Abstract Title

Executive Cognitive Dysfunction Associated with Total Serum Protein and Bilirubin in Severe Obesity

Presenter Name

Steve Bell

RAD Assignment Number

1003

Abstract

Background: Obesity confers increased risk for several major chronic medical conditions. Studies also have suggested that obesity may carryincreased riskfor future dementia. Recent research has pointed toward obesity’s role in acceleratingage-related cognitive dysfunction; however the underlying process has not been elucidated. The purpose of this study was to explore psychological and biological parameters that may be associated with cognitive dysfunction in severe obesity.

Hypothesis: Obese subjects (OB) will have greater deficits in executive cognitive function (EXE) than normal weight controls (NW). Common psychological and biological markers that may predict EXE were explored.

Methods: Secondary data analysis of a one-year prospective study in a communitybariatricsurgical setting. OB (n=71) (Mean age=44.6 years, Mean BMI=43 kg/m2) underwent pre- and post-surgical assessments. NW matched for age and gender (n=30) were assessed for comparison.Self-report surveyassessed indicators of psychological dysfunction. Fasting blood samples were taken to analyze common clinical indicators. TheStrooptest was used to determine EXE.Independent t-testwas used to analyze EXE between OB and NW. Relationships between EXE with biological and psychological indicators were explored using Pearson correlation.Significantlycorrelated variables were used in logistic regression to ascertain their ability to predict high or low EXE. Repeated measure t-tests were used to compare changes for OB in EXE at one-year post-surgery.

Results: OB hadsignificantly lower EXEthan NW at baseline (t=-2.491, p=.017). EXE was significantly correlated with Total Protein (r=-.279, p=.015) and Total Bilirubin (r=.327, p=.004). Logistic regression for Protein and Bilirubin was significant in predicting cognitive status (X2=8.117, p=.017). Individually each approached significance (Protein p=.060, Bilirubin p=.059). EXE was improved for OB at one year post-surgery EXE (t=-3.216, p=.004).

Conclusion: Increases in Total Protein and decreases in Total Bilirubin may be earlybiomarkersof executive dysfunction in severe obesity. These associations may represent distal markers of higher inflammation and lower antioxidant status and are consistent with other work on possible mechanisms for neuropsychiatric sequelae of obesity. Weight loss may ameliorate cognitive risk.

Presentation Type

Poster

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Executive Cognitive Dysfunction Associated with Total Serum Protein and Bilirubin in Severe Obesity

Background: Obesity confers increased risk for several major chronic medical conditions. Studies also have suggested that obesity may carryincreased riskfor future dementia. Recent research has pointed toward obesity’s role in acceleratingage-related cognitive dysfunction; however the underlying process has not been elucidated. The purpose of this study was to explore psychological and biological parameters that may be associated with cognitive dysfunction in severe obesity.

Hypothesis: Obese subjects (OB) will have greater deficits in executive cognitive function (EXE) than normal weight controls (NW). Common psychological and biological markers that may predict EXE were explored.

Methods: Secondary data analysis of a one-year prospective study in a communitybariatricsurgical setting. OB (n=71) (Mean age=44.6 years, Mean BMI=43 kg/m2) underwent pre- and post-surgical assessments. NW matched for age and gender (n=30) were assessed for comparison.Self-report surveyassessed indicators of psychological dysfunction. Fasting blood samples were taken to analyze common clinical indicators. TheStrooptest was used to determine EXE.Independent t-testwas used to analyze EXE between OB and NW. Relationships between EXE with biological and psychological indicators were explored using Pearson correlation.Significantlycorrelated variables were used in logistic regression to ascertain their ability to predict high or low EXE. Repeated measure t-tests were used to compare changes for OB in EXE at one-year post-surgery.

Results: OB hadsignificantly lower EXEthan NW at baseline (t=-2.491, p=.017). EXE was significantly correlated with Total Protein (r=-.279, p=.015) and Total Bilirubin (r=.327, p=.004). Logistic regression for Protein and Bilirubin was significant in predicting cognitive status (X2=8.117, p=.017). Individually each approached significance (Protein p=.060, Bilirubin p=.059). EXE was improved for OB at one year post-surgery EXE (t=-3.216, p=.004).

Conclusion: Increases in Total Protein and decreases in Total Bilirubin may be earlybiomarkersof executive dysfunction in severe obesity. These associations may represent distal markers of higher inflammation and lower antioxidant status and are consistent with other work on possible mechanisms for neuropsychiatric sequelae of obesity. Weight loss may ameliorate cognitive risk.