Identification of State Markers in Anorexia Nervosa: Replication and Extension of Inflammation-Associated Biomarkers Using Multiplex Profiling.

Background: Proteomics offers potential for detecting and monitoring anorexia nervosa (AN) and its variant, atypical AN (atyp-AN). However, research has been limited by small protein panels, a focus on adult AN, and lack of replication. Methods: In this study, we performed Olink multiplex profiling of 92 inflammation-related proteins in females with AN/atyp-AN (n = 64), all of whom were ≤90% of expected body weight, and age-matched healthy control individuals (n = 44). Results: Five proteins differed significantly between the primary AN/atyp-AN group and the healthy control group (lower levels: HGF, IL-18R1, TRANCE; higher levels: CCL23, LIF-R). The expression levels of 3 proteins (lower IL-18R1, TRANCE; higher LIF-R) were uniquely disrupted in participants with AN in our primary model. No unique expression levels emerged for atyp-AN. In the total sample, 12 proteins (ADA, CD5, CD6, CXCL1, FGF-21, HGF, IL-12B, IL18, IL-18R1, SIRT2, TNFSF14, TRANCE) were positively correlated with body mass index and 5 proteins (CCL11, FGF-19, IL8, LIF-R, OPG) were negatively correlated with body mass index in our primary models. Conclusions: Our results replicate the results of a previous study that demonstrated a dysregulated inflammatory status in AN and extend those results to atyp-AN. Of the 17 proteins correlated with body mass index, 11 were replicated from a previous study that used similar methods, highlighting the promise of inflammatory protein expression levels as biomarkers of AN disease monitoring. Our findings underscore the complexity of AN and atyp-AN by highlighting the inability of the identified proteins to differentiate between these 2 subtypes, thereby emphasizing the heterogeneous nature of these disorders.

We examined 73 inflammation proteins in adolescent girls with anorexia nervosa (AN) and atypical AN and compared them with age-matched healthy control girls. Significant differences were found, driven by 5 key proteins (lower: HGF, IL-18R1, TRANCE; higher: CCL23, LIF-R). Three proteins (TRANCE, LIF-R, IL-18R1) uniquely distinguished low-weight participants with AN from control participants. Our study reveals distinct inflammation patterns in AN and atypical AN and sheds light on potential state-specific factors that underlie these disorders.

Identification of State Markers in Anorexia Nervosa: Replication and Extension of Inflammation Associated Biomarkers Using Multiplex Profiling in Anorexia Nervosa and Atypical Anorexia Nervosa.

Proteomics provides an opportunity for detection and monitoring of anorexia nervosa (AN) and its related variant, atypical-AN (atyp-AN). However, research to date has been limited by the small number of proteins explored, exclusive focus on adults with AN, and lack of replication across studies. This study performed Olink Proseek Multiplex profiling of 92 proteins involved in inflammation among females with AN and atyp-AN (N = 64), all < 90% of expected body weight, and age-matched healthy controls (HC; N=44). After correction for multiple testing, nine proteins differed significantly in the AN/atyp-AN group relative to HC group ( lower levels: CXCL1, HGF, IL-18R1, TNFSF14, TRANCE; higher levels: CCL23, Flt3L, LIF-R, MMP-1). The expression levels of three proteins ( lower IL-18R1, TRANCE; higher LIF-R) were uniquely disrupted in females with AN. No unique expression levels emerged for atyp-AN. Across the whole sample, twenty-one proteins correlated positively with BMI (ADA, AXIN1, CD5, CD244, CD40, CD6, CXCL1, FGF-21, HGF, IL-10RB, IL-12B, IL18, IL-18R1, IL6, LAP TGF-beta-1, SIRT2, STAMBP, TNFRSF9, TNFSF14, TRAIL, TRANCE) and six (CCL11, CCL23, FGF-19, IL8, LIF-R, OPG) were negatively correlated with BMI. Overall, our results replicate the prior study demonstrating a dysregulated inflammatory status in AN, and extend these results to atyp-AN (AN/atyp-AN all < 90% of expected body weight). Of the 27 proteins correlated with BMI, 18 were replicated from a prior study using similar methods, highlighting the promise of inflammatory protein expression levels as biomarkers of disease monitoring. Additional studies of individuals across the entire weight spectrum are needed to understand the role of inflammation in atyp-AN.

Accountability in promoting representation of historically marginalized racial and ethnic populations in the eating disorders field: A call to action.

Promoting representation of historically marginalized racial and ethnic populations in the eating disorders (EDs) field among professionals and the populations studied and served has long been discussed, with limited progress. This may be due to a reinforcing feedback loop in which individuals from dominant cultures conduct research and deliver treatment, participate in research, and receive diagnoses and treatment. This insularity maintains underrepresentation: EDs in historically marginalized populations are understudied, undetected, and undertreated. An Early Career Investigators Workshop generated recommendations for change that were not inherently novel but made apparent that accountability is missing. This paper serves as a call to action to spearhead a paradigm shift from equality to equity in the ED field. We provide a theoretical framework, suggest ways to disrupt the feedback loop, and summarize actionable steps to increase accountability in ED leadership and research toward enhancing racial/ethnic justice, equity, diversity, and inclusion (JEDI). These actionable steps are outlined in the service of challenging our field to reflect the diversity of our global community. We must develop and implement measurable metrics to assess our progress toward increasing diversity of underrepresented racial/ethnic groups and to address JEDI issues in our providers, patients, and research participants.

Change in normative eating self-efficacy is associated with six-month weight restoration following inpatient treatment for anorexia nervosa.

Anorexia nervosa (AN) is a disorder characterized by rigid and restrictive eating behaviors, resulting in significantly low body weight. While specialized behavioral intensive treatment programs can reliably support individuals with AN to normalize eating and weight control behaviors and achieve weight restoration, prognostic factors predicting relapse following treatment are unclear. We examined whether changes in (i) normative eating self-efficacy, (ii) body image self-efficacy, (iii) drive for thinness, and (iv) body dissatisfaction from inpatient admission to six-month follow-up were associated with weight restoration status at program discharge and at six-month follow-up. The sample comprised 146 participants with AN admitted to a meal-based inpatient-partial hospitalization program. Participants completed questionnaires at inpatient admission and six months following program discharge. Additionally, at follow-up, participants reported the frequency of engaging in normalized eating behaviors since discharge (e.g. eating with others and preparing a balanced meal). The majority (73.3%) of participants attained a BMI > 19 at discharge and 59.6% were weight restored at six-month follow-up. Change in normative eating self-efficacy was significantly associated with weight restoration at follow-up, whereas change in body image self-efficacy, drive for thinness, and body dissatisfaction were not. For each one unit increase in normative eating self-efficacy, patients were 4.65 times more likely to be weight restored at follow-up (p = .002). Additionally, individuals reporting a higher frequency of normalized eating behaviors at follow-up were more likely to be weight restored. Normative eating self-efficacy and normalized eating behaviors may represent vital treatment targets for relapse prevention interventions for this high-risk population.