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Psychosomatics 49:399-406, September-October 2008
doi: 10.1176/appi.psy.49.5.399
© 2008 Academy of Psychosomatic Medicine
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Eating Pathology in Adolescents With Celiac Disease

Andreas Karwautz, M.D., Gudrun Wagner, M.Sc., Gabriele Berger, M.D., Ursula Sinnreich, M.D., Vasileia Grylli, Ph.D., and Wolf-Dietrich Huber, M.D.

Received September 3, 2006; revised January 9, 2007; accepted January 19, 2007. From the Medical University of Vienna (Austria) Eating Disorders Unit at the Dept. of Child and Adolescent Psychiatry and Gastroenterology Unit at the Dept. of Pediatrics and Adolescent Medicine. Send correspondence and reprint requests to Prof. Andreas Karwautz, Dept of Child and Adolescent Psychiatry, Medical Univ. of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. e-mail: andreas.karwautz{at}meduniwien.ac.at
© 2008 The Academy of Psychosomatic Medicine


  ABSTRACT

 
TOP
 ABSTRACT
INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 
BACKGROUND: Celiac disease (CD), treated by a gluten-free diet, may represent a nonspecific trigger for the development of eating pathology, particularly in adolescence. OBJECTIVE: The authors sought to perform a systematic study on eating pathology in CD. METHOD: CD patients were assessed for eating disorders by questionnaire, and body mass index was recorded. RESULTS: There was a higher rate of eating pathology in CD patients than would be expected, especially, a higher rate of bulimia nervosa. This subgroup reported more noncompliance with the gluten-free diet and had higher scores on most eating-related questionnaires. In most cases, diagnosis of CD preceded the onset of eating pathology. CONCLUSION: The authors recommend asking early-adolescent CD patients whether they are also dieting for aesthetic reasons.


  INTRODUCTION

 
TOP
 ABSTRACT
 INTRODUCTION
METHOD
 RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 
In adolescence, chronic medical diseases may lead to psychological burden, severe psychiatric disturbance, deterioration of compliance, and coping problems. The mechanisms relating chronic disease to psychological disturbance have been described in a vast literature.1–3 A number of these studies have investigated the relationship between chronic illnesses and eating pathology.4–6 Specifically, diabetes mellitus type 1 (DM-1) has been frequently shown to be related to a higher prevalence rate of eating pathology in adolescent populations.7–9 However, there are some prevalence studies of eating disorders in young women with DM-1 that negate this finding, with data demonstrating that eating disorders are no more common than in similar non-diabetic populations.10–13

Celiac disease (CD), also known as celiac sprue and gluten-sensitive enteropathy, is a common, immune-mediated condition triggered by the ingestion of gluten. Gluten causes an injury of the small intestinal mucosa, leading to partial, subtotal, and total atrophy. Removal of gluten from the diet leads to full clinical remission and restoration of the small intestinal mucosa. The protein gluten consists of glutenins and prolamins, which, in wheat, are called gliadins; in barley, hordeins; in rye, secalins; and, in oats, avenins.14 Environmental (such as viral or bacterial infections, or food), genetic (HLA type), and immunological factors influence the occurrence of celiac disease. Depending on the grade and the extension of the mucosal damage, patients present with various symptoms caused by intestinal malabsorption. Failure to thrive, diarrhea, vomiting, bad temper, inappetence, and anemia are the most common symptoms at presentation. CD commonly affects people in early childhood and adolescence, with an age at onset similar to DM-1.

Auto-antibodies, such as anti-endomysial antibodies (EMA) and anti-tissue-transglutaminase-antibodies (ATGA), can be used as a screening tool, but small-bowel biopsy is still required for a diagnosis of CD.15,16

There are several reasons why CD could serve as a risk factor for the development of an eating problem in some adolescents, via a number of mechanisms: Chronic dietary restraint, gluten-free diet (GFD), food preoccupation, food awareness, interference with growth, pubertal delay, weight gain during treatment, the nonspecific burden of chronic illness, and impaired development of autonomy could act as vulnerability factors and triggers for this course.

Because the GFD is currently the only therapy for celiac disease, the high and persistent awareness of food and food intake required of patients may act as a risk factor for altered eating behavior.17,18 GFD puts a chronic, restrictive burden on the patient19 and has several other disadvantages, each of which may act as a specific risk factor for developing eating problems: For example, gluten-free products are less palatable, often more expensive, and not always available in all restaurants or shops, thus creating negative peer-group pressure. Food labeling is not consistent. Most importantly, contamination of gluten-free food may occur at each stage of production, thereby leading to gastrointestinal symptoms. Treatment-induced weight gain can also act as a risk factor,20,21 especially in adolescence. Many children with CD are underweight and present with growth retardation. Among women with CD, BMI was below 20 in 29% of the patients.22 As a result, a reduced quality of life and a problematic acceptance and noncompliance with dietary regime23 is frequently seen in the majority of children and adolescents with CD, in particular, those between 12 and 17 years. of age.24

The pathogenesis of the comorbidity between CD and eating disorders can be explained by different mechanisms leading to eating pathology in this population: self-control of eating behavior is indispensable for successful treatment in CD. Permanent preoccupation with food and the right selection of food drives the cognitive focus increasingly onto eating behavior. On the other hand, restrictive or controlled food intake can increase the risk of binge eating, which, consequently, could lead to compensatory weight behaviors. Thus, the diagnosis of CD in adolescence may lead to weight gain when following the GFD, which, in turn, might increase body dissatisfaction and trigger the development of eating pathology by increased dieting, bingeing, and the use of compensatory behaviors.25

In addition to these specific problems, psychiatric symptoms and disorders (according to the brilliant systematic study by Pynnönen et al.26) are common in CD. Major depressive disorder, dysthymic disorder, panic disorder, and behavioral disturbances have been observed in adult and adolescent CD patients.27–30 Psychiatric symptoms appear to be most prevalent in subjects affected by severe classical CD with onset at an early age.27 Focusing on eating pathology, CD has been found to be a covert problem in patients presenting with an eating disorder and has to be considered as a differential diagnosis in all syndromes associated with malabsorption, abdominal bloating and discomfort, and growth and pubertal delay (Yucel et al.31 presented the case of one adult woman). We found four case reports finding an association between eating disorder and CD.26,28,32,33 Seven percent of 29 CD patients (N=2) had an eating-disorder lifetime diagnosis, and CD preceded the eating-disorder diagnosis.26 However, so far, there have been no systematic studies specifically focusing on eating pathology in adolescent patients with CD.

We therefore aimed to perform the first systematic study on the prevalence and clinical manifestations of eating pathology in a larger group of adolescents with CD, to look at the time course and gender differences, and also to compare eating pathologies in CD patients with those in DM-1 patients and in normative control subjects. We specifically aimed 1) to assess the current and lifetime rates of eating pathology in adolescent patients with CD; 2) to evaluate the temporal relationship between the diagnosis of CD and the onset of eating pathology; 3) to compare the clinical features of CD and the findings of questionnaires measuring eating-related pathology in patients with and without eating pathology, including the evaluation of gender differences; and 4) to compare the prevalence rates of eating pathology as well as the results of the eating-disorder questionnaires in CD with those in DM-1.


  METHOD

 
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 
Participants and Procedure
We approached adolescent patients diagnosed with CD after small-bowel biopsy. We used a two-stage design, screening patients with CD for eating pathology and related psychopathology in the first stage, using the Eating Disorder Inventory (EDI–2) and the Eating Disorder Examination Questionnaire (EDE–Q), calculating body-mass index (BMI), taking a detailed medical and social history, and estimating relevant laboratory data (EMA, ATGA). In the second stage, all patients meeting predetermined cut-off criteria and a similar number of patients below the cut-off (see below; randomly selected from all patients below cut-off) were interviewed for eating-disorder pathology (both current and lifetime) by use of the Eating Disorder Examination (EDE).

Cut-off criteria were either 1) a BMI <10th percentile and an EDE–Q Restraint, Shape or Weight Concern scale score ≥2; or 2) current bingeing, vomiting, use of laxatives, or eating gliadin-containing food in order to influence shape and weight (assessed by EDE–Q and one additional and modified item regarding gliadin); or 3) one of the following: EDI–2 scores: Drive for Thinness ≥9, Bulimia ≥5, Body Dissatisfaction ≥15.

The classification of eating disorders was based on the Eating Disorder Examination interview. Patients were diagnosed with a full-syndrome eating disorder according to DSM–IV (anorexia nervosa; bulimia nervosa; or eating disorders, not otherwise specified). Violating dietary restrictions ("gluten purging") in order to cause diarrhea and influence shape and weight have been included in purging behaviors.

We also assessed milder forms of eating disorders, called subclinical EDs (SED; as reported in Grylli et al.7) which were diagnosed in patients who met one of the following criteria: 1) occasional binge eating (3 or more episodes; for subsyndromal binge eating disorder, almost all of the proposed research criteria of binge eating disorder have been met except one), or occasional purging (including "gluten purging") during the past 3 months; 2) repeated chewing and spitting-out of food to prevent weight gain (at least once per week over the preceding 3 months or twice per week during the past 4 weeks); or 3) regular extreme dietary restraint (<2.1 mega-joules/day) or excessive exercising (more than 120 minutes, 5 times per week) for the purpose of weight loss during the past 4 weeks, in the absence of binge eating; or 4) problems with body image or eating attitudes, as indicated by a mean score of 2-or-more on the EDE Weight Concern subscale or a mean score of 2-or-more on the EDE Shape-Concern subscale.

We assessed lifetime as well as current eating-disorder status; 339 adolescent patients with CD (age range: 10 years–20 years) were approached through the Gastroenterology Unit, Dept. of Pediatrics, Medical University of Vienna, the Celiac Societies of Austria and Germany (self-help-organizations for CD patients), and the pediatric hospital centers in Austria. Fifty-six patients had to be excluded from further analysis because they did not meet the inclusion criteria: 4 did not fulfill the 1-year CD duration criterion; 16 had comorbidity (DM-1, ulcerative colitis, Crohn’s disease); 2 were intellectually challenged and not able to take part; 5 had no proven CD diagnosis; and 29 did not return the Stage 1 questionnaires; thus, 283 CD patients met full inclusion criteria. For control purposes, data from Austria28 on DM-1 (assessed with similar procedures and instruments), published previously,7 and EDI–2 data derived from schools (N=1,080 girls, mean age 17.7 years; standard deviation [SD]: 2.2; N=580 boys, mean age 13.7 years; SD: 2.0)28 were used. The control populations were similar in age and sex.

Measures for Stage 1
The Eating Disorders Inventory (EDI–2; German version34)
This is a widely-used self-report measure designed for the assessment of attitudinal and behavioral dimensions relevant to EDs. The EDI–2 has 91 items (in 11 subscales) and has also been validated in school children age 10–20 years.34 We adapted this version for use in CD patients (e.g., asking for "dieting for shape and weight reasons" instead of "unspecified dieting" in order to reduce the false-positive answers in a population adhering to a diet for medical reasons).

The Eating Disorder Examination Questionnaire (EDE–Q)
This is the self-report version of the Eating Disorder Examination (EDE), a semistructured interview for the assessment of the specific eating-disorder psychopathology. We used the German version, which was validated by Hilbert et al.35 In samples with anorexia nervosa, bulimia nervosa, and atypical eating disorders, and nonclinical, subclinical, and psychiatric comparison groups, the EDE–Q subscales of Dietary Restraint, Eating Concern, Weight Concern, and Shape Concern, and the global score were highly internally consistent. The German version of the EDE–Q appears well-suited for the assessment of specific eating-disorder psychopathology in clinical research and practice.35

IgA Anti-Endomysial Antibodies (EMA) in serum have been measured by means of indirect immunofluorescence assay, using cryostat sections of monkey esophagus (INOVA Diagnostics Inc., San Diego, CA, U.S.). Any positive readings (+ to +++++) in the immunofluorescence of a serum diluted 1:10 were considered as positive. IgA endomysial antibodies are considered the most powerful screening tool because sensitivity and specificity both almost approach 100%.36 IgA transglutaminase antibodies (ATGA) have been determined by using an chromogenic enzyme immunoassay, based on human recombinant antigen (Eu-tTG, Fa Eurospital, Trieste, Italy). Both EMA and ATGA show high sensitivity and specificity in the various phases of CD and have proven to be effective in screening tests for atypical forms as well as for silent or latent CD and for overall compliance with treatment in patients with CD.37

Measure at Stage 2
The Eating Disorders Examination/ Version 12.0 D (German version; Hilbert38)
This is a semistructured diagnostic interview that quantifies the symptoms, behavior, and psychopathology of eating disorders and allows eating disorders to be diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders (DSM).39 This interview is the gold standard for the standardized assessment of eating disorders and has good reliability and validity. For the purposes of our study, we use a modified version to evaluate CD-specific behaviors related to eating disorders and to determine whether eating behavior was motivated by CD management or by "weight and shape" reasons. (All involved investigators have received rater training by Dr. A. Hilbert/Marburg/Lahn, Germany.)

Statistical Analysis
We used t-tests, U tests, chi-square tests, and Fisher’s exact tests, and ANCOVA, as appropriate. To account for multiple testing, the Bonferroni post-hoc correction method was used. All statistical procedures were performed with SPSS for Windows (Version 14).


  RESULTS

 
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
DISCUSSION
 CONCLUSION
 REFERENCES
 
Participants
Of all 283 CD patients (210 girls, age 14.8 [3.0] years; 73 boys, age 13.9 [2.7] years) screened for eating pathology, 200 (70.7%) scored below cut-off, and 83 (29.3%) were above cut-off for eating pathology. In the second wave, 168 patients with CD were interviewed in-person with the EDE over the telephone. All 83 patients above the cut-off (100%) and 85 (42.5%) below were interviewed; thus, there was a similar number in both groups. Four patients above cut-off could not be reached for the EDE interview. (Demographics and clinical characteristics are shown in Table 1.)


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TABLE 1. Demographics and Celiac-Disease Characteristics in Teen-Aged Girls With Celiac Disease/Eating Pathology Versus Those With Celiac Disease/No Eating Pathology



Antibodies in the CD Population
The latest available IgA antiendomysial antibodies (EMA) titer in serum revealed a positive value in 25% of the female adolescent patients and in 10% in the male patients (the female/male difference was significant: {chi}2 = 5.03; p=0.025). The latest available IgA and IgA transglutaminase antibody (ATGA) values were positive in 16.9% and 24.2% of the girls, respectively, and in 13.6% and 10% of the boys, respectively (the female/male difference was significant for IgG ({chi}2 = 4.9; p=0.032).

Prevalence of Eating Pathology in CD
We analyzed the lifetime history and current presence of eating pathology (eating disorder [ED] and subclinical eating disorder [SED]) in 283 adolescent patients with CD. All patients affected by an ED or SED were girls. Eleven girls (4.8%) had a lifetime history of ED (1 anorexia; 4 bulimia nervosa; 6 eating disorder, not otherwise specified), and 8 (3.9%) had a current ED (all 8 with eating disorder, not otherwise specified). Also, 21 girls (10.2%) had a lifetime history of SED, and 22 (10.7%) had a current SED.

Antibody Comparison of CD With and Without Eating Pathology
There were significant differences between the EMA and ATGA-IgG scores between patients with CD + eating pathology and those without (28% versus 14.4%), but only a trend for higher values of ATGA-IgA in those with SED. Latest available EMA and IgG values were significantly more often positive in those with comorbid eating pathology. Patients with comorbid eating pathology were more often noncompliant with their GFD (defined here as noncompliant with diet ≥2 times per month; Table 1).

Findings in Female CD Patients
The girls with eating pathology (N=32) were older and had a higher BMI than those without eating pathology (N=174). Thus, we included age and BMI in the further ANCOVA comparisons as covariates. Age at diagnosis of CD and the duration since the diagnosis of CD did not differ in the two groups (Table 1). Regarding the time order of onset of CD and ED, we found that 85.7% of the patients had the CD diagnosis earlier than the ED diagnosis, and in only 14.3% did the ED precede the CD diagnosis. In those with CD before ED, the time period between diagnosis of CD and onset of eating pathology was between 2 and 17 years (mean: 9.87; SD: 4.7). Looking at clinical presentation, we found the following weight-loss behaviors among the girls with CD and eating pathology (all EDs and SEDs taken together: N=32): 58.1% used dieting, 12.9% used excessive exercising, 19.4% used vomiting, and 3.2% abused laxatives. Female CD patients with and without eating pathology differed in several scales of self-report questionnaires measuring eating-related psychopathology and ED symptoms: except for maturity fears and perfectionism, which showed only a trend toward higher scores in those affected by a comorbid ED or SED, all other scales of the EDI–2, the EDE–Q and the EDE Interview were significantly more pathological in the group with comorbid eating pathology (including BMI and age as covariates in the ANCOVA). Comparing the EDI–2 findings in girls with CD and those from a large number of normative controls similar in age (published by Rathner and Waldherr34) showed significantly less pathology in the entire group as well as in those without eating pathology.

Findings in Male CD Patients
We found no male patient with ED or SED. In general, the male patients had significantly less eating pathology, as compared with a large number of normative control subjects matched for age,34 except for the scales Drive for Thinness, Bulimia, Body Dissatisfaction, and Maturity Fears. The male CD patients also had a significantly lower EDI–2 Total score than the control subjects.

Comparison of Patients with CD and DM-1
To gain insight into the specificity of our data for CD, we compared adolescents with CD+eating pathology to a population of adolescents similar in age suffering from DM-1+eating pathology (Table 2). The results of the DM-1 prevalence study, which used the same methodology, have previously been reported.7 Female CD patients had lower prevalence rates of EDs (5.3%) and SEDs (10.2%) than female patients with DM-1 (EDs: 11.5%, SEDs: 13.5%), but these were not statistically significant (except for "eating disorder, not otherwise specified," which was more common in DM-1: 9.4% versus 2.9%). Comparing patients with CD and DM-1 and comorbid EDs and SED on weight-loss measures, we found no significant difference between the two groups, other than "insulin manipulation" as an important measure of DM-1 patients (26.1%) and "vomiting" in one-fifth of cases with CD (19.4%). "Dieting for shape and weight reasons" was the most common behavior found in CD patients with EDs (58.1%), whereas "excessive exercising" was not as common in CD (12.9%) as in DM-1 patients (30.4%).


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TABLE 2. Eating-Disorder Diagnoses According to EDE Interview and Weight-Loss Measures in Adolescent Female Patients With Celiac Disease or Type 1 Diabetes




  DISCUSSION

 
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
CONCLUSION
 REFERENCES
 
We performed the first systematic study on the prevalence and clinical manifestations of eating pathology in a larger group of adolescents with celiac disease (CD), looked at time-course and sex differences, and compared the clinical and eating-disorder (ED)-relevant data in CD patients with and without comorbid EDs and subclinical EDs (SEDs), as well as with normative control subjects and DM-1 patients.

We found a higher rate of EDs and SEDs in the patients with CD than would be expected from prevalence estimates generally agreed on for female adolescents in the United States and European countries (0.5% anorexia nervosa, 1.0% bulimia nervosa, as reported by Hoek40). The prevalence rate of ED (not otherwise specified) was 2.9% in female CD patients; however, there are no generally accepted rates for nonspecific ED in the literature that can be used for comparison. We found no male cases with EDs or SEDs, which is comparable to the low rates in all United States and European studies. Diagnosis of CD preceded the onset of an ED or first symptoms of eating pathology by between 2 and 17 years in the majority of cases (86%); thus, if there is a causal connection between CD as chronic illness and the development of an ED, this evidence could be strengthened by the data reported here. Looking at clinical presentation, we found that more than half of CD patients with an ED used dieting for shape and weight reasons; one-fifth used vomiting and exercising, and laxative abuse was relatively uncommon in this population.

Comparing female CD patients with and without eating pathology, the former were older and had a higher current mean BMI. Patients with eating pathology reported more noncompliance with their GFD, thus leading us to suspect that those with more diet noncompliance could be harboring an eating disorder.

Patients with eating pathology had, as expected, higher scores on nearly all EDI–2, EDE–Q, and EDE scales than CD patients without eating pathology. Female CD patients, regardless of their eating-disorder status, scored lower on all scales than normative control subjects (also including undiagnosed eating-disordered subjects), and female CD patients without eating pathology showed less eating-related pathology measured using the EDI–2 than did normative school controls. Less eating pathology has also been found in diabetes populations, who also rated lower in several scales measuring psychological symptoms and body complaints,1 thus leading to the speculation that some adolescents with chronic diseases present as "supernormal" in self-report measures. Boys with CD did not suffer from EDs or SEDs; however, the boys without CD had significantly lower eating pathology than did school control subjects.

Comparing female CD and DM-1 patients similar in age and using similar assessment strategies, we found a trend toward lower prevalence rates of EDs and SEDs in CD patients, which was statistically significant only for those with nonspecific ED.

For reasons of specificity, we compared CD and DM-1 populations and found no significant clinical difference between the two groups (besides insulin manipulation as an important measure in DM-1 patients and vomiting in one-fifth of CD+ED patients). Dieting for shape and weight reasons, however, was most commonly used in CD+ED, whereas excessive exercising was not as common in CD as in DM-1 patients.

This study has both strength and limitations. It is the first systematic study with a larger number of young CD patients from a relatively homogeneous socioeconomic background. We investigated prevalence and clinical aspects of EDs with a two-stage design and contemporary self-report and interview measures and sex- and age-matched control groups.

We have not interviewed a group of schoolchildren with the EDE, and there are no available Austrian prevalence data on EDs. To overcome this, we also compared our CD group (without eating pathology) with controls from the literature34 and with earlier published data on DM-1.7,41 Interviews performed via telephone could yield results different from those of face-to-face interviews; however, a recent study found that participants tend to answer significantly more carefully via phone, even on very sensitive topics.42 Further studies are required to look at predictors for the development of eating pathology in CD patients.

We recommend that healthcare professionals who treat patients with CD be aware of the possibility of eating pathology, particularly in those patients with a higher BMI and positive IgG and EMA antibodies. Clinicians should routinely inquire about weight and "shape" concerns, dieting, and vomiting for weight control. The use of eating-disorder screening instruments for the early identification of eating pathology would be useful and should be implemented in the treatment of patients with CD.

Clinic-based group interventions or more intensive treatments, including family-based components, should be provided for those with eating pathology, given that they have shown effectiveness in a diabetic population.25,43 However, we need further systematic research on intervention strategies for eating pathology in patients with CD.


  CONCLUSION

 
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 CONCLUSION
REFERENCES
 
Results of this first large systematic study on comorbidity of CD and eating disorders/subclinical eating disorders indicate that female adolescent CD patients, particularly, those with a higher BMI and who were older, had higher prevalence rates of eating pathology than expected,. We recommend asking CD patients about dieting for shape and weight reasons in early adolescence. Results also confirmed that CD and DM-1 are chronic illnesses that place adolescents at greater risk for developing disordered eating behavior than their peers without such chronic illness.9 We suggest assessing this problem with investigator-based interviews, rather than with self-report measures, although this method has effectively identified youths with eating pathology.


  ACKNOWLEDGMENTS

 
This study was presented in part at the Annual Meeting of the Academy for Eating Disorders, Barcelona, Spain, June 2006.

We thank all the patients, the cooperating centers (LKH Wels, LKH Klagenfurt, LKH Villach, Preyerkinderspital, LKH Graz, LKH Salzburg), the Austrian and the German Celiac Society, and medical students Astrid Eisenkölbl, Martina Cislakova, and Helga Hürner for their invaluable help in conducting the study.

We are grateful to Dr A. Hilbert for training us in the use of the German version of the EDE; Prof. Dr. Christian Wöber, Medical University of Vienna, for helpful comments on the manuscript; and Prof. Dr. Barbara Cooper, McMaster University, Hamilton, Ontario, Canada, and Prof. James G. Cooper, Syracuse University, Florence, Italy, for correcting the English text.

This study was supported by a grant of the "Jubiläumsfonds of the Austrian National Bank" (grant 11086) to AK.


  REFERENCES

 
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 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 CONCLUSION
 REFERENCES
 

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