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AbstractObjectivesAdolescents with functional abdominal pain (FAP) often experience pain and other gastrointestinal symptoms in the context of eating, which may place them at risk for eating disorders. This study compared disordered eating and its sequalae in adolescents with FAP to those with chronic headache.MethodsParticipants in this retrospective chart review study were 270 adolescents and young adults (mean age 15.9; standard deviation [SD] = 1.63; 60% female) attending an intensive, interdisciplinary pain treatment program, including 135 youth with FAP and an age‐ and gender‐matched control group with a primary pain diagnosis of chronic headache. Information was extracted related to eating‐ and weight‐related symptoms.ResultsIndependent t‐tests and χ2 analyses found that compared with adolescents with chronic headache, patients with FAP showed significantly more eating pathology as reflected by scores on the Eating Attitudes Test—26 (EAT‐26) (p < 0.001), endorsement of pain‐related restrictive eating (p < 0.01), eating disorder history (p < 0.001), and avoidant restrictive food intake disorder (ARFID) diagnoses (p < 0.001). Compared to those with chronic headache, significantly more patients with FAP had lost 10 pounds or more (p < 0.01) and a higher proportion were underweight (p < 0.001). Among all participants, a history of exclusion diets used to manage symptoms significantly increased the risk for ARFID (p < 0.001).ConclusionThe results of this study highlight the increased risk of eating‐related concerns among youth with FAP, as well as the judicious use of exclusion diets to manage symptoms in these patients.

Introduction Subjectively experienced cognitive difficulties are common in youth with postural orthostatic tachycardia syndrome. The pathophysiological and psychological contributions of these cognitive impairments remain unclear. Method Participants were 96 adolescents and young adults diagnosed with postural orthostatic tachycardia syndrome and admitted to an intensive pain treatment program. Participants completed cognitive assessment and measures of postural orthostatic tachycardia syndrome symptoms, pain intensity, pain catastrophizing, anxiety, depression, and functional disability. Results Self-reported autonomic symptom intensity, but not severity of heart rate change, was associated with cognitive performance. Symptoms of depression were associated with decreases in most measures of cognitive functioning. Pain intensity, pain catastrophizing, and depression but not cognitive scores and physiological measures, were significant predictors of disability. Conclusion Depression appears to be a significant contributor to the cognitive difficulties in youth with postural orthostatic tachycardia syndrome. These findings highlight the importance of assessing and treating affective symptoms in this population along with medical and lifestyle approaches to treating postural orthostatic tachycardia syndrome symptoms.

Abstract Objective Anorexia nervosa (AN) and atypical AN are conceptualized as distinct illnesses, despite similar characteristics and sequelae. Whereas DSM‐5 differentiates youth with AN and atypical AN by the presence of clinical ‘underweight’ (i.e., 5th BMI percentile for age‐and‐sex (BMI%)), we hypothesized that using this weight cut‐off to discern diagnoses creates a skewed distribution for premorbid weight. Method Participants included hospitalized youth with AN ( n = 165, 43.1%) and atypical AN ( n = 218, 56.9%). Frequency analyses and chi‐square tests assessed the distribution of premorbid BMI z ‐scores (BMIz) for diagnosis. Non‐parametric Spearman correlations and Stepwise Linear regressions examined relationships between premorbid BMIz, admission BMIz, and weight loss in kg. Results Premorbid BMIz distributions differed significantly for diagnosis ( p < .001), with an underrepresentation of ‘overweight/obesity’ (i.e., BMI% ≥ 85th) in AN. Despite commensurate weight loss in AN and atypical AN, patients with premorbid ‘overweight/obesity’ were 8.31 times more likely to have atypical AN than patients with premorbid BMI% < 85th. Premorbid BMIz explained 57% and 39% of the variance in admission BMIz and weight loss, respectively. Discussion Findings support a homogenous model of AN and atypical AN, with weight loss predicted by premorbid BMI in both illnesses. Accordingly, premorbid BMI and weight loss (versus presenting BMI) may better denote the presence of an AN‐like phenotype across the weight spectrum. Findings also suggest that differentiating diagnoses with BMI% < 5th requires that youth with higher BMIs lose disproportionately more weight for an AN diagnosis. This is problematic given unique treatment barriers experienced in atypical AN. Public significance Anorexia nervosa (AN) and atypical AN are considered distinct conditions in youth, with differential diagnosis hinging upon a presenting weight status of ‘underweight’ (i.e., BMI percentile for age‐and‐sex (BMI%) < 5th). In our study, youth with premorbid ‘overweight/obesity’ (BMI% ≥ 85th) disproportionately remained above this threshold, despite similar weight loss. Coupled with prior evidence for commensurate characteristics and sequelae in both diagnoses, we propose that DSM‐5 differentiation of AN and atypical AN inadvertently reinforces weight stigma and may contribute to treatment disparities in atypical AN.

AbstractBackgroundFood intake is regulated by homeostatic and hedonic systems that interact in a complex neuro‐hormonal network. Dysregulation in energy intake can lead to obesity (OB) or anorexia nervosa (AN). However, little is known about the neurohormonal response patterns to food intake in normal weight (NW), OB, and AN.Material & MethodsDuring an ad libitum nutrient drink (Ensure®) test (NDT), participants underwent three pseudo‐continuous arterial spin labeling (pCASL) MRI scans. The first scan was performed before starting the NDT after a > 12 h overnight fast (Hunger), the second after reaching maximal fullness (Satiation), and the third 30‐min after satiation (postprandial fullness). We measured blood levels of ghrelin, cholecystokinin (CCK), glucagon‐like peptide (GLP‐1), and peptide YY (PYY) with every pCASL‐MRI scan. Semiquantitative cerebral blood flow (CBF) maps in mL/100 gr brain/min were calculated and normalized (nCBF) with the CBF in the frontoparietal white matter. The hypothalamus (HT), nucleus accumbens [NAc] and dorsal striatum [DS] were selected as regions of interest (ROIs).ResultsA total of 53 participants, 7 with AN, 17 with NW (body‐mass index [BMI] 18.5–24.9 kg/m2), and 29 with OB (BMI ≥30 kg/m2) completed the study. The NW group had a progressive decrease in all five ROIs during the three stages of food intake (hunger, satiation, and post‐prandial fullness). In contrast, participants with OB showed a minimal change from hunger to postprandial fullness in all five ROIs. The AN group had a sustained nCBF in the HT and DS, from hunger to satiation, with a subsequent decrease in nCBF from satiation to postprandial fullness. All three groups had similar hormonal response patterns with a decrease in ghrelin, an increase in GLP‐1 and PYY, and no change in CCK.ConclusionConditions of regulated (NW) and dysregulated (OB and AN) energy intake are associated with distinctive neurohormonal activity patterns in response to hunger, satiation, and postprandial fullness.

The striking rise in adolescent eating disorders since the severe acute respiratory coronavirus syndrome 2 pandemic has amplified demands for specialty eating disorders services and contributed to protracted delays in care. In the context of these delays, patients are at risk for increased weight loss, medical instability, escalating disease progression and poor prognosis. Primary care providers (PCPs) are frequently the first point of contact for young patients with eating disorders and are often left to bridge the gap while families struggle to establish specialty care. Yet, beyond case detection and medical comanagement, there are no evidence-based guidelines that can assist PCPs to prepare families for treatment, halt disease progression, and begin the lengthy process of weight and nutritional restoration in efforts to reduce medical complications and support a favorable prognosis. We present the case of a 13-year-old girl with a restrictive eating disorder to illustrate how PCPs can use intervention principles and strategies derived from evidence-based eating disorder treatment to successfully manage adolescent patients until they can access specialty treatment. We offer concrete guidelines for decision-making, as well as suggested behavioral and medical interventions for the PCP. With evidence-based tools, PCPs are well-positioned to support young patients with restrictive eating disorders and their family members as they begin the process of recovery from an eating disorder.

ABSTRACT: Background: When adolescents present with symptoms of unexplained weight loss, underweight, or poor appetite, eating disorders (EDs) are commonly on the list of differential diagnoses. However, the relationship of these symptoms to other psychiatric disorders is often less clear. Methods: Using the Rochester Epidemiology Project database, a retrospective cohort study of adolescents (13–18 years) with billing diagnoses of weight loss, underweight, or loss of appetite was conducted between January 2005 and December 2017. Patients who presented with conditions commonly associated with weight loss, underweight, or poor appetite (e.g., cancer) were excluded. This study sought to examine the proportion of patients who received ED and psychiatric diagnoses within 5 years of the index visit and patient characteristics associated with these diagnoses. Results: Of 884 patients diagnosed with symptoms of unexplained weight loss, underweight, or poor appetite, 662 patients (M age = 15.8; SD = 1.6; 66.0% female) met study criteria. Within 5 years of the index visit, the lifetime prevalence of all psychiatric disorders was 70% (n = 461) and of EDs was 21% (n = 141). For both psychiatric disorders and EDs, sex and race were significantly associated with receiving a diagnosis within 5 years. Decrease in body mass index (BMI) percentile was associated with receiving an ED diagnosis, whereas the highest historical BMI percentile was associated with receiving a psychiatric diagnosis. Conclusion: Patients presenting with symptoms of unexplained weight loss, underweight, or poor appetite are at risk not only for EDs but also for other psychiatric disorders that may require further assessment and follow-up.

AbstractBackgroundIntegrative Cognitive Affective Therapy (ICAT) is an empirically supported treatment for bulimia nervosa (BN) in adults. However, it is unclear whether a modified version, Integrative Cognitive Affective Therapy–Adolescent (ICAT‐A) is feasible and beneficial for adolescents. This study evaluated the feasibility of ICAT‐A for adolescents with BN or subthreshold BN.MethodsEight adolescents with BN or subthreshold BN (mean age = 16.1) were enroled in the study. At baseline and end of treatment, adolescents who participated in ICAT‐A completed the Eating Disorder Examination (EDE) and self‐report measures of eating disorder symptoms, depression, anxiety, self‐esteem and functional impairment.ResultsRetention for the intervention (75%) suggests that the majority of participants found the intervention acceptable. Although all treatment completers participated in the clinician‐administered assessment (EDE), compliance with end of treatment self‐report questionnaires was compromised by the COVID‐19 pandemic, which occurred during the treatment course of the majority of the sample. At the end of treatment, all 6 adolescents who completed the ICAT‐A intervention were in full eating disorder remission based on EDE scores, with large effect sizes identified for reductions in EDE global scores (d = 2.71), objective binge episodes (d = 0.91), subjective binge episodes (d = 1.06) and compensatory behaviours (d = 1.72).ConclusionResults suggest that ICAT‐A is a feasible treatment that has promise for the treatment of adolescents with BN. Future studies are necessary to establish the efficacy of ICAT‐A for adolescent BN.