota
and inflammatory bowel disease, it would be forward-
thinking to consider dietary regimens that optimise
microbiota health in addition to meeting caloric goals
in the treatment of patients with eating disorders.
Specifically, while there is ongoing debate about whether
a typical diet of people in developed countries has causal
links to autoimmunity triggering new-onset inflam­
matory bowel disease, it is interesting to note the
evidence supporting the association of dysbiosis and
inflammatory bowel disease, especially in paediatric
Crohn’s disease.16 Reproducible research has shown that
there is loss of microbial diversity and total abundance of
commensal gut bacteria in patients with inflammatory
bowel disease, specifically depletion of bacteria from the

phyla Firmicutes and Bacteroidetes.50 Loss of bacterial
species from these phyla allows increased interactions of
the host immune system with the environmental
antigens within the mucosal lining of the intestinal
tract.17 Although the question of causality about diet and
inflammatory bowel disease continues, research has
shown that a diet high in animal fats and processed foods
is associated with an increased risk of developing Crohn’s
disease and ulcerative colitis. Conversely, regular intake
of foods rich in dietary plant fibres has been shown
to be protective against new-onset inflammatory
bowel disease.51 Therefore, in the management and
rehabilitation of patients with known eating disorders,
thoughtful consideration about incorporating plant-
based fibres in meals would optimise gut bacterial health
in a population with known dysbiosis.
Type 1 diabetes
Diabetes is one of the most common chronic conditions in
youth (less than 20 years), affecting approximately 0∙2% of
children and adolescents in the USA.52 Around 87% of new
cases of diabetes in adolescents are classified as type 1
diabetes,52 characterised by partial or total deficiency of
insulin production due to autoimmune destruction of
pancreatic β cells. More than 50% of patients with type 1
diabetes present after the age of 10 years.52 Weight loss,
along with polyuria and polydipsia, is one of the classic
presenting symptoms, and is often followed by rapid
weight gain after initiation of insulin therapy.53
Eating disorders represent one of the most common
psychiatric diagnoses in adolescents with type 1 diabetes,54
with a prevalence twice as high as in individuals without
diabetes.55 Although a coexisting eating disorder might
be more common in female adolescents,56 in a large
population-based study, adolescent males with type 1
diabetes were twice as likely to report body development
concerns and unhealthy methods of weight control
compared with their male peers without type 1 diabetes.4
Several factors associated with type 1 diabetes could put
these adolescents at risk for developing an eating disorder,
including but not limited to: disruption in typical eating
patterns, including having to calculate the carbohydrate
content of every meal and continually having to evaluate
the effect of food and exercise on blood glucose levels;
rapid weight changes at time of diagnosis and initial
treatment; psychological distress at time of diagnosis and
stressors of living with a chronic disease; and body image
emphasis as part of typical adolescent development.57,58
Intentional omission of insulin for weight loss purposes
is probably the most common unhealthy weight control
method used by patients on insulin therapy.54,58,59 This
behaviour has rendered the informal term diabulimia, a
portmanteau of diabetes and bulimia.54,58 Without insulin,
glucose cannot be metabolised, resulting in hyper­
glycaemia, glycosuria, and weight loss. The subsequent
hyperglycaemic state, as evidenced by elevated glycated
haemoglobin A1c (HbA1c), not only accelerates the
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Review
development of chronic complications of type 1 diabetes
but also increases the risk for acute medical complications
such as diabetic ketoacidosis.54 It is not surprising,
therefore, that intentional insulin omission is associated
with a three-times increase in mortality and a reduced
mean age of death by more than 10 years.60 The opposite
behaviour, intentional insulin overdose, has also been
described in patients with type 1 diabetes and bulimia
nervosa, done specifically to abate cravings for binge
eating.61 Although excess insulin leads to hypoglycaemia,
HbA1c in these patients is also typically elevated, suggesting
an overall hyperglycaemic state, probably from binge
eating followed by compensatory insulin omissions.
Carbohydrate avoidance is commonly observed in
patients with anorexia nervosa. With coexisting type 1
diabetes, carbohydrate restriction or elimination can
decrease insulin needs and lower HbA1C, which in turn
might be misinterpreted as an improvement in glycaemic
control. This behaviour also increases the risk for
starvation ketoacidosis and the rare complication of
euglycaemic diabetic ketoacidosis.62 Additionally, it also
impairs appropriate hepatic storage of substrates needed
for gluconeogenesis, thus increasing the risk of hypo­
glycaemia during the initial nutritional rehabilitation of
these patients.63 In patients with undiagnosed type 1
diabetes, the course of re-feeding could be atypical with
an inappropriately slow rate of weight gain, unusual
hunger or increase in appetite, or glycosuria. As
carbohydrate restriction lowers HbA1c, this serological
test could be unreliable in the evaluation of diabetes in
these patients.64 Other screening tests, such as 2 h
postprandial blood glucose levels, might be more helpful.
Type 2 diabetes
Type 2 diabetes is characterised by insulin resistance and
impaired glucose metabolism. Its incidence has
increased in children and adolescents, especially in the
USA, where it might be as frequent as type 1 in some
regions of the country.65 Obesity is the most common
comorbidity in youth (less than 20 years) with type 2
diabetes.65 As unhealthy weight control behaviours are
more common in overweight and obese people,66 it
should not be surprising that in the multicentre TODAY
study67 of adolescents with recent diagnosis of type 2
diabetes, 6% of the participants met criteria for clinical
binge eating, and 20% for subclinical binge eating. Binge
eating was associated with higher levels and rates of
extreme obesity, global eating disorder scores, depressive
symptoms, and impaired quality of life.67 In a systematic
review and meta-analysis of observational studies,
patients with bulimia nervosa were found to have an
increased risk for developing type 2 diabetes across all
studies, whereas for individuals with binge eating
disorder, the increased risk was seen only in cross-
sectional studies, but not in cohort studies.68 This finding
was important as obesity is more common in binge
eating disorder than in bulimia nervosa.69 The increased
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Thyroid disorders
Endocrinological dysfunction affecting the thyroid axis is
Thyroid gland
often seen in eating disorders.70 Normally, thyroxine is
metabolised into triiodothyronine by monodeiodination
at its outer ring. In starvation states, however, the
decreased secretion of leptin from adipose tissue
mediates thyroxine monodeiodination to occur at the
inner ring instead,72 resulting in the preferential
formation of reverse triiodothyronine, the metabolically
I I inactive isomer of triiodothyronine (figure 2).70 This
H
NH2
HO O C C H change results in low triiodothyronine euthyroid sick
H COOH syndrome, character­ ised by low triiodothyronine but
I I
Normal state Malnutrition
usually normal thyroxine and thyroid-stimulating
Thyroxine hormone (TSH) concentrations. Low triiodothyronine
I I I I
euthyroid sick syndrome is more commonly seen in
HO O R HO O R anorexia nervosa than in bulimia nervosa,70 with some
I
studies suggesting that low triiodothyronine is seen more
I
specifically during the periods between binge eating.73
Triiodothyronine Reverse triiodothyronine (inactive)
The decrease in triiodothyronine is a com­ pensatory
adaptation in starvation states to lower metabolic needs
Figure 2: Mechanism for low triiodothyronine euthyroid sick syndrome in malnutrition
and decrease energy imbalance, but it results in
In the normal state, thyroxine is converted to triidonthyonine (grey arrows). In malnutrition, thyroxine is bradycardia, hypothermia, and delayed deep tendon
preferentially converted to reverse triiodonthyronine (red arrows). R=CH2CH(NH2)(COOH) group attached to the reflexes.70 Following weight restoration, triiodothyronine
inner aromatic ring. concentrations normalise with resolution of these
clinical signs.70
Thyrotoxicosis factitia is another cause of reversible
Thyroid- Free Total Antibodies Other
stimulating thyroxine triiodothyronine abnormalities in thyroid function tests in patients with
hormone eating disorders. In thyrotoxicosis factitia, exogenous
Hashimoto’s Increased Decreased Decreased Thyroid peroxidase thyroid hormone is taken surreptitiously or in excess for
thyroiditis and weight control purposes.74 The resulting biochemical
antithyroglobulin profile is similar to that of hyperthyroidism, with low TSH
antibodies
and elevated thyroxine or triiodothyronine, or both. In
Low Normal or Normal or Decreased None Reversible with
contrast to true hyperthyroidism, the supraphysiological
triiodothyronine decreased decreased weight
euthyroid sick restoration thyroid hormones in thyrotoxicosis factitia lead to a
syndrome hypoactive thyroid gland with decreased iodine uptake,
Graves’ disease Decreased Increased Increased Thyroid- Enlarged thyroid so there is no enlargement of the thyroid gland (goiter).74
stimulating gland (goiter), Serum thyroglobulin and faecal thyroxine concentrations
immunoglobulin increased
radioactive
might be helpful in differentiating thyrotoxicosis factitia
iodine uptake from a true thyroid pathology.74 In thyrotoxicosis factitia,
Thyroiditis factitia Decreased Increased Increased None Decreased serum thyroglobulin concentrations are decreased and
thyroglobulin, faecal thyroxine concentrations elevated, whereas in either
increased faecal
silent thyroiditis or true hyperthyroidism, the reverse
thyroxine
pattern is expected (table 2).74
Table 2: Laboratory and imaging tests associated with different thyroid disturbances Although not as commonly seen as thyrotoxicosis
factitia or low triiodothyronine euthyroid sick syndrome,
a true thyroid pathology could also coexist with an eating
risk seen in bulimia nervosa could be in part due to an disorder, although there are no large population-based
association with hyperinsulinaemia or polycystic ovarian studies assessing its prevalence among patients with
syndrome, or both,70 which were not factored into the eating disorders. To date, there has only been a limited
analysis of the review. Hyper­ insulinaemic states, number of published case reports on the topic (17 on
commonly seen in type 2 diabetes due to impaired hyperthyroidism coexisting with an eating disorder, all
glucose metabolism, stimulate appetite and could in female patients,75–77 and two on hypothyroidism and
contribute to binge eating.70,71 These observations suggest anorexia nervosa, both in adolescents78,79). The prevalence
that patients with type 2 diabetes should be screened for of both disorders, however, might be higher than what
unhealthy methods of weight control, and that patients is suggested by the medical literature. In a study of
with binge eating disorder and bulimia nervosa should 50 adult women attending a thyroid clinic, three women
similarly be screened for type 2 diabetes. with hypothyroidism aged 26–29 years met criteria

6 www.thelancet.com/child-adolescent Published online January 9, 2019 http://dx.doi.org/10.1016/S2352-4642(18)30386-9


for bulimia nervosa.80 However, as two of the three
women also endorsed intentionally abusing their thyroid
hormone for weight loss, these cases could actually
represent thyrotoxicosis factitia rather than a truly
shared asso­ciation between hypothyroidism and bulimia
nervosa.
In the case reports of hyperthyroidism,75–77 elevated
triiodothyronine concentrations were associated with
binge eating or purging behaviours in adults but not in
adolescents. These behaviours also improved with
treatment of their thyroid disorder and normalisation of
triiodothyronine concentrations. Binge eating was likely
the result of appetite increase caused by elevated
triiodothyronine, similar to the relationship between
binge eating and hyperinsulinaemia discussed earlier.
In the case reports76,78,79 in which the thyroid disease and
the eating disorder were both diagnosed at the time of
presentation, the diagnosis of a thyroid pathology was
often masked because of normal thyroxine or triiodo­
thyronine concentrations, even when a goiter was
present. Yet, in all of these cases, TSH concentrations
were slightly above or below normal limits. With weight
restoration, thyroid function tests gradually became
more consistent with the underlying thyroid pathology,
whether hypothyroidism or hyperthyroidism. The initial
re-feeding course in these patients was often atypical as
well. For instance, in a case of undiagnosed hypo­
thyroidism, sinus bradycardia persisted despite weight
gain.78 In a case of undiagnosed hyperthyroidism, the re-
feeding course was notable for an inappropriately slow
weight gain, rise of heart rate above the normal range,
and temperature reaching low-grade pyrexia.76 In another
patient, the hyperthyroid-induced hypermetabolic state
coupled with dietary restrictions from the eating disorder
led to multivitamin deficiency with subsequent severe
polyneuropathy from deficient amounts of vitamins E,
B6, and folic acid,77 and could have increased the risk of
electrolyte deficiencies in another patient.75
Treatment of the underlying thyroid disorder can be
challenging in the setting of an eating disorder due to a
patient’s desire to remain in a hypermetabolic state to
facilitate weight loss, fear of weight gain with treatment,
and self-induced vomiting of the thyroid medication. As
a result, non-adherence was commonly observed in
patients with hyperthyroidism, and thyroid medication
abuse (as in thyrotoxicosis factitia) has been observed in
individuals with hypothyroidism.
Conclusion
Eating disorders and some chronic gastrointestinal
and endocrine diseases begin during adolescence and
frequent­­
ly present with similar symptoms. The
conditions can be misdiagnosed inter­ changeably, but
they can also coexist, making manage­ment challenging.
Adolescents with a suspected eating disorder should be
screened for coeliac disease, inflammatory bowel disease,
diabetes, and thyroid disease, especially when symptoms
www.thelancet.com/child-adolescent Published online January 9, 2019 http://dx.doi.org/10.1016/S2352-4642(18)30386-9 7
Review
Search strategy and selection criteria
We searched PubMed and MEDLINE for articles published
between Jan 1, 1995, and June 30, 2018 with the terms:
(“chronic disease”, “diabetes mellitus”, “celiac disease”,
“inflammatory bowel diseases”, “ulcerative colitis”, “thyroid
disease”) AND (“anorexia nervosa”, “binge eating disorder,”
“avoidant restrictive food intake disorder” OR “bulimia
nervosa”) according to PRISMA guidelines. These specific
chronic medical illnesses were selected on the basis of the
chronic medical diseases most frequently encountered in
adolescents with eating disorders treated in a large
specialised multidisciplinary adolescent eating disorder
treatment programme located within a tertiary care
children’s hospital. We focused on comorbid medical diseases
in which the coexistence of both diseases could make
management difficult. We searched only for articles published
in English or those translated into English involving
adolescents or young adults and excluded animal studies
(appendix). Additionally, supplemental searches for the See Online for appendix
separate topics in this Review were done. We included
randomised controlled trials, observational studies,
retrospective studies, meta-analyses, review articles,
editorials, case reports, and other relevant articles.
are not typical for the eating disorder. Similarly,
adolescents with chronic gastrointestinal and endocrine
diseases should be screened for unhealthy methods of
weight control. When an eating disorder coexists with a
chronic disease, frequent communication among health-
care professionals is advised. The con­tinued discovery of
possible genetic, immunological, and environmental
factors shared by eating disorders and chronic medical
diseases will increase our under­ standing of the
mechanisms under­ lying the shared pathogenesis of
these conditions.
Contributors
NHG drafted the manuscript. JTA did the systematic review.
NHG contributed to the introduction, search strategy and selection
criteria, diagnostic criteria, epidemiology, and conclusion.
JTA contributed to the sections on diabetes and thyroid disorders.
KTP contributed to the sections on coeliac disease and inflammatory
bowel disease. All authors reviewed and edited the manuscript and
accept responsibility for the accuracy and integrity of the work.
Declaration of interests
KTP reports grants from the Crohn’s & Colitis Foundation, Takeda
Pharmaceutical, Abbvie, Prometheus, and Inova Diagnostics, all outside
the submitted work. JTA and NHG declare no competing interests.
Acknowledgments
Supported in part by The Mary Gallo Endowed Postdoctoral Fellowship
Fund (JTA), National Institutes of Health—National Institute of Diabetes
and Digestive and Kidney Diseases (DK094868), Crohn’s & Colitis
Foundation (KTP), and National Institutes of Health—Eunice Kennedy
Shriver National Institute of Child Health and Human Development
(RO1 HD082166; NHG).
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