Pediatric Loss of Control Eating and High-Sensitivity C-Reactive Protein Concentrations

Shank, Lisa M.; Tanofsky‐Kraff, Marian; Kelly, Nichole R.; Schvey, Natasha A.; Marwitz, Shannon E.; Mehari, Rim D.; Brady, Sheila M.; Demidowich, Andrew P.; Broadney, Miranda M.; Galescu, Ovidiu; Pickworth, Courtney K.; Yanovski, Susan Z.; Yanovski, Jack A.

doi:10.1089/chi.2016.0199

Cited by 28 publications

(22 citation statements)

References 75 publications

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“…Indeed, prior studies show that snack intake better distinguishes youth with LOC eating from youth without LOC eating than total intake [14, 15], and may account for the associations between LOC eating and metabolic syndrome components [10] and C-reactive protein, a measure of chronic inflammation [9]. Thus, impacting dessert and snack food intake, specifically, may be an important target of excess weight gain prevention.…”

Section: Discussionmentioning

confidence: 99%

“…The endorsement of recent LOC eating is associated with greater depressive and anxiety symptoms [2–4], lower self-esteem [5, 6], higher likelihood of overweight and obesity [7], more physiological markers of stress [8, 9], and a greater odds of presenting with components of the metabolic syndrome [10]. Of particular concern are data demonstrating that LOC eating places youth at undue risk for excess weight and fat gain [11, 12] and exacerbation of metabolic syndrome components [13].…”

Section: Introductionmentioning

confidence: 99%

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Examination of the interpersonal model of loss of control eating in the laboratory

Shank

Crosby

Grammer³

et al. 2017

Comprehensive Psychiatry

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Background The interpersonal model of loss of control (LOC) eating proposes that interpersonal problems lead to negative affect, which in turn contributes to the onset and/or persistence of LOC eating. Despite preliminary support, there are no data examining the construct validity of the interpersonal model of LOC eating using temporally sensitive reports of social stress, distinct negative affective states, and laboratory energy intake. Method 117 healthy adolescent girls (BMI: 75th–97th %ile) were recruited for a prevention trial targeting excess weight gain in adolescent girls who reported LOC eating. Prior to the intervention, participants completed questionnaires of recent social stress and consumed lunch from a multi-item laboratory test meal. Immediately before the test meal, participants completed a questionnaire of five negative affective states (anger, confusion, depression, fatigue, anxiety). Bootstrapping mediation models were conducted to evaluate pre-meal negative affect states as explanatory mediators of the association between recent social stress and palatable (desserts and snack-type) food intake. All analyses adjusted for age, race, pubertal stage, height, fat mass percentage, and lean mass. Results Pre-meal state anxiety was a significant mediator for recent social stress and palatable food intake (ps < .05). By contrast, pre-meal state anger, confusion, depression, and fatigue did not mediate the relationship between social stress and palatable food intake (ps > .05). Discussion Pre-meal anxiety appears to be the salient mood state for the interpersonal model among adolescent girls with LOC eating. Interventions that focus on improving both social functioning and anxiety may prove most effective at preventing and/or ameliorating disordered eating and obesity in these adolescents.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Examination of the interpersonal model of loss of control eating in the laboratory

Shank

Crosby

Grammer³

et al. 2017

Comprehensive Psychiatry

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“…youth (Shank et al, 2017) who report LOC eating have increased markers of inflammation relative to their peers. It is important for future research to examine how LOC eating impacts specific components of metabolic health.…”

Section: Discussionmentioning

confidence: 99%

“…It is also possible that LOC eating impacts cardiometabolic health through nonspecific pathways, such as inflammation. Cross‐sectional analyses have shown that adults (Succurro et al, ) and youth (Shank et al, ) who report LOC eating have increased markers of inflammation relative to their peers. It is important for future research to examine how LOC eating impacts specific components of metabolic health.…”

Section: Discussionmentioning

confidence: 99%

Remission of loss of control eating and changes in components of the metabolic syndrome

Shank

Tanofsky‐Kraff

Radin

et al. 2018

Intl J Eating Disorders

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Objective Pediatric loss of control (LOC) eating prospectively predicts the worsening of metabolic syndrome components. However, it is unknown if remission of LOC eating is associated with improvements in metabolic health. Therefore, we conducted a secondary analysis of a trial that enrolled adolescent girls with LOC eating, examining whether LOC remission (vs. persistence) at end-of-treatment was associated with changes in metabolic syndrome components at 6-month follow-up. Method One hundred three adolescent girls (age 14.5±1.7y; BMI-z 1.5±0.3; 56.3% non-Hispanic White, 24.3% non-Hispanic Black) with elevated weight (75th-97th BMI %ile) and reported LOC eating were assessed for metabolic syndrome components at baseline and again six months following the interventions. The main effects of LOC status at end-of-treatment (persistence vs. remission) on metabolic syndrome components (waist circumference, lipids, glucose, and blood pressure) at 6-month follow-up were examined, adjusting for baseline age, depressive symptoms, LOC frequency, fat mass, and height, as well as race, change in height, change in fat mass, and the baseline value of each respective component. Results Youth with LOC remission at end-of-treatment had lower glucose (83.9±6.4 vs. 86.5±5.8 mg/dL; p = .02), higher high-density lipoprotein cholesterol (50.3±11.8 vs. 44.8±11.9 mg/dL; p = .01), and lower triglycerides (84.4±46.2 vs. 96.9±53.7 mg/dL; p = .02) at 6-month follow-up compared to youth with persistent LOC, despite no baseline differences in these components. No other component significantly differed by LOC eating status (ps > .05). Discussion Reducing LOC eating in adolescent girls may have a beneficial impact on some components of the metabolic syndrome.

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“…All-in-all, it is intriguing to note that independent sources have now pinpointed that easy access to hyper-caloric/ industrially manipulated food has posed the basis for the rise of childhood obesity. This early pathologic weight gain, in turn, has been recognized as the one factor in the increase of the inflammatory tune [71], a chronic bias that seems to pervade us since early in life. Indeed, this inflammatory background might be the reason to thrive for IBD and the tens of the inflammatory "Western" disorders named above These profound changes, as expected, have significantly impacted our overwhelming microbiome population, which, as emphasized above, crowds our gut with some 10 4 microbic individuals.…”

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confidence: 99%

The gut immune system, inflammatory bowel diseases, and the body immune homeostasis: modern treatment strategies

Actis¹

2016

Prog Health Sci

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The digestive tract is nowadays conceived as a barrier organ constituted by a mucosal membrane separating the gut lumen from the inner milieu. The gut lumen is laden by a myriad of antigens brought about by the diet, but also pertaining to the overwhelming bacterial species of the gut microbiome. The mucosal cell population comprehends epithelial cells, and a variety of immune reactive cells. Of them, the mononuclear types effecting innate responses are endowed by membrane signaling receptors and, as a rule, are sensing the polysaccharides of bacterial cell walls; non-tolerated signals may then push the chain reaction on, to end in full activation of inflammation mediators. Acquired immunity is in turn mainly effected by T-cell types, some of them, behaving as autoreactive cells, may induce metastatic inflammation beyond bowel boundaries, partly explaining the so-called extra-intestinal manifestations of inflammatory bowel disease (IBD). The scenario is further complicated by the possible influence of epigenetic factors: diet, stress, smoking, drugs. Being IBD a low-penetrance disorder, for the full phenotype to develop, a critical mass of the above listed factors (typically, a disturbed membrane permeability, an immune stimulus, and an epigenetic factor) must occur. In the century since the full description of IBD, a variegated plethora of measures have been attempted. Some updated designs are now under scrutiny. Microbiota engineering, apoptosis modulation, and diet modification are just a few of the measures that we are arbitrarily describing here.

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Pediatric Loss of Control Eating and High-Sensitivity C-Reactive Protein Concentrations

Cited by 28 publications

References 75 publications

Examination of the interpersonal model of loss of control eating in the laboratory

Examination of the interpersonal model of loss of control eating in the laboratory

Remission of loss of control eating and changes in components of the metabolic syndrome

The gut immune system, inflammatory bowel diseases, and the body immune homeostasis: modern treatment strategies

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