Inflammatory dysregulation in women with an eating disorder: Relationships with altered emotional reactivity. Issue 10 (21st August 2021)

• Record Type: Journal Article
• Authors: Diaz‐Marsa, Marina; MacDowell, Karina; de laTorre‐Luque, Alejandro; Caso, Javier R.; Faya, Mar; Gutierrez, Silvia; Soto, Marta; Pemau, Andres; Diaz‐Carracedo, Patricia; Carrasco‐Diaz, Alvaro; Leza, Juan C.; Graell, Montserrat; Carrasco, Jose L.
• Is Part Of: International journal of eating disorders. Volume 54:Issue 10(2021)
• Page Start: 1843
• Page End: 1854
• Publication Date: 2021-08-21
• Subjects: cytokines -- eating disorder -- emotional processing -- emotional reactivity -- inflammation; Appetite disorders -- Periodicals; Ingestion disorders -- Periodicals; Eating disorders -- Periodicals; 616.8526
• DOI: 10.1002/eat.23598
• Languages: English
• ISSNs: 0276-3478

Abstract

Abstract: Background: Some studies suggest that inflammatory signaling dysregulation may contribute to eating disorder (ED) pathophysiology. However, little is known about the influence of inflammatory response on altered processes seen among patients with ED, such as emotional processing and reactivity. Objectives: The objectives were: (a) to investigate the systemic inflammatory response in ED women; and (b) to analyze the role of inflammatory markers in emotional reactivity. Method: Concentrations of several intercellular and intracellular inflammatory mediators (cytokines, prostaglandin by‐products and enzymes, TBARS, and MAPK proteins) were quantified in plasma and PBMCs from 68 women with an ED ( m = 22.01 years, SD = 9.15) and 35 healthy controls ( m = 18.54 years, SD = 4.21). Moreover, emotional reactivity to affective pictures (those without either food or thinness content) was studied using the adult (>18 years old) sample ( n = 41). Results: Between‐group differences were revealed for most markers (TNF‐α, PGE2, COX2, and ratio of activated MAPK proteins), pointing to increased inflammatory response in patients ( p < .01). Women with ED showed heightened emotional reactivity, regardless of picture valence. Principal components derived from inflammatory markers showed an explanatory loading on patient's emotional reaction, in terms of valence and arousal. Conclusion: This study corroborates the altered systemic inflammatory response in patients with ED. The inflammatory dysregulation may contribute to ED phenotype, as seen by its relationship with heightened emotional reactivity, even though the inflammatory markers were not evaluated throughout the emotional reactivity protocol.